Tag Archives: ciprofloxacin

Ciprofloxacin Depletes Exosomal DNA

Journal of Extracellular Vesicles, “Biological properties of extracellular vesicles and their physiological functions”

The study, “Antibiotic-induced release of small extracellular vesicles (exosomes) with surface-associated DNA” published in Nature, found that, “ciprofloxacin induced the release of both DNA (mitochondrial and chromosomal sequences) and DNA-binding proteins on the exofacial surfaces of small extracellular vesicles referred to in this paper as exosomes.” And, “Our results reveal for the first time that prolonged low-dose ciprofloxacin exposure leads to the release of DNA associated with the external surface of exosomes.”

In the discussion section of “Antibiotic-induced release of small extracellular vesicles (exosomes) with surface-associated DNA” the authors expand on their findings:

“Exposure of Jurkat cells to ciprofloxacin has been shown to induce oxidative stress, production of reactive oxygen species, mitochondrial dysfunction, inhibition of the respiratory chain and decrease of mitochondrial membrane potential leading to mitophagy47. Our MS analysis has also confirmed the above biological processes in Jurkat cells. Importantly, the presence of ciprofloxacin has been reported to lead to the loss of mtDNA28, 29 and an aneuploidy caused by the genotoxic stress of Jurkat cells30, 48. Genotoxic stress response has been shown to induce the release of nucleosomes by leukemic myeloid cells49. In the present study, mitochondrial damage of ciprofloxacin-exposed Jurkat cells has been evidenced by the abundance of mtDNA, and the nucleoid protein FEN1, as well as numerous other mitochondrial proteins in the secreted vesicles. Ciprofloxacin inhibits both the bacterial DNA gyrase and the mammalian topoisomerase II enzymes responsible for proper DNA replication50. Given that ciprofloxacin mainly inhibits the mitochondrial isoform of mammalian topoisomerase II29, its presence induces mtDNA fragmentation as well as subsequent gradual decrease in mtDNA content29.”

And also note that:

“We found that the exosomal DNA release-inducing effect was not solely observed in the case of Jurkat cells as we also detected ciprofloxacin-induced release of exofacial EV DNA in the case of the pancreatic cancer cell line MiaPaCa. These results demonstrate that DNA-associated EVs may be released from various types of cells after long-term ciprofloxacin exposure.”

These findings are interesting, and I think consequential and explanatory.

But, I am guessing that most people reading this need some more information about what the excerpts above mean. I know I did (and I had to read it about five times).

First, understanding “Antibiotic-induced release of small extracellular vesicles (exosomes) with surface-associated DNA” requires a little knowledge of what extracellular vesicles and exosomes are.

Extracellular vesicles (EVs) are “lipid bilayer-delimited particles that are naturally released from a cell and, unlike a cell, cannot replicate. EVs range in diameter from near the size of the smallest physically possible unilamellar liposome (around 20-30 nanometers) to as large as 10 microns or more, although the vast majority of EVs are smaller than 200 nm. They carry a cargo of proteins, nucleic acids, lipids, metabolites, and even organelles from the parent cell. Most cells that have been studied to date are thought to release EVs, including some bacterial, fungal, and plant cells that are surrounded by cell walls. A wide variety of EV subtypes have been proposed, defined variously by size, biogenesis pathway, cargo, cellular source, and function, leading to a historically heterogenous nomenclature including terms like exosomes and ectosomes.” (Source)

Exosomes are a subtype of extracellular vesicles. “Exosomes are best defined as extracellular vesicles that are released from cells upon fusion of an intermediate endocytic compartment, the multivesicular body (MVB), with the plasma membrane.” (Source) More information (that’s only basic if you have a heavy science background) about exosomes can be found in “Q&A: What are exosomes, exactly?

Basically, they’re molecules secreted from cells that affect other cells (sometimes positively, sometimes negatively).

Here’s a series of videos that give a really high-level, shiny and high-production-value explanation of exosomes and extracellular vesicles:

Additionally, here are some interesting tidbits about extracellular vesicles (EVs) and exosomes gathered from various articles:

“In the past decade, extracellular vesicles (EVs) have been recognized as potent vehicles of intercellular communication, both in prokaryotes and eukaryotes. This is due to their capacity to transfer proteins, lipids and nucleic acids, thereby influencing various physiological and pathological functions of both recipient and parent cells. While intensive investigation has targeted the role of EVs in different pathological processes, for example, in cancer and autoimmune diseases, the EV-mediated maintenance of homeostasis and the regulation of physiological functions have remained less explored.” (Source)

“EVs alone regulated the expression of numerous genes related to inflammation and signaling.” (Source)

“EVs are carriers of pathogen-associated and damage-associated molecular patterns, cytokines, autoantigens and tissue-degrading enzymes. In addition to a possible role in the pathogenesis of a number of inflammatory conditions, such as infections and autoimmune diseases, EVs, including microvesicles (also known as microparticles), exosomes and apoptotic vesicles, have therapeutic potential and might be used as biomarkers for inflammatory diseases.” (Source)

“another significant role of EVs has emerged in the removal of unwanted molecular material as a means for cell maintenance.” (Source)

“This report is the first show that numbers of blood-derived EVs are elevated in patients suffering from CFS/ME, indicating their potential involvement in disease pathogenesis. This promising finding may not only provide insights into the mechanisms involved in the disease but also shows that EVs may be useful for early diagnosis of illness. Moreover, isolation of circulating EVs coupled to our prototype for their detection by LFIA may constitute a powerful diagnostic tool, which can be performed in a single step and in minutes. We concluded that EVs may play a critical role in CFS/ME. Studies with larger sample size, outcome measures and different study designs (i.e. cross-sectional vs. longitudinal cohorts) are now urgently needed. These studies should stratify subgroups according to illness onset and progression, and assess patients at baseline and following induction of post-exertional malaise (PEM), using the 2-day cardiopulmonary exercise test (CPET).” (Source)

“Mast cells, being capable of both degranulation and subsequent recovery, have recently attracted substantial attention as also being rich sources of secreted extracellular vesicles (including exosomes and microvesicles).” (Source)

Both extracellular vesicles and exosomes contribute to processes that are related to many illnesses (including multi-symptom chronic illnesses like ME/CFS and autoimmune diseases, as well as cancer), as well as some of the processes behind those diseases such as inflammation, mast cell activation, cellular signaling and communication, etc. Neither extracellular vessicles nor exosomes are bad though – they are neither good nor bad. They are a natural function, and their relationship to these disease processes may be to spread the disease or prevent the disease, depending on many more factors than I can even begin to fathom.

I surmise and assume though, that removal and depletion of DNA from exosomes, is not a healthy or productive thing to do. And as this study showed, ciprofloxacin, and probably other fluoroquinolones, remove/deplete DNA from exosomes.

Can the removal of DNA from exosomes trigger inflammation? Can the depletion of DNA from exosomes change the inter-cellular communication in ways that trigger illnesses? Extracellular vesicles and exosomes are involved with the immune system, so can depletion of DNA from exosomes trigger immune dysregulation or autoimmune diseases? In depleting DNA from exosomes, does ciprofloxacin trigger disease? We know that ciprofloxacin can trigger multi-symptom chronic illness – is the depletion of exosomal DNA the mechanism through which it “floxes” people?

I don’t know the answers to those questions, and I doubt that the scientists who know much more about cellular processes than I do know those answers either. But “Antibiotic-induced release of small extracellular vesicles (exosomes) with surface-associated DNA” raises some really interesting questions, and provides some interesting and insightful links for those of us who are exploring what occurs in the body of a “floxed” person.

Sources*:

Nature, “Antibiotic-induced release of small extracellular vesicles (exosomes) with surface-associated DNA

BMC Biology, “Q&A: What are exosomes, exactly?

Journal of Extracellular Vesicles, “Biological properties of extracellular vesicles and their physiological functions

Cellular and Molecular Life Sciences, “Critical role of extracellular vesicles in modulating the cellular effects of cytokines.

Nature Reviews. Rheumatology., “Emerging role of extracellular vesicles in inflammatory diseases.

Journal of Extracellular Vesicles, “Circulating extracellular vesicles as potential biomarkers in chronic fatigue syndrome/myalgic encephalomyelitis: an exploratory pilot study

Seminars in Cell and Developmental Biology, “Mast cell secretome: Soluble and vesicular components.

*I found these sources through the post “Nature’s Quinolones: The 4Qs” on FluoroquinoloneThyroid.com – you should check it out – it’s great.

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New Study Finds that Ciprofloxacin Depletes Mitochondrial DNA

An excellent article about the effects of ciprofloxacin (a fluoroquinolone antibiotic) on mitochondrial DNA was recently published in the journal, Nucleic Acids Research. The article, Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2, by Anu Hangas, Koit Aasumets, Nina J Kekäläinen, Mika Paloheinä, Jaakko L Pohjoismäki, Joachim M Gerhold, and Steffi Goffart, gives a great amount of insight into the damage that ciprofloxacin does to mitochondria, and I recommend that you read it (linked through the article title). I’m going to go over the article in this post, and point out some of the more interesting findings.

First, a bit of background information to help readers to understand the article.

Mitochondria are the energy centers of our cells. There are over ten million billion mitochondria in the human body (Lane p. 1). Each cell (with a few exceptions) contains an average of 300-400 mitochondria that are responsible for generating cellular energy through a process called ATP (Adenosine Triphosphate). Mitochondria regulate energy production, aging, epigenetic signaling between and within cells and many other important functions. Proper functioning of mitochondria is vital, and when mitochondria are not operating properly, a wide range of disease states can ensue (2).

Mitochondria have their own DNA (mtDNA) that is separate from (though it interacts with) nuclear DNA. The structure of mtDNA is similar to that of bacterial DNA, and it is widely thought that mitochondria descended from ancient bacteria. The similarities between bacteria and mitochondria should make everyone take pause to think about how antibiotics of all kinds are affecting mitochondrial health. This post, and the article that it is based on, only focuses on the effects of ciprofloxacin, a fluoroquinolone antibiotic, on mitochondrial health, but if you want to read about the effects of other antibiotics on mitochondria, the article “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells” is a great place to start.

There are enzymes in our cells called topoisomerases. According to the wikipedia article for topoisomerase:

Topoisomerases are enzymes that participate in the overwinding or underwinding of DNA. The winding problem of DNA arises due to the intertwined nature of its double-helical structure. During DNA replication and transcription, DNA becomes overwound ahead of a replication fork. If left unabated, this torsion would eventually stop the ability of DNA or RNA polymerases involved in these processes to continue down the DNA strand.

In order to prevent and correct these types of topological problems caused by the double helix, topoisomerases bind to DNA and cut the phosphate backbone of either one or both the DNA strands. This intermediate break allows the DNA to be untangled or unwound, and, at the end of these processes, the DNA backbone is resealed again. Since the overall chemical composition and connectivity of the DNA do not change, the DNA substrate and product are chemical isomers, differing only in their global topology, resulting in the name for these enzymes. Topoisomerases are isomerase enzymes that act on the topology of DNA.[1]

Bacterial topoisomerases and human topoisomerases proceed via similar mechanisms for managing DNA supercoils.

The mechanism of action for all fuoroquinolones is that they are topoisomerase interruptors. The FDA warning label for ciprofloxacin states that the mechanism of action for ciprofloxacin is, “The bactericidal action of ciprofloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination.”

Here is a video that describes how fluoroquinolones work, and how they interrupt topoisomerase and thus interrupt the process of bacterial (and mitochondrial, as we shall discuss below) DNA replication.

I have argued, and I believe, that EVERY drug that is a topoisomerase interruptor, should be thought of as a chemotherapy drug. All other topoisomerase interrupting drugs ARE chemo drugs. But fluoroquinolones are thought of as antibiotics, and handed out as if they are inconsequential. They are extremely consequential though, and they are hurting too many people. More information on fluoroquinolones being chemo drugs can be found in the post, “Cipro, Levaquin and Avelox are Chemo Drugs.”

Now to highlight some of the important parts of Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2.

The abstract of the article, Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2, notes that:

“Loss of Top2β or its inhibition by ciprofloxacin results in accumulation of positively supercoiled mtDNA, followed by cessation of mitochondrial transcription and replication initiation, causing depletion of mtDNA copy number. These mitochondrial effects block both cell proliferation and differentiation, possibly explaining some of the side effects associated with fluoroquinolone antibiotics.”

When you look into the multiple roles of mitochondria–from controlling cellular energy production to aging, and the links between mitochondrial damage and various multi-symptom chronic illnesses (from ME/CFS to autism to autoimmune diseases), yes, most definitely, the damaging effects of fluoroquinolones on mitochondria can certainly explain many, if not all, of the side effects associated with fluoroquinolone antibiotics.

The study found that, “In agreement with the in vitro assay, also HeLa cells treated with ciprofloxacin or doxorubicin rapidly accumulated supercoiled mtDNA (Figure 3A).”

This accumulation of supercoiled mtDNA led to a “change in topology” of the mitochondria, and a depletion of the mitochondrial DNA. Per the article:

“The change in topology caused by the inhibition of mitochondrial Top2 was connected with an impairment of mtDNA replication. 7S DNA, the 650bp ssDNA strand incorporated at the D-loop region of mtDNA, was rapidly depleted upon ciprofloxacin, ethidium bromide and doxorubicin treatment.”

Ciprofloxacin treatment not only depleted mtDNA, it also inhibited mtDNA synthesis:

“ciprofloxacin treatment reduced mtDNA copy number by 18% within 3 days (Figure 3C). As at the same time the growth rate of ciprofloxacin-treated cells was strongly reduced doubling time 170.2 h versus 22.7 h in untreated controls (Supplementary Figure S4), the observed depletion reflects a nearly complete inhibition of mtDNA synthesis.”

Ciprofloxacin treatment, and the resulting supercoiled mtDNA, also stalled mtDNA replication.

“Ciprofloxacin caused a strong reduction in these intermediates already after 2 h treatment (Figure 3E). After 20 h, this effect was clearly enhanced, with the strand-asynchronous intermediates being replaced by strand-coupled replication intermediates, a hallmark of mtDNA replication stalling (25,31–33).”

It was also found that ciprofloxacin inhibited the increase of mtDNA that typically comes with building muscle. It was found that:

“The impairment of mtDNA maintenance by ciprofloxacin not only disturbed cellular proliferation and the physiological increase of mtDNA copy number during muscle maturation, it also effectively impaired the fusion of confluent myoblasts to multinuclear myotubes (Figure 4E) and cell differentiation as indicated by the reduced expression of the heavy chain of Myosin II, a marker of differentiated skeletal muscle (Figure 4F).”

In the paragraph that the above quote was taken from, it was stated that “This increase (of mtDNA when muscle matures) was completely abolished by ciprofloxacin.” I’ve said it multiple times before, but, again, fluoroquinolones should NEVER be given to athletes (or anyone who values their ability to move, or have their heart beat).

In the article’s discussion section, this summary of the demonstrated damage done by ciprofloxacin was given:

“Ciprofloxacin caused a dramatic effect on mtDNA topology, blocking replication initiation, reducing copy number and inhibiting mitochondrial transcription (Figures 2B3AE and 4A). Ciprofloxacin, the third most commonly used antibacterial antibiotic, stops the cleavage/re-ligation reaction of type II topoisomerases midway, generating double-strand breaks, persistent protein–DNA adducts and reduces also the overall enzyme activity (30). Its toxicity to mitochondria has been reported in various studies, suggesting a broad range of mechanisms including topoisomerase inhibition, oxidative stress, altered calcium handling and photosensitization (38–40). In our study, we observed ciprofloxacin to clearly reduce Top2 topoisomerase activity both in vitro and in vivo, but did not find any indication of increased mtDNA double-strand breaks (Figure 3AC). However, ciprofloxacin did impair the overall mtDNA integrity in post-mitotic cells (Figure 4D). As our detection method (long-range PCR) does not distinguish between strand-breaks, abasic sites or base alterations inhibiting Taq polymerase, the observed effect might be caused by oxidative damage, which fluoroquinolones have been reported to induce in a variety of cell types (41,42).”

And the study’s authors also surmise that many of the severe adverse effects of fluoroquinolones are due to the depletion of mtDNA caused by the drugs:

“The severe side effects of ciprofloxacin and other fluoroquinolones include tendinopathies such as tendon rupture, joint inflammation, muscle weakness, central and peripheral neuropathies, epilepsy and psychological symptoms such as depression. These symptoms have been proposed to be connected to enhanced oxidative stress (42,54,55), but the molecular mechanism remained unclear. The reduction of mtDNA copy number and mitochondrial transcription caused by the altered topology of mtDNA might result in severe dysregulation of the electron transport chain complexes, as known to occur under ciprofloxacin treatment (56), lead to respiratory chain dysfunction and cause the observed enhanced oxidative stress.

Ciprofloxacin has also been reported to interfere with physiologically significant cell differentiation processes, such as spermatogenesis (57), brain development (41), bone mineralization (58), as well as to induce renal toxicity and heart arrhythmia (59). While the molecular mechanisms of these adverse effects are yet unclear, mitochondria play a central role in all of these physiological processes, making mitochondrial impairment a likely culprit for the disturbed cellular physiology.”

Throughout the article, the effects of ciprofloxacin are compared to the effects of another topoisomerase interrupting drug, doxorubicin. Per its wikipedia post, Doxorubicin “is a chemotherapy medication used to treat cancer.[3] This includes breast cancer, bladder cancer, Kaposi’s sarcoma, lymphoma, and acute lymphocytic leukemia.” The authors of Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2 noted that, “Interestingly, doxorubicin had a similar, but milder inhibitory effect on mtDNA replication than ciprofloxacin.” Why, yes, it is interesting that a drug that is marketed and dispensed as an antibiotic is more damaging than a similar drug that is marketed and dispensed as a chemotherapy drug. It’s very interesting indeed. It is also interesting that another topoisomerase interrupting chemotherapeutic drug, topotecan, was found to increase the expression of genes related to autism (“Topoisomerases facilitate transcription of long genes linked to autism“).

The Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2, authors conclude their article with two points. First, that very little is known about the consequences of mtDNA supercoiling. “Although central in bacterial genome maintenance, the whole phenomena of DNA supercoiling and its functional implications are virtually unstudied in mitochondria and calls for future research.” Yes, future research is needed, and better late than never. But nalidixic acid, the backbone of all fluoroquinolone antibiotics, was first used clinically in 1967. Shame on the medical and scientific communities for not studying the effects of fluoroquinolones on mtDNA earlier. We should have known more about the consequences of these drugs long before millions of prescriptions had been doled out, and millions of people affected.

Second, the authors of Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2 conclude by stating, “As fluoroquinolone antibiotics are widely used and effective drugs against a number of important bacterial pathogens, their dosage, systemic enrichment and side-effects should be reviewed in the mitochondrial context, and their clinical use should be considered with great care.” Yes, indeed, the effects of fluoroquinolones on mitochondria should be given long, hard, thoughtful consideration by every doctor, pharmacist, scientist, and every relevant person in the FDA and other regulatory agencies.

Ciprofloxacin impairs mitochondrial DNA replication initiation through inhibition of Topoisomerase 2 is an eye-opening article with groundbreaking research. Yes, more research needs to be done. But the research that has been done, that is described in the article, is greatly appreciated. Thank you to all the authors – Anu Hangas, Koit Aasumets, Nina J Kekäläinen, Mika Paloheinä, Jaakko L Pohjoismäki, Joachim M Gerhold, and Steffi Goffart.

 

Floxie Hope Podcast Episode 26 – Tamara

I had the pleasure of interviewing Tamara for Episode 26 of The Floxie Hope Podcast.

Please check out the podcast through this link:

https://itunes.apple.com/us/podcast/floxie-hope-podcast/id945226010

You can also read about Tamara’s journey:

https://floxiehope.com/tamaras-story-cipro-toxicity/

Tamara wrote her recovery story back in 2014. She has since had a beautiful, healthy, vivacious little girl, and her life has changed significantly in the last 4 years.

She speaks about her journey through fluoroquinolone toxicity, and how her life has changed in the last 4+ years since she was hurt by Cipro in this episode of The Floxie Hope Podcast.

Thank you for sharing your journey, Tamara!

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Subscriptions, reviews, and shares of The Floxie Hope Podcast are greatly appreciated! Please let me know if you have questions about how to do any of those things.

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EMA Hearing on Fluoroquinolone Toxicity Part 1

The Pharmacovigilance Risk Assessment Committee (PRAC) of the European Medicines Agency (EMA) held a hearing regarding the risks of permanent and disabling effects of fluoroquinolones (i.e. Fluoroquinolone Toxicity) on Wednesday June 13, 8018. More than 100 patient testimonials were submitted to the PRAC, and several dozen people who suffered from fluoroquinolone toxicity testified before the PRAC in-person.

The patients who testified were asked to answer three questions:

  1. What is your view on the role of quinolones and fluoroquinolones in the treatment of infections?
  2. What is your view of the risks associated with quinolone and fluoroquinolone use?
  3. In your opinion, what further measures could be taken to optimize the safe use of quinolones and fluoroquinolones?

You can watch the hearing, and listen to the patient testimonials, through this video:

All of the patient testimonials were moving, thought-provoking, and insightful. Thank you to all who testified – many of whom traveled hundreds of miles/kilometers to get to the hearing. It is because of the people who testified (including those who testified in writing) that the PRAC now knows how truly devastating fluoroquinolones are. Hopefully they will be moved to action by the testimonials provided.

A transcript of the hearing will be published, and I will link to it when it is available. In the meantime, I will highlight some of the testimonials given during the hearing. I highly recommend that you watch the video, as the words directly from the victims’ mouths are much more powerful than my synopsis.

Elizabeth Carmouche testified that she was given ciprofloxacin as a prophylactic “in case” she got a urinary tract infection or travelers’ diarrhea while on holiday. She only took two of the prescribed pills, and has been suffering from the devastating effects of those pills for more than two years. She went from being an active to a woman with no pain, to suffering from severe joint, muscle, tendon, and bone pain, as well as peripheral neuropathy. She testified that doctors were unable to help her, and many dismissed the connection between ciprofloxacin and her ill health. She asserted that the following measures need to be taken:

  1. There needs to be official recognition of fluoroquinolone toxicity syndrome, and doctors need to be made fully aware of what the syndrome entails.
  2. Bayer, and the other pharma companies that produce fluoroquinolones, need to identify the precise mechanism of damage done by fluoroquinolones, and those companies need to establish a protocol for healing those who have been hurt by fluoroquinolones.
  3. Patients damaged by fluoroquinolones should be treated and guided by medical professionals.
  4. A red-flag system needs to be put in patient records so that those who have experienced an adverse reaction to a fluoroquinolone are never given fluoroquinolones again.

In closing, Elizabeth notes that fluoroquinolones are linked to mitochondrial damage, and that mitochondrial damage is linked to many diseases including Parkinson’s, Alzheimer’s, and other serious and severe diseases.

The next presenter was a pharmacist from Northern Spain named Manex Bettan Arguinzoniz (Bettan). He was just 37 years old when ciprofoxacin destroyed his body, mind, and health. He went from being athletic and able to play with his children, to being unable to do many of the activities that he loves. Despite being a pharmacist, he was unaware of the debilitating, disabling, and devastating effects of ciprofloxacin. He also found that his doctors and other specialists were unaware of the extent of the damage done by fluoroquinolones. His doctor (who is also his father in law) was only convinced of the link between Bettan’s health problems and ciprofloxacin when another doctor who had studied at the Mayo Clinic noted the reality of the link. Bettan suggests that fluoroquinolones be restricted so that they are only used in life-or-death situations in hospitals. He suggests that a stronger, possibly black-box, warning be added so that patients are aware of the dangers of fluoroquinolones.

One of the EMA PRAC members asked Bettan if he got his information about fluoroquinolone toxicity from patient testimonials or scientific papers. He answered that he read many papers about fluorouinolones. There are hundreds of research papers about fluoroquinolones and the damage they do listed on https://floxiehope.com/fluoroquinolones-links-resources/.

The next presenter was Richard Cooknell. Richard was a firefighter before he was poisoned by quinolones. He is still unable to work, and suffers from many ill effects. He asserts that quinolones are used too widely, and that their use should be restricted to life-or-death situations. Richard points out that fluoroquinolones are often inappropriately prescribed for non-bacterial chronic prostatitis. He also points out that there is no information in the warning label about the effects of fluoroquinolones being permanently disabling, or that adverse reactions can be delayed. Richard was able to gain a diagnosis of fluoroquinolone toxicity by a rheumatologist, and he asked that fluoroquinolone toxicity be more officialy recognized and diagnosed by more doctors.

Richard points out that his prostatitis was non-bacterial, as many cases of prostatitis are, and that he never should have been given fluoroquinolones for a non-bacterial ailment. The post, “Cipro is no better than a PLACEBO at treating chronic prostatitis / chronic pelvic pain syndrome” goes over some information about this.

Richard also points out that NSAIDs and steroids have caused set-backs for him and many other victims of fluoroquinolones toxicity.

The next speaker was Markus Hamedinger. Markus suffers from tendon and joint pain, and has received a confirmed diagnosis of fluoroquinolone toxicity. Fluoroquinolone toxicity has severely affected Markus’s life, and he is unable to do many of the activities that he used to enjoy. His symptoms have not improved in the 2+ years that he has been sick.

Markus asserts that fluoroquinolones are used too often, and that they are inappropriately used when other, safer, antibiotics could be used. He notes the delayed adverse reactions to fluoroquinolones are a factor in keeping the effects of fluoroquinolones under-recognized. He says that doctors need to be made aware of exactly which infections need to be treated by fluoroquinolones, and which infections can be treated with other antibiotics. He also states that fluoroquinolone use should be banned in agriculture, to prevent exposure to fluoroquinolones from occurring through meat consumption.

The PRAC Chairwoman asked a question about repeated exposure making the reaction worse, and Markus noted that his reactions got worse and worse with each fluoquinolone exposure.

The next presenter was Miriam Knight. Miriam also presented on behalf of Raymond Miller and Geoffrey Robinson. Miriam is the co-founder of Quinolone Toxicity Support UK, and is also an administrator for Fluoroquinolone Toxicity Victims in Europe.

Miriam asserts that there is no role of quinolones/fluoroquinolones in the treatment of disease. She notes that mitochondrial DNA wasn’t known, studied, or acknowledged when quinolones were developed, and that they are chemotherapeutic agents.

Miriam points out that despite the official death toll from quinolones being low, there are many people who are hurt by these drugs in fatal ways – including aortic aneurysm.

Miriam notes the damage done by quinolones to mitochondrial DNA, and how mitochondrial DNA damage effects individuals differently depending on a variety of factors.

Miriam asserts, “There will never be a safe use of quinolones. They will always cause damage, observed or not.” And she also states that if removing them from the market is impossible, they should at least be severely restricted.

Miriam also asserts that quinolone toxicity should be a diagnosable illness with a diagnosis code. This is incredibly important in getting it acknowledged and quantifying the damage done by quinolones.

Miriam connects the dots between chronic pain, fibromyalgia, ME/CFS and fluoroquinolone toxicity.

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There are several dozen other testimonials. In the interest of the attention-spans of those reading this, I am going to split my notes about the hearing into several posts. This is the first of __ (tbd) posts about the hearing.

THANK YOU to all who testified. The testimony provided is wonderful, thoughtful, passionately delivered, and those who provided it represented themselves and the “floxie” community wonderfully!

End note – To those who testified, if I misspelled your name, please let me know. Also, if anyone would like me to publish their testimony directly, please send it over. Thank you!

 

 

 

Can Floxies Drink Alcohol?

Many people have asked me if they can/should drink alcohol post-flox.

As with most things, the answer is – it depends, and everyone is different.

Some Floxies tolerate alcohol fine, while others don’t.

Alcohol is, of course, bad for you. It’s hard on the liver, and can lead to cirrhosis and alcoholic hepatitis. It burdens your liver’s detoxification abilities and hinders your ability to get rid of other toxins. Alcohol wreaks havoc on the gut microbiome, and can encourage candida growth. Alcohol weakens the immune system, and can make you more succeptible to other illnesses. I could go on and on because there are hundreds of articles about the harm that alcohol inflicts on the human body. No matter how many videos come out about tequila being a probiotic, or articles there are about wine containing resveritrol, alcohol is not a health elixir. It is not good for you.

HOWEVER, it is quite fun (IMO), and it even has some health benefits–it’s a painkiller and it reduces feelings of stress and anxiety. Alcohol has enough redeeming qualities that billions of people around the world, most of whom are aware of the negative effects of alcohol, consume it. I do, and so do many other floxies.

When I first got floxed, I stopped drinking for a while. My body was going hay-wire in every conceivable way, and I didn’t want to contribute to my problems by knowingly consuming a substance that is bad for me. I think that abstaining from alcohol during the acute phase of fluoroquinolone toxicity was the right thing for me to do.

Once my body stabilized (i.e. it stopped feeling like a bomb was going off in my body, and I even had some improved/normal days) I started having a drink every once in a while. Even though I could drink, I found that my tolerance for alcohol was greatly diminished. Before I got floxed I could handle three-ish drinks in an evening (and I thoroughly enjoyed drinking them). After getting floxed, my tolerance was one drink a night (that was barely enjoyable). I didn’t even want to drink more than that–I struggle to explain why, but I just felt done after 3/4 of a drink. Over time (I am now a bit over 5 years post-flox) my tolerance increased, and I can now comfortably have two alcoholic beverages in an evening. That’s plenty for me, in my personal opinion of how much I should/shouldn’t drink.

I never experienced a relapse in fluoroquinolone toxicity symptoms as a direct result of drinking alcohol, but other people have, and I encourage everyone who wants to drink post-flox to be very careful and cautious with alcohol consumption. Comments such as this one, from Bob (and the comment just above it when you click on the link, from Ann), are examples of alcohol triggering an increase in, or relapse of, fluoroquinolone toxicity symptoms:

After getting floxed I had relapses to alcohol which I only drank on vacation. I suspect this is due to severe kill off of gut flora. I am afraid to drink anymore.

This comment from Mark also notes that alcohol consumption can lead to fluoroquinolone toxicity symptom flares:

I cheated this weekend and drank alcohol/ate dairy. You know what? It flared up my cipro symptoms full force. Knee joints started cracking like crazy, achilles heal flare, etc. I’m convinced that we are all suffering an overgrowth of yeast and the faster we can get that under control, the healthier we will be.

Some people have a more moderate reaction to alcohol post-flox. This comment, from Ruth, is really interesting and insightful. Though she can drink alcohol without issue, she typically abstains:

I am able to drink again but my tolerance is greatly reduced. It won’t actually harm your gaba receptors because alcohol acts on gaba-b instead of gaba-a. I think it promotes healing.

When the alcohol downgrades the gaba-b subunit, I think the body makes repairs to some of the a subunits in order to put things back in balance.

I think when the FQ took out some of your gaba-a receptors your body gave you extra gaba-b receptors. This can make you a lot more receptive to the effects of alcohol. The b unit seems to be able to replace itself faster. That’s why alcohol withdrawal lasts a lot less long than benzodiazepine withdrawal. This is all just my theory. I have nothing to back it up with except my own experience.

Last year I got drunk at the Racine Zoo by accident. They hosted a teacher’s night and served spiked punches with no indication that they were alcoholic. I had what they had labeled as “Lesson Learned Lemonade.” I was thirsty so I slammed a big cup. At first I felt super relaxed and I thought that my nervous system must really be healing. Maybe it was that walk on the beach… and then I felt it. I knew it had been alcoholic. I ended up drunk off my ass, but not so bad that I couldn’t say “gamma amino butyric acid,” ha, ha. I got a brief relapse from that experience, of symptoms I had not had in a long time. After that ended my base line seemed higher.

So I think alcohol is not completely bad. However, it can devastate your gut microbiome, so I am very careful about it. I had a tiny tiny bit of Bailey’s at Christmas. I enjoyed it. Other than the holidays I abstain from alcohol for the sake of my healthy flora.

Although it won’t stop your nervous system from healing, remember that psych symptoms can also stem from an imbalance of healthy vs. unhealthy microbes. Alcohol can worsen that situation considerably so for the foreseeable future it is better to abstain. Farther down the road you will probably be able to have a beer now and then with no ill effects.

Some people have even found that alcohol has helped them. It is a pain reliever and relaxant. It reduces anxiety and stress – even the anxiety and stress that comes with getting poisoned by a pharmaceutical. Stress and anxiety reduction are crucial for healing from fluoroquinolone toxicity. Both Bronwen and Barbara noted that they felt better with moderate alcohol consumption.

Bronwen’s Comment:

As far as booze goes, I actually found one drink helped lessen my symptoms a bit when they were getting overwhelming in the evening – much to my surprise, but I have only ever read one other person that found the same thing – most find the opposite. Again, test yourself! I certainly could not have more than one drink. The liver is struggling along with the other organs, as the clearing house for toxins, so alcohol puts another burden on it.

Barbara’s Comment:

My saving grace is I am allowed wine 😁😁 hallelujah .I have been able to drink alcohol from the begining and in certain times when the pain was bad I swear it helped.

As you can see, reactions to alcohol post-flox vary considerably. So, what should your take-away from this post be? Should you drink alcohol, or not? I can’t answer that for you, because I have no idea how you respond to alcohol, or how much you enjoy consuming it. If alcohol isn’t your drug of choice, and you don’t particularly like it, don’t start drinking because some people have responded positively to its benefits. If you want to drink alcohol, it is, of course, best to do it in moderation. If you want to avoid all things that may trigger a relapse, or that are generally bad for the body, by all means, don’t drink. As with all advice for my floxie friends – it depends, everyone is different, and be careful.

 

Fluoroquinolone Antibiotics Increase Risk of Birth Defects

A few years ago, a friend from high school who was in her second trimester of pregnancy with her second child, reached out to me to ask me what antibiotics she should avoid. She had pneumonia, and was on her way to the doctor’s office. I told her that she should steer clear fluoroquinolones (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, and Floxin/ofloxacin).

Being an empowered and skeptical person, my friend didn’t just take my word for it that fluoroquinolones were dangerous, she did her own research and noted that the warning label for Cipro/ciprofloxacin stated:

Pregnancy Category C There are no adequate and well-controlled studies in pregnant women. CIPRO should not be used during pregnancy unless the potential benefit justifies the potential risk to both fetus and mother. An expert review of published data on experiences with ciprofloxacin use during pregnancy by TERIS–the Teratogen Information System–concluded that therapeutic doses during pregnancy are unlikely to pose a substantial teratogenic risk (quantity and quality of data=fair), but the data are insufficient to state that there is no risk.2

With that information in-hand, she was empowered to adamantly refuse the prescription for Cipro that her doctor wanted to give her, and instead insisted that she get a prescription for a safer antibiotic (a pregnancy category B antibiotic).

I was relieved beyond words when she told me that she had refused the Cipro prescription. She wasn’t going to get floxed, and whatever effects the Cipro may have had on her baby were avoided.

Study Indicates that Fluoroquinolones May Increase Risk of Birth Defects

A recent study in the British Journal of Pharmacology, “Use of antibiotics during pregnancy and the risk of major congenital malformations: a population based cohort study” has shown that, “antibiotics in the class called quinolones — ciprofloxacin, levofloxacin and others — are particularly dangerous and should be avoided in pregnancy.”

The study, which “followed 139,938 mothers of babies born in Quebec from 1998 to 2008, tracking their antibiotic use in the first trimester, and their babies’ birth defects through the first year of life” found that:

Moxifloxacin exposure was associated with a 5-fold increased risk of respiratory system malformations and ofloxacin use with an 8-fold increased risk of MCMs. However, these results should be interpreted with caution given the small number of exposed cases.

Teratogenicity of quinolone has been reported in the literature in animal and experimental studies [50, 51]. Indeed, quinolones can act as DNA gyrase inhibitors and also as mitotic inhibitors [52]. This may partially damage DNA and induce fetal malformation, which supports our findings [52].

The other antibiotics examined were also more dangerous during pregnancy than I think any pregnant woman should feel comfortable with, but fluoroquinolones were found to be particularly dangerous.

Too Many Pregnant Women are Prescribed Fluoroquinolone Antibiotics

My friend had a healthy son, and he is now a happy and healthy toddler. She took antibiotics (but not fluoroquinolone antibiotics) during pregnancy, but her son was not negatively affected.

My friend was fortunate. However, most pregnant women don’t have a high school friend who incessantly posts about the dangers of fluoroquinolones, and many of them take fluoroquinolones during pregnancy without being aware of the risks these drugs pose to them or their babies. Doctors who prescribe fluoroquinolones to pregnant women, when there are safer alternative antibiotics, are endangering women and children, and there is nothing okay about that.

***

New York Times, “Certain Antibiotics May Increase Risk of Birth Defects

British Journal of Clinical Pharmacology, “Use of antibiotics during pregnancy and the risk of major congenital malformations: a population based cohort study

***

 

 

Fluoroquinolones and Statins: A Recipe for Rhabdomyolysis

In May, 2017, WSB-TV 2 Atlanta aired the story, “Clark Howard says near-fatal disease possibly caused by popular antibiotic,” in which the story of how Clark Howard, a popular consumer expert and host of the nationally syndicated Clark Howard Show, was hurt by a combination of ciprofloxacin (a fluoroquinolone antibiotic) and generic Lipitor (a statin). Mr. Howard had a severe and life-threatening reaction to these drugs, and he is quoted in the story as saying, “I felt like death,” and “It was a struggle to walk five steps.” Mr. Howard was admitted to the hospital where he was diagnosed with rhabdomyolysis–a condition where muscles break down rapidly, causing severe strain on the kidneys and, potentially, death.

Both fluoroquinolones alone, and fluoroquinolones combined with statins, have been documented to cause rhabdomyolysis.

Here are some articles about fluoroquinolone-induced rhabdomyolysis:

Here is a news story about Chris Dannelly, who was killed after levofloxacin-induced rhabdomyolysis:

Additionally, here are some articles about fluoroquinolone plus statin induced rhabdomyolysis:

Both fluoroquinolones and statins are known to damage mitochondria, and they are both fluorinated drugs. They are also both widely prescribed–to millions of people annually–often concurrently.

In the article “Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population” a description of the basic science behind fluoroquinolone-induced muscle damage (and rhabdomyolysis) is described. The following is a quote from “Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population“:

Muscle: Basic Science

Although the etiology of fluoroquinolone-associated muscle disorders has yet to be fully elucidated, evidence supports a relationship with both latent myopathic disorders and the fluorine atom in fluoroquinolones. Despite no history of myopathy, an electromyogram (EMG) performed on a 54- year old woman with apparent ofloxacin-induced rhabdomyolysis demonstrated evidence of myopathy [85]. The patient’s myalgias and muscle weakness resolved upon discontinuation of ofloxacin. It is unknown whether the myopathic findings on EMG were related to the acute rhabdomyolysis or an underlying myopathy. In another case, a 33-year-old man thought to have norfloxacin-induced rhabdomyolysis was found to be susceptible to malignant hyperthermia by in vitro contracture tests [86], which raises the question of a possible link between the 2 conditions. His clinical complaints of myalgia and weakness and laboratory abnormalities resolved 6 months after discontinuing the norfloxacin. The researchers hypothesized that a similar muscle deficit may have accounted for the patient’s susceptibility to malignant hyperthermia and rhabdomyolysis induced by fluoroquinolones. Both malignant hyperthermia and fluoroquinolone-associated muscle disorders are thought to be triggered by a fluorine-containing compound [86]. To further investigate this possible connection, the same French investigators studied muscle function in 3 patients who presented with myalgia, tendinopathy, and arthralgia associated with fluoroquinolone exposure [87]. These results were compared with 3 patients exposed to fluoroquinolones who had no adverse events and 9 subjects with no known muscle disease who had not taken fluoroquinolones. Muscle contraction and metabolism were investigated through the use of histology, in vitro contracture tests, and 31P magnetic resonance spectroscopy (31P MRS). The 3 patients with fluoroquinolone-associated myalgia and weakness displayed similar metabolic abnormalities, whereas the 3 subjects exposed to fluoroquinolones with no adverse effects displayed normal metabolic profiles. These findings led the researchers to conclude that the adverse effects recorded in the 3 patients were related to a pre-existing muscular anomaly revealed by fluoroquinolone treatment. Further support for the hypothesis that fluorine may be the trigger for fluoroquinolone associated myopathy comes from the fact that no adverse muscular events have been reported with unfluorinated quinolones. In addition, steroid myopathy is thought to occur more frequently with fluorinated steroids (ie, dexamethasone and triamcinolone) than with nonfluorinated steroids (ie, prednisone or hydrocortisone) [88-90]. The researchers recommended that any patient experiencing myalgias associated with fluoroquinolone exposure should undergo noninvasive muscle metabolic testing with 31P MRS along with a subsequent muscle biopsy for histoenzymology and contracture tests if a metabolic disorder is found.

Muscle: Clinical Manifestations

A variety of muscle syndromes have been reported in association with fluoroquinolone use, ranging from mild myalgias to life-threatening rhabdomyolysis[78,85-87,91-95]. In fact, some investigators have proposed that myalgias may be the most common adverse effect of fluoroquinolone use [78]. Symptoms, which typically consist of diffuse muscle pain with or without weakness [86,87,91] and perhaps a predilection for proximal muscle groups [85,92], appear to manifest within 1 week after initiation of fluoroquinolone treatment [94] and often resolve within 1-4 weeks after discontinuation of the medication [78,86,91,92], although symptoms that persisted up to 6 months have been reported [86]. Statins may potentiate fluoroquinolone-associated myopathy (emphasis added) [91,92]. Furthermore, an association may exist between an underlying myopathic process and the development of myalgias and/or rhabdomyolysis after fluoroquinolone exposure, as previously discussed.

It is interesting that the authors of “Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population” attribute myalgia and rhabdomyolysis to the fluorine atom that is added to quinolones to form fluoroquinolones. The toxicity of fluorine is often overlooked by researchers and “floxies” alike, in part because of the politics associated with assertions that fluorine and fluoride are toxic (they are). As the first sentence in the quote (“Although the etiology of fluoroquinolone-associated muscle disorders has yet to be fully elucidated”) notes though, the exact mechanism through which fluoroquinolones, statins, and fluoroquinolones and statins together, cause adverse reactions is not fully known.

What is known is that fluoroquinolones, and fluoroquinolones combined with statins, can cause rhabdomyolysis, and that rhabdomyolysis can be deadly.

If you are a “floxie” that is on statins, I highly recommend that you talk to your doctor about the case reports linked above and the possibility of rhabdomyolysis and other myalgias being induced by fluoroquinolones, statins, or both.

If you have existing myalgias, including fibromyalgia, I suggest that you take the quote above to your doctor and get off of all fluorinated drugs–as they have been shown to exacerbate myalgias.

I hope that the millions of people on statins, and their doctors, recognize that fluoroquinolones should not be given to people on statins because the two drugs combined can increase the likelihood of rhabdomyolysis and other myalgias.

I’m sorry that Mr. Howard was hurt by ciprofloxacin and generic Lipitor, but hopefully the publicity that his story is getting will serve as a warning for others.

 

Floxie Hope Podcast Episode 21 – James

James is featured in Episode 21 of The Floxie Hope Podcast.

Check it out:

https://itunes.apple.com/us/podcast/floxie-hope-podcast/id945226010

http://www.floxiehopepodcast.com/episode-021-james/

James also shared his story in writing, and you can read it here – https://floxiehope.com/james-story-hurt-by-metronidazole-then-cipro/. He goes into more detail in the podcast though, and I highly recommend that you listen in. Thank you for sharing your story, James!

James was 24 years old when he was floxed. He lost his grip strength after taking a single pill. After that, he experienced pain, burning pain in his legs, his eyes hurt, he had floaters in his vision, visual snow, loss of ability to sweat, weight loss, stiff and weak legs, nerve pain, brain fog, and anxiety.

He was acutely sick for 9 months. Even though he has recovered to the point where he is able to do his job again, he is not quite at 100% yet. He’s getting there though. He has a new perspective on health, healing, and happiness that is helping him immensely.

Thank you for listening to James’ insightful and uplifting story!

(Again, I apologize about the sound quality. There is still a lot of beneficial information in the podcast, despite the static and echoes.)

 

Happy Birthday Grandma!

grandma

Today is my Grandma’s birthday. Happy birthday, Gram! I hope you have a wonderful day!

My Grandma is one of my favorite people in the world and I love her very much.

My Grandma was incredibly, wonderfully supportive through my journey through fluoroquinolone toxicity. As soon as I said, “I’m sick,” before I even knew why or how I was sick, she took me seriously. When I realized what was making me sick, she never questioned me. She never downplayed or dismissed my experience with fluoroquinolone toxicity–she just believed me. She was always on my side, and it didn’t seem like it ever occurred to her to believe the medical establishment, or anyone else, over me.

When she broke her hip a few years after I got floxed, my Grandma immediately put Cipro on her list of medications that she was not to be given. She knew that it was dangerous because of what I had gone through, and she didn’t want what happened to me to happen to her. Her refusal to take Cipro meant a lot to me. It signified that she believed me, and that she didn’t believe that my reaction was something rare or dismissible. It meant that she listened. I write about my experience with fluoroquinolone toxicity not to relive what happened, or to wallow in it, but to warn people so that they don’t go through the same thing I did. It means a lot when people listen, and it meant a lot to me that my Grandma listened to me, and that she refused to take the drug that hurt me. I’ve never had to fight with a doctor about a fluoroquinolone prescription for a loved one, but, I’m pretty sure that if I did get into an argument with a doctor about whether or not a fluoroquinolone prescription was appropriate for my Grandma, she would take my side.

I am lucky in that I have a lot of wonderfully supportive people in my life. I always felt like everyone in my family loved me and wanted what was best for me. I have always known that I am loved and cherished. I have always known that all of my loved ones were on my side. They are all appreciated!

Not all “floxies” have supportive loved ones. Some people don’t believe that their floxed loved one is really sick. Some people don’t try to understand what their floxed loved one is going through. Some people have family members who are dismissive of fluoroquinolone toxicity, and who don’t believe that it’s “real.” Some people have family members who believe that fluoroquinolones can’t be dangerous, and that adverse reactions can’t be devastating, even though there is plenty of documented evidence that fluoroquinolones ARE dangerous and adverse reactions ARE devastating. It saddens me when I hear of people who are not supported by their loved ones as they go through the difficulty of fluoroquinolone toxicity.

I appreciate the support of all my family members, and, today, on my Grandma’s birthday, I am especially appreciative of her.

You are loved, Gram. Happy Birthday! xoxo

 

fluoroquinolone-lawsuit-banner-trulaw

Letter from Bayer to Doctors Regarding Cipro and Avelox

bayer-letter1

bayer-letter2

The above letter, from Bayer to health care professionals reads:

August 22, 2016

IMPORTANT DRUG WARNING

Subject: Important Changes in the Avelox (moxifloxacin hydrochloride) and Cipro (ciprofloxacin) Complete Prescribing Information – New Limitations of Use and Safety Information for Fluoroquinolones

Dear Health Care Professional:

Bayer HealthCare Inc. and Merck & Co., Inc. would like to inform you of imprtant changes to the prescribing information for fluoroquinolone antibiotics for systemic use in the United States, including Avelox (moxifloxacin hydrochloride) and Cipro (ciprofloxacin).

Limitation of Use and Safety Information for Fluoroquinolone Drugs

To communicate important safety information for fluoroquinolone antibiotics, the U.S. Food and Drug Administration (FDA) has requested that all license holders of these products, including Bayer for Avelox and Cipro, implement a class label change.

These labeling changes provide for revisions to the Indications and Usage section of the package insert to include a new limitation of use statement for acute bacterial sinusitis, uncomplicated urinary tract infections, acute uncomplicated cystitis, and acute bacterial exacerbation of chronic bronchitis, to reserve systemic fluoroquinolones for treatment in patients who have no alternative treatment options. In addition to the Boxed Warning, Warnings and Precautions, and Information for Patients sections of the package insert and the Medication Guide have been revised to include information regarding the risk of disabling and potentially irreversible serious adverse reactions of tendinitis and tendon rupture, peripheral neuropathy, and central nervous system effects that can occur together in the same patient.

The labels of fluoroquinolones already had a Boxed Warning for tendinitis, tendon rupture, and worsening myasthenia gravis. The labels also included warnings about the risks of peripheral neuropathy and central nervous system effects. Other serious risks associated with fluoroquinolones are described in the labels, such as cardiac, dermatologic, and hypersensitivity adverse reactions. This information about the risk of disabling and potentially irreversible serious adverse reactions is based on the FDA’s review of postmarketing adverse event reports from the FDA Adverse Event Reporting System (FAERS). This safety information was discussed at a November 5, 2015 joint meeting of the Antimicrobial Drugs Advisory Committee and the Drug Safety and Risk Management Advisory Committee.

Prescriber Action:

Health care professionals should not prescribe systemic fluoroquinolones to patients who have other treatment options for acute bacterial sinusitis, acute bacterial exacerbation of chronic bronchitis, acute uncomplicated cystitis, and uncomplicated urinary tract infections. Health care professionals should encourage patients to read the Medication Guide that describes the safety issues associated with fluoroquinolones. The Medication Guide is required to be given to the patient with each fluoroquinolone prescription. Stop fluoroquinolone treatment immediately if a patient reports serious side effects, and switch to a non-fluoroquinolone antibacterial drug to complete the patient’s treatment course.

Reporting Adverse Events:

Health care professionals are encouraged to report adverse events to FDA’s MedWatch reporting system by visiting www.fda.gov/medwatch or calling 1-800-FDA-1088.

If you wish to request further information for AVELOX, please contact Merck National Service Center at 1-800-526-4099. If you wish to request further information for CIPRO, please contact Bayer Service Center at 1-888-842-2937.

Please refer to the accompanying Important Information about AVELOX and CIPRO for complete indication and other important risks. Please also see the enclosed Prescribing Information, including BOXED WARNINGS and Medication guide for AVELOX and CIPRO.

Bayer HealthCare is the license holder for AVELOX and CIPRO. Under terms of a marketing agreement, Merck markets AVELOX in the United States.

Sincerely,

Dario F. Mirski, M.D.

Senior Vice President and Head Medical Affairs Americas

Bayer HealthCare Pharmaceuticals, Inc.

Enclosures: AVELOX and CIPRO Full Prescribing Information

 

The Avelox and Cipro prescribing information can be found HERE and HERE.

 

I’m honestly feeling speechless right now–I have no idea how to respond to this. The letter speaks for itself. I never thought I would see the words, “Health care professionals should not prescribe systemic fluoroquinolones to patients who have other treatment options for acute bacterial sinusitis, acute bacterial exacerbation of chronic bronchitis, acute uncomplicated cystitis, and uncomplicated urinary tract infections,” or that doctors and patients alike should be warned of “disabling and potentially irreversible serious adverse reactions” of fluoroquinolones, or that, “the risk of disabling and potentially irreversible serious adverse reactions of tendinitis and tendon rupture, peripheral neuropathy, and central nervous system effects that can occur together in the same patient,” from Bayer. But, there it is, on Bayer letterhead–a letter to health care professionals regarding the real, serious, often permanent risks of fluoroquinolones.

I hope that this letter is being distributed far and wide, and that it reaches every doctor, P.A., nurse, and other medical provider in the country.

I hope that Johnson & Johnson sends out a similar letter regarding Levaquin (levofloxacin).

I hope that doctors heed these warnings, and stop prescribing fluoroquinolones outside of life-threatening situations.

I hope that these letters do something other than mitigate the risks and losses that Bayer anticipates from lawsuits having to do with the updated Cipro and Avelox warning labels.

I hope that some of the motivation for this letter is Bayer wanting to do the right thing and warn patients and health care providers alike about the dangerous side-effects of their drugs.

I hope that we in the “floxie” community can celebrate this. I see this letter as a very big deal. When I started this site in 2013, I didn’t think that I would ever see a letter like this. It, along with the warning label changes that prompted it, should be celebrated.

 

flu tox get help you need banner click lisa

 

Publicizing Fluoroquinolone Warnings

I have such mixed feelings about the FDA’s response to the November, 2015 Antimicrobial Drugs Advisory Committee meeting regarding fluoroquinolone safety. On one hand, I feel like they really did hear those who testified, and they not only listened, they responded in a way that showed that they listened. The FDA did what the Antimicrobial Drugs Advisory Committee recommended they do: they updated fluoroquinolone warnings to note that, “the serious side effects associated with fluoroquinolone antibacterial drugs generally outweigh the benefits for patients with acute sinusitis, acute bronchitis, and uncomplicated urinary tract infections who have other treatment options.” They not only updated the warning labels, they updated the black-box warnings–the most severe warning a drug can have. I am truly grateful for the steps forward in acknowledging fluoroquinolone adverse-reactions, and I’m hopeful that the updated warning labels will lead physicians and patients to realize that fluoroquinolones are dangerous drugs with potentially devastating consequences.

I wonder though, what good is an updated warning label? In the post, Who Reads the Drug Warning Labels? I go over the problem of people not knowing what is on the warning labels. Are physicians going to read the updated warning labels? Are patients? Is anyone other than the “floxie” community going to realize that the warning labels have been changed?

I appreciate the action taken by the FDA–I really do–but are updated warning labels actually going to change anything? Will fewer people get injured and killed by fluoroquinolones? I certainly hope that a significant portion of doctors hear about the warning label changes, and stop prescribing fluoroquinolones, but, unfortunately, the FDA isn’t taking any major steps to make this happen.

The FDA has no plans to inform individual doctors about the recent warning label changes made to fluoroquinolone warning labels. Even though the black-box warnings, again–the most severe warning label a drug can receive, have been updated to note that fluoroquinolones are associated with disabling and potentially irreversible serious adverse reactions, the FDA is not going to tell doctors about the changes. No “dear doctor” letter will be issued by the FDA. They will not do a massive publicity campaign to let physicians or patients know that the warning labels have been updated. They know about the dangers of fluoroquinolones, and, in their own way, they acknowledge them, but they’re not proactively communicating what they know to patients or physicians.

Since the FDA isn’t going to issue a “dear doctor” letter, it will likely be helpful if we (the people in the fluoroquinolone toxicity community, and those who care about drug safety) give the information the FDA has released to our doctors, local hospitals, and media.

I encourage everyone reading this to please, please, please send this information (that is directly from the FDA) to your doctors, the media, your friends, your loved ones, and anyone else who you think may benefit from the information. People need to know how dangerous Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, and Factive/gemifloxacin are. In order for them to know how dangerous these drugs are, we need to tell them.

Please forward these FDA releases to those who need this information:

  1. 5/12/16 – Fluoroquinolone Antibacterial Drugs: Drug Safety Communication – FDA Advises Restricting Use for Certain Uncomplicated Infections
  2. 7/26/16 – FDA Drug Safety Communication: FDA updates warnings for oral and injectable fluoroquinolone antibiotics due to disabling side effects
  3. July, 2016 Drug Safety Labeling Changes

Since most people don’t actually click on links, I’m also going to copy and paste what the FDA notices said (feel free to share this post with anyone who needs the information too).

Fluoroquinolone Antibacterial Drugs: Drug Safety Communication – FDA Advises Restricting Use for Certain Uncomplicated Infections:

AUDIENCE: Internal Medicine, Family Practice, Pharmacy, Patient

ISSUE: FDA is advising that the serious side effects associated with fluoroquinolone antibacterial drugs generally 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.

An FDA safety review has shown that fluoroquinolones when used systemically (i.e. tablets, capsules, and injectable) 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.

As a result, FDA is requiring the drug labels and Medication Guides for all fluoroquinolone antibacterial drugs to be updated to reflect this new safety information. FDA is continuing to investigate safety issues with fluoroquinolones and will update the public with additional information if it becomes available.

See the FDA Drug Safety Communication for a list of currently available FDA approved fluoroquinolones for systemic use.

BACKGROUND: The safety issues described in the Drug Safety Communication were also discussed at an FDA Advisory Committee meeting in November 2015.

RECOMMENDATION: Patients should contact your health care professional immediately if you experience any serious side effects while taking your fluoroquinolone medicine. Some signs and symptoms of serious side effects include tendon, joint and muscle pain, a “pins and needles” tingling or pricking sensation, confusion, and hallucinations. Patients should talk with your health care professional if you have any questions or concerns.

Health care professionals should stop systemic fluoroquinolone treatment immediately if a patient reports serious side effects, and switch to a non-fluoroquinolone antibacterial drug to complete the patient’s treatment course.

Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA’s MedWatch Safety Information and Adverse Event Reporting Program:

  • Complete and submit the report Online: www.fda.gov/MedWatch/report

  • Download form or call 1-800-332-1088 to request a reporting form, then complete and return to the address on the pre-addressed form, or submit by fax to 1-800-FDA-0178

FDA Drug Safety Communication: FDA updates warnings for oral and injectable fluoroquinolone antibiotics due to disabling side effects:

SAFETY ANNOUNCEMENT

The U.S. Food and Drug Administration (FDA) approved changes to the labels of fluoroquinolone antibacterial drugs for systemic use (i.e., taken by mouth or by injection). These medicines are associated with disabling and potentially permanent side effects of the tendons, muscles, joints, nerves, and central nervous system that can occur together in the same patient. As a result, we revised the Boxed Warning, FDA’s strongest warning, to address these serious safety issues. We also added a new warning and updated other parts of the drug label, including the patient Medication Guide.

We have determined that fluoroquinolones should be reserved for use in patients who have no other treatment options for acute bacterial sinusitis, (ABS), acute bacterial exacerbation of chronic bronchitis (ABECB), and uncomplicated urinary tract infections (UTI) because the risk of these serious side effects generally outweighs the benefits in these patients. For some serious bacterial infections the benefits of fluoroquinolones outweigh the risks, and it is appropriate for them to remain available as a therapeutic option.

Patients must contact your health care professional immediately if you experience any serious side effects while taking your fluoroquinolone medicine. Some signs and symptoms of serious side effects include unusual joint or tendon pain, muscle weakness, a “pins and needles” tingling or pricking sensation, numbness in the arms or legs, confusion, and hallucinations. Talk with your health care professional if you have any questions or concerns (see List of Serious Side Effects from Fluoroquinolones).

Health care professionals should not prescribe systemic fluoroquinolones to patients who have other treatment options for acute bacterial sinusitis (ABS), acute bacterial exacerbation of chronic bronchitis (ABECB), and uncomplicated urinary tract infections (UTI) because the risks outweigh the benefits in these patients. Stop fluoroquinolone treatment immediately if a patient reports serious side effects, and switch to a non-fluoroquinolone antibacterial drug to complete the patient’s treatment course (see List of Currently Available FDA-approved Fluoroquinolones for Systemic Use).

Fluoroquinolones are antibiotic medicines that work by killing or stopping the growth of bacteria that can cause illness. They are FDA-approved to prevent or treat certain serious bacterial infections.

The labels of fluoroquinolone medicines already have a Boxed Warning for tendinitis, tendon rupture, and worsening of myasthenia gravis. The labels also include warnings about the risks of peripheral neuropathy and central nervous system effects. Other serious risks associated with fluoroquinolones are described in the labels, such as cardiac, dermatologic, and hypersensitivity reactions. After FDA’s 2013 review that led to the additional warning that peripheral neuropathy may be irreversible, FDA evaluated post-marketing reports* of apparently healthy patients who experienced disabling and potentially permanent side effects involving two or more body systems after being treated with a systemic fluoroquinolone (see Data Summary). We evaluated only reports submitted to FDA, so there are likely additional cases of which we are unaware. The side effects occurred within hours to weeks after starting the fluoroquinolone, and at the time we received the reports, the side effects had continued for an average of 14 months to as long as 9 years after stopping the medicines. Several cases reported that some side effects stopped or improved after discontinuation of the medicine; others reported the side effects worsened or continued.

We previously communicated about these safety issues associated with fluoroquinolones in May 2016. Additional communications about related safety issues associated with fluoroquinolones occurred in August 2013 (peripheral neuropathy) and July 2008 (tendinitis and tendon rupture). The safety issues described in this Drug Safety Communication were also discussed at an FDA Advisory Committee meeting in November 2015.

In addition to updating information in the Boxed Warning, we are also including information about these safety issues in the Warnings and Precautions section of the label. The Indications and Usage section contains new limitation-of-use statements to reserve fluoroquinolones for patients who do not have other available treatment options for acute bacterial sinusitis (ABS), acute bacterial exacerbation of chronic bronchitis (ABECB), and uncomplicated urinary tract infections (UTI). The patient Medication Guide that is required to be given to the patient with each fluoroquinolone prescription describes the safety issues associated with these medicines. We are continuing to assess safety issues with fluoroquinolones as part of FDA’s usual ongoing review of drugs and will update the public if additional actions are needed.

We urge health care professionals and patients to report side effects involving fluoroquinolone antibacterials and other drugs to the FDA MedWatch program, using the information in the “Contact FDA” box at the bottom of the page.

ADDITIONAL INFORMATION FOR PATIENTS

  • Fluoroquinolone antibiotic medicines are associated with disabling and potentially permanent serious side effects that can occur together in the same patient and should not be used to treat certain uncomplicated infections. These uncomplicated infections include acute bacterial sinusitis (ABS), acute worsening of bacterial chronic bronchitis (ABECB), and uncomplicated urinary tract infections (UTI).
  • These side effects can involve the tendons, muscles, joints, nerves, and central nervous system, and can occur within hours to weeks after starting a fluoroquinolone medicine.
  • FDA has updated the Boxed Warning in the labels, added new warnings, and has revised the patient Medication Guide of all fluoroquinolone antibiotics.
  • Contact your health care professional immediately if you experience any serious side effects while you are taking your fluoroquinolone medicine.
  • Before starting a new fluoroquinolone medicine, inform your health care professional if you have previously experienced any serious side effects with another antibiotic.
  • Serious side effects involving the tendons, muscles, joints and nerves include:
    • Swelling or inflammation of the tendons
    • Tendon rupture
    • Tingling or pricking sensation (“pins and needles”)
    • Numbness in arms or legs
    • Muscle pain
    • Joint pain
    • Joint swelling
  • Serious central nervous system side effects include:
    • Depression
    • Hallucinations
    • Suicidal thoughts
    • Confusion
    • Anxiety
  • Other side effects include:
    • Abnormally rapid or irregular heart beat
    • Ringing or buzzing in the ears
    • Vision problems
    • Skin rash
    • Sensitivity of skin to sunlight
    • Headache
    • Trouble falling asleep
    • Fatigue
  • Read the patient Medication Guide you receive with your fluoroquinolone antibiotic prescriptions, which explains the benefits and risks of the medicine.
  • Talk to your health care professional if you have questions or concerns about fluoroquinolone antibiotic medicines.
  • We communicated safety information associated with fluoroquinolones in May 2016, August 2013, andJuly 2008.
  • Report side effects from a fluoroquinolone or any drug to your health care professional and the FDA MedWatch program, using the information in the “Contact FDA” box at the bottom of this page.

ADDITIONAL INFORMATION FOR HEALTH CARE PROFESSIONALS

  • FDA has approved label changes that reserve the use of fluoroquinolone antibacterial medicines when treating acute bacterial sinusitis (ABS), acute bacterial exacerbation of chronic bronchitis (ABECB), and uncomplicated urinary tract infections (UTI) for patients who do not have alternative treatment options.

  • FDA has also updated the Boxed Warning and the Warnings and Precautions sections of the labels and revised the patient Medication Guide of the fluoroquinolone drug class to describe the serious risk of multiple disabling and potentially irreversible adverse reactions that can occur together.

  • These adverse reactions primarily include tendinitis and tendon rupture, muscle pain, muscle weakness, joint pain, joint swelling, peripheral neuropathy, and central nervous system effects.

  • The adverse reactions can occur within hours to weeks after starting treatment with a fluoroquinolone medicine.

  • Discontinue the fluoroquinolone medicine immediately at the first signs or symptoms of any serious adverse reaction.

  • Avoid fluoroquinolones in patients who have previously experienced serious adverse reactions associated with fluoroquinolones.

  • Serious Adverse reactions of the musculoskeletal system and peripheral nervous system include:

    • Tendinitis/Tendon rupture

    • Muscle pain

    • Muscle weakness

    • Joint pain

    • Joint swelling

    • Peripheral Neuropathy

    • Serious Central nervous system effects include:

      • Psychosis
      • Anxiety
      •  Insomnia
      • Depression
      • Hallucinations
      • Suicidal thoughts
      • Confusion
    • Other adverse reactions include:

      • Exacerbation of myasthenia gravis
      • Prolongation of the QT interval
      • Hypersensitivity reactions/anaphylaxis
      • Photosensitivity/phototoxicity
      • Blood glucose disturbances
      • Clostridium difficile-associated diarrhea
    • Encourage patients to read the Medication Guide that they receive with their fluoroquinolone prescriptions.

    • FDA convened a public advisory committee meeting in November 2015 to discuss the risks and benefits of fluoroquinolone antibacterial medicines for the treatment of ABS, ABECB, and uncomplicated UTI. We also communicated safety information associated with fluoroquinolones in May 2016, August 2013, and July 2008.

    • Report adverse reactions involving a fluoroquinolone or any drug to the FDA MedWatch program, using the information in the “Contact FDA” box at the bottom of this page.

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Levaquin/levofloxacin Warning Label Changes (Please see July, 2016 Drug Safety Labeling Changes for the other fluoroquinolone label changes:

BOX WARNING (revised)

WARNING: SERIOUS ADVERSE REACTIONS INCLUDING TENDINITIS, TENDON RUPTURE, PERIPHERAL NEUROPATHY, CENTRAL NERVOUS SYSTEM EFFECTS AND EXACERBATION OF MYASTHENIA GRAVIS

  • Fluoroquinolones, including LEVAQUIN®, have been associated with disabling and potentially irreversible serious adverse reactions that have occurred together including:
    • Tendinitis and tendon rupture
    • Peripheral neuropathy
    • Central nervous system effects
  • Discontinue LEVAQUIN immediately and avoid the use of fluoroquinolones, including LEVAQUIN, in patients who experience any of these serious adverse reactions. Fluoroquinolones, including LEVAQUIN, may exacerbate muscle weakness in patients with myasthenia gravis. Avoid LEVAQUIN in patients with known history of myasthenia gravis.
  • Because fluoroquinolones, including LEVAQUIN, have been associated with serious adverse reactions, reserve LEVAQUIN for use in patients who have no alternative treatment options for the following indications:
    • Acute exacerbation of chronic bronchitis
    • Acute uncomplicated cystitis
    • Acute sinusitis

WARNINGS AND PRECAUTIONS

Disabling and Potentially Irreversible Serious Adverse Reactions Including Tendinitis and Tendon Rupture, Peripheral Neuropathy, and Central Nervous System Effects (addition)
  • Fluoroquinolones, including LEVAQUIN, have been associated with disabling and potentially irreversible serious adverse reactions from different body systems that can occur together in the same patient. Commonly seen adverse reactions include tendinitis, tendon rupture, arthralgia, myalgia, peripheral neuropathy, and central nervous system effects (hallucinations, anxiety, depression, insomnia, severe headaches, and confusion). These reactions can occur within hours to weeks after starting LEVAQUIN. Patients of any age or without pre-existing risk factors have experienced these adverse reactions.
  • Discontinue LEVAQUIN immediately at the first signs or symptoms of any serious adverse reaction. In addition, avoid the use of fluoroquinolones, including LEVAQUIN, in patients who have experienced any of these serious adverse reactions associated with fluoroquinolones.
Tendinitis and Tendon Rupture replaces Tendinopathy
  • Fluoroquinolones, including LEVAQUIN, have been associated with an increased risk of tendinitis and tendon rupture in all ages. This adverse reaction most frequently involves the Achilles tendon, and has also been reported with the rotator cuff (the shoulder), the hand, the biceps, the thumb, and other tendons. Tendinitis or tendon rupture can occur, within hours or days of starting LEVAQUIN, or as long as several months after completion of fluoroquinolone therapy… Tendinitis and tendon rupture can occur bilaterally.
  • The risk of developing fluoroquinolone-associated tendinitis and tendon rupture is increased in patients over 60 years of age, in patients taking corticosteroid drugs, and in patients with kidney, heart or lung transplants. Other factors that may independently increase the risk of tendon rupture include strenuous physical activity, renal failure, and previous tendon disorders such as rheumatoid arthritis. Tendinitis and tendon rupture have also occurred in patients taking fluoroquinolones who do not have the above risk factors. Discontinue LEVAQUIN immediately if the patient experiences pain, swelling, inflammation or rupture of a tendon. Avoid fluoroquinolones, including LEVAQUIN, in patients who have a history of tendon disorders or have experienced tendinitis or tendon rupture.
Peripheral Neuropathy (new sentences added)
  • Fluoroquinolones, including LEVAQUIN, have been associated with an increased risk of peripheral neuropathy. Cases of sensory…
  • …minimize the development of an irreversible condition…Avoid fluoroquinolones, including LEVAQUIN, in patients who have previously experienced peripheral neuropathy.

ADVERSE REACTIONS

  • The following serious and otherwise important adverse drug reactions are discussed in greater detail in other sections of labeling:
    • Disabling and Potentially Irreversible Serious Adverse Reactions (addition)
    • Tendinitis and Tendon Rupture (replaces Tendon Effects)

PATIENT COUNSELING INFORMATION

Serious Adverse Reactions
  • Advise patients to stop taking LEVAQUIN if they experience an adverse reaction and to call their healthcare provider for advice on completing the full course of treatment with another antibacterial drug. Inform patients of the following serious adverse reactions that have been associated with LEVAQUIN or other fluoroquinolone use:
  • Disabling and potentially irreversible serious adverse reactions that may occur together: Inform patients that disabling and potentially irreversible serious adverse reactions, including tendinitis and tendon rupture, peripheral neuropathies, and central nervous system effects, have been associated with use of LEVAQUIN and may occur together in the same patient. Inform patients to stop taking LEVAQUIN immediately if they experience an adverse reaction and to call their healthcare provider. (addition)
  • Tendinitis and tendon rupture replaces Tendon Disorders

MEDICATION GUIDE

What is the most important information I should know about LEVAQUIN?

Tendon rupture or swelling of the tendon (tendinitis).

  • Stop taking LEVAQUIN immediately and get medical help right away…
  • Worsening of myasthenia gravis (a problem that causes muscle weakness). Tell your healthcare provider if you have a history of myasthenia gravis before you start taking LEVAQUIN. (addition)

What is LEVAQUIN?

  • LEVAQUIN should not be used in patients with acute exacerbation of chronic bronchitis, acute uncomplicated cystitis, and sinus infections, if there are other treatment options available.
  • LEVAQUIN should not be used as the first choice of antibacterial medicine to treat lower respiratory tract infections cause by a certain type of bacterial called Streptococcus pneumoniae.

Before you take LEVAQUIN, tell your healthcare provider if you:

  • have a disease that causes muscle weakness (myasthenia gravis); LEVAQUIN should not be used in patients who have a known history of myasthenia gravis.
  • have nerve problems; LEVAQUIN should not be used in patients who have a history of a nerve problem called peripheral neuropathy

How should I take LEVAQUIN?

Do not skip any doses of LEVAQUIN, or stop taking it, even if you begin to feel better, until you finish your prescribed treatment unless:

  • you have nerve problems. See “What is the most important information I should know about LEVAQUIN?”

  • you have central nervous system problems. See “What is the most important information I should know about LEVAQUIN?”

     

All help in spreading the word about these FDA warnings will be greatly appreciated!

 

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First Do No Harm – By Barbara Arnold

The following was written by Barbara Arnold and published in a magazine aimed toward ex-pats living in Spain. When Barbara sent it to me she said, “If it saves one person from taking this poison, then I will be happy. I am trying to get it translated to Spanish so I can send it to the Spanish papers here.
I urge every floxie that is well enough to try and get articles published in any magazine local paper etc. It’s certainly helped me focus my anger in a positive way, and maybe eventually it will become better known about.”

I also encourage all of my floxie friends to write something like what Barbara wrote below. It is important to focus your anger in a positive way, and it is even healing. Writing, advocating, and helping others through this mess have been vital parts of my healing process. I suspect that those things can be healing for other people as well, and I encourage each of my floxie friends to write, advocate, and help others in whatever way you feel comfortable. 

Thank you, Barbara, for speaking out and passionately advocating for those in medicine to think about the Hippocratic Oath when they prescribe fluoroquinolones!

FIRST DO NO HARMWritten by Barbara Arnold.

Before Doctor can practice they have to take “The Hippocratic oath”, First do no harm. Unfortunately harm is being done to hundreds of thousands, maybe even millions of people across the world by Doctors prescribing antibiotics from a group called FLUOROQUINOLONES.

For me, it all started nearly 2 years ago when I went to the Doctor with bronchitis. I had no idea then that my life was about to change, in the most awful drastic way possible and that for the next two years to date I would still be  suffering from the debilitating side effects from ciprofloxacin an antibiotic from the group called FLUOROQUINOLONES. At the same time I was given cortisone injections the result of which was like a bomb going off in my body. It started with searing pain in my Achilles tendons, at the time I stupidly believed that it was caused by changing my high heeled shoes to low heels and then walking to far. I had no idea that my body was being POISONED by a treatment for a simple thing like Bronchitis. I had great difficulty walking but I believed it would soon get better. HOW WRONG I WAS. 

I had mentioned to the nurse who was administrating the cortisone injection that I was having trouble walking, and did he think it was anything to do with the injections. He told me it couldn’t be as cortisone is an anti-inflammatory. At this point I did not connect the dots. I later found out these drugs are contra indicated to anyone over 60yrs and even worse especially alongside cortisone injections. Fluoroquinolones leach magnesium from the cells and as you get older you have less magnesium to begin with. The pain got worse to the point I ruptured a tendon causing a bruise the size of “England” on the inside of my right leg and I could   barely walk a few yards. At the same time I started to get Chronoc Fatigue to the point where I could hardly keep my eyes open. I had dizziness and balance problems.

For the next three months and many visits to my Doctor, I eventually saw a Rheumatologist who diagnosed my condition as “side effects of ciprofloxacin”.

From that point onwards I started to do my own research on Fluoroquinolones. The results were MIND BLOWING I found out that these antibiotics were being used for simple bladder infections, bronchitis and sinus infections. This was the equivalent of using a sledge hammer to kill a fly. There are many other safer antibiotics that could be used without the devastating side effects that can be caused by Fluoroqinolones. I was told I was a RARE CASE and that my Doctor had never heard of this before. Unfortunately this is totally untrue, as the symptoms of fluoroquine poisoning are vast and in some people the reaction does not occur until months later. Therefore a lot of misdiagnosis is going on. Here are some of the symptoms that can occur but are not limited to, weeks or even months later.

MUSCULOSKELETAL DAMAGE WITH DEGENERATION OF CARTILAGE AND TENDONS. DAMAGE TO THE MITOCHONDRIA (the power cells that give us energy} DETATCHED RETINAS, NEURO PROBLEMS, ANXIETY, PANIC ATTACKS. PERIPHERAL NEUROPATHY IE, BURNING, DAMAGED NERVES,, PAIN, OXIDATIVE DAMAGE IN MAMMALIAN CELLS, CELL DEATH, INSOMNIA, DIFFICULTY BREATHING, PALPITATIONS, SKIN RASH, VOMITING, HIVES LOSS OF MUSCLE STRENGTH, BRAIN FOG. These are just a few of fluoroquinolone poisoning symptoms. There are many many more.

As things got worse I had to result to using  a wheelchair as it was extremely painful to walk. As well as the pain, my legs felt like I was dragging along lead weights. During the months that followed I had various blood tests which showed NOTHING apart from high ferritin levels. I was referred to another Rheumatologist who treated me more or less with contempt as no test she did showed anything wrong. I had  learned that there was a BLACK BOX WARNING in America about this group of antibiotics and when I told her about this, that the Black Box Warning is the highest warning you can get in America, she scoffed at me and declared “This is Spain not America.”  This kind of arrogance and ignorance is allowing others to suffer in the most devastating ways. Subsequently, some 18 months later, the Food and Drug Administration has just issued an advisory to ALL DOCTORS IN THE UNITED STATES, to cease using these dangerous drugs to all patients unless it is a life or death situation.

I have spent thousands of pounds in natural supplements trying to cure myself as Doctors do not have any answers. However there are some Doctors willing to listen now as they or some-one in their family have been effected. by this group of chemotherapy drugs. YES they are chemo drugs because they destroy good cells as well as bad. They do damage down to the very DNA and in some people they leave permanent nerve damage. I am presently seeing an integrative Doctor who is also a Medical Doctor. He is in Marbella and I have to travel 5 hours to see him. I have no choice if I want to recover. The medical health care system here poisoned me and now I have to heal myself with all the costs that, that incurs.

I fully understand that Doctors do the best they can and cannot be expected to know the side effects of every drug they prescribe, but this group of drugs are completely different as they are one of the most dangerous drugs on the market, It was the responsibility of the  health representatives to inform Doctors of this. They were negligent in their duty of care and because of that I, and many other’s have been sentenced to years of suffering. This has been known about since the 1970’s. The attitude of the pharmaceutical companies beggars belief. It is only now with the event of the world-wide web that this is becoming common knowledge   If you think you have been effected by any of these drugs go to http://www.floxiehope.com. There is a mine of information there from fellow sufferers and Doctors who are now beginning to take notice. I urge every-one that reads this to be very very careful that you are not prescribed any antibiotic from this group namely ….CIPROFLOXACIN, LEVAQUIN/LEVOFLOXACIN, AVELOX/MOXIFLOXACIN OR FLOXIN/OFLOXACIN.

To conclude, not everyone that takes these drugs suffers the side effects initially but eventually maybe years later this has been known to happen. There are likely genetic factors that make some people  more susceptible to suffer adverse reactions to fluoroquinolones than others. Human bodies are complex and how a drug reacts in a human body is difficult to predict. I just wish Doctors took their  “Hippocratic Oath” more seriously and FIRST DO NO HARM.

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Fluoroquinolones Removed From the Market

Several fluoroquinolones have been removed from the market because they caused acute toxicity and death. The fluoroquinolones that have been removed from the market are not terribly different from the ones that remain on the market in terms of damage done or damage mechanisms.

Here are some of the fluoroquinolones that have been removed from the market:

Omniflox/temafloxacin

In 1992 the fluoroquinolone antibiotic Omniflox/temifloxacin was removed from the US market after causing three deaths.

To note the removal from the market, the FDA released the following statement:

            “The Food and Drug Administration today announced that Abbott Laboratories of Abbott Park, Ill., is voluntarily recalling the broad-spectrum anti-infective drug Omniflox (temafloxacin) tablets, and will halt all further distribution of the drug.

This action is being taken because of severe adverse events associated with the use of the drug that have been reported to the company and to FDA in the first three months of marketing.

Temafloxacin was approved in late January 1992 and marketed in mid-February.  Since that time there have been approximately 50 reports of serious adverse reactions, including three deaths.  There were several cases of severe low blood sugar, especially in very elderly patients with decreased kidney function.  Among the severe reactions there were a number of cases of an unusual complex of adverse reactions consisting of hemolitic anemia (destruction of red blood cells) and other blood cell abnormalities.”

The fluoroquinolones that remain on the market also impair kidney function. From the 2013 Science Daily article, Risk of kidney disease doubled with use of fluoroquinolone antibiotics, “The risk of acute kidney disease is doubled for people taking oral fluoroquinolone antibiotics, according to a new study.” The article pointed out that the risk of acute kidney disease was increased for patients taking cipro/ciprofloxacin, levaquin/levofloxacin, avelox/moxifloxacin and floxin/ofloxacin – fluoroquinolones that remain on the market today.

The fluoroquinolones that remain on the market also cause blood-sugar abnormalities, including severe low blood sugar. A large 2013 study out of Taiwan looked at more than 78,000 patient records and found that, “The researchers found that patients with diabetes who had taken fluoroquinolone antibiotics had higher rates of both hyperglycemia and hypoglycemia compared with those who had taken macrolide antibiotics.” (source) Additionally, in the article, Fluoroquinolone antibiotics and type 2 diabetes mellitus, it is noted that, “Exposure to fluoroquinolone antibiotics is postulated as a risk factor for subsequent development of type 2 diabetes. It is hypothesized that fluoroquinolones induce an intracellular magnesium deficit that can lead to insulin resistance.”

Raxar/grepafloxacin

Raxar/grepafloxacin was removed from the worldwide market in 1999. The FDA withdrawal notice stated:

RAXAR is a fluoroquinolone antibiotic indicated for the treatment of infections caused by strains of bacteria susceptible to grepafloxacin in the following diseases: community-acquired pneumonia; acute bacterial exacerbations of chronic bronchitis; uncomplicated gonorrhea (urethral in males and endocervical and rectal in females); non-gonococcal urethritis and cervicitis.

Glaxo Wellcome has recently concluded an extensive review of the safety of RAXAR and determined that due to an effect of RAXAR on cardiac repolarization, manifested as QT interval prolongation on the electrocardiogram (ECG), some patients may be at risk of a very rare but serious ventricular arrhythmia known as torsade de pointes when treated with the product.

The warning label for Levaquin/levofloxacin (and the other fluoroquinolones that remain on the market) notes that:

“Prolongation of the QT interval and isolated cases of torsade de pointes have been reported. Avoid use in patients with known prolongation, those with hypokalemia, and with other drugs that prolong the QT interval.”

Additionally, a study entitled “Azithromycin and Levofloxacin Use and Increased Risk of Cardiac Arrhythmia and Death” compared the risk of cardiac arrhythmia for U.S. Veterans taking amoxicillin, azithromycin and levofloxacin. The study concluded that:

“Compared with amoxicillin, azithromycin resulted in a statistically significant increase in mortality and arrhythmia risks on days 1 to 5, but not 6 to 10. Levofloxacin, which was predominantly dispensed for a minimum of 10 days, resulted in an increased risk throughout the 10-day period.”

Just like Raxar/grepafloxacin, the fluoroquinolones that are still on the market prolong the QT interval and cause torsade de pointes, which can lead to arrhythmia and death.

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Zagam/sparfloxacin

Zagam/Sparfloxacin was also removed from the market because it caused QT interval prolongation.

Zagam/Sparfloxacin also caused incidents of Stevens Johnson Syndrome:

“When a patient using  Zagam develops SJS or TEN after taking the fluoroquinolone antibiotic treatment, the individual’s topmost skin cells die and fall off. This leaves the deeper layers exposed and unprotected, making it likely for a patient to experience infection and scarring. The sensitive mucous membrane also becomes exposed when the upper layer of skin sloughs off, and may be prone to blistering.” (source)

Trovan/trovafloxacin

Trovan/Trovafloxacin was removed from the market because of its high potential for inducing serious, sometimes fatal liver damage (hepatotoxicity). The wiki entry for Trovafloxacin notes that:

In June 1999 the U.S. Food and Drug Administration advised doctors to limit the prescription of Trovan after it had been found “strongly associated” with 14 cases of acute liver failure and six deaths. The FDA had received over 100 reports of liver problems in people taking Trovan, which was at that time being prescribed at a rate of 300,000 patients per month in the United States. Two days later the Committee for Proprietary Medicinal Products recommended to the European Commission that marketing approval of Trovan be suspended for a year.

One of the best articles about the hepatotoxicity of Trovan/Trovofloxacin is Trovafloxacin, a fluoroquinolone antibiotic with hepatotoxic potential, causes mitochondrial peroxynitrite stress in a mouse model of underlying mitochondrial dysfunction. The article, Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria, by some of the same authors, is also enlightening. Liver damage, mitochondrial damage, and ROS overload/oxidative stress are all intricately connected. I highly recommend that you read the two articles linked to (but, man, they’re both really difficult articles). I suspect that both articles hold many of the keys to understanding all fluoroquinolone toxicity reactions. In the post, Article Breakdown – “Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria,” I go over some of the implications Mechanisms of Pathogenesis in Drug Hepatotoxicity Putting the Stress on Mitochondria has for floxies.

Interestingly, Trovan/Trovafloxacin has another area of shady history. In Kano, Nigeria, it was used in an improperly conducted trial on children with meningitis. Per the wiki entry for Trovafloxacin:

In 1996, during a meningitis epidemic in Kano, Nigeria, the drug was administered to approximately 200 [3] infected children. Eleven children died in the trial: five after taking Trovan and six after taking an older antibiotic used for comparison in the clinical trial. Others suffered blindness, deafness and brain damage, common sequalae of meningitis that have not been seen in patients treated with trovafloxacin for other infection types.[4][5][6] An investigation by the Washington Post concluded that Pfizer had administered the drug as part of an illegal clinical trial without authorization from the Nigerian government or consent from the children’s parents.[7] The case came to light in December 2000 as the result of an investigation by The Washington Post, and sparked significant public outcry. The most serious error was the falsification and backdating of an ethics approval leader by the lead investigator of the trial, Dr. Abdulhamid Isa Dutse. Dr. Dutse is now the chief medical officer of Aminu Kano Teaching Hospital. The result of the trial was that children treated with oral trovafloxacin had a 5% (5/100) mortality rate compared to a 6% (6/100) mortality rate with intramuscular ceftriaxone.

Between 2002 and 2005 the victims of the Trovan tests in Nigeria filed a series of unsuccessful lawsuits in the United States. However, in January 2009, the United States Court of Appeals for the Second Circuit ruled that the Nigerian victims and their families were entitled to bring suit against Pfizer in the United States under the Alien Tort Statute. A US$75 million settlement with the State of Kano was reached July 30, 2009.[8] Additionally two lawsuits also remain pending in New York, United States.[8] According to Wikileaked US embassy cables, Pfizer’s country manager admitted that “Pfizer had hired investigators to uncover corruption links to federal attorney general Michael Aondoakaa to expose him and put pressure on him to drop the federal cases.”[9]

Additional information about the Kano trial can be found in The Guardian article, Pfizer pays out to Nigerian families of meningitis drug trial victims.

Tequin/gatifloxacin

Tequin/Gatifloxacin was pulled from the market because it caused severe blood sugar reactions such as hyperglycemia and hypoglycemia.

The New England Journal of Medicine article, Outpatient Gatifloxacin Therapy and Dysglycemia in Older Adults, noted that:

“Between April 2002 and March 2004, we identified 788 patients treated for hypoglycemia within 30 days after antibiotic therapy. As compared with macrolide antibiotics, gatifloxacin was associated with an increased risk of hypoglycemia (adjusted odds ratio, 4.3; 95 percent confidence interval, 2.9 to 6.3). Levofloxacin was also associated with a slightly increased risk (adjusted odds ratio, 1.5; 95 percent confidence interval, 1.2 to 2.0), but no such risk was seen with moxifloxacin, ciprofloxacin, or cephalosporins. We then identified 470 patients treated for hyperglycemia within 30 days after antibiotic therapy. As compared with macrolides, gatifloxacin was associated with a considerably increased risk of hyperglycemia (adjusted odds ratio, 16.7; 95 percent confidence interval, 10.4 to 26.8), but no risk was noted with the other antibiotics. Risks were similar in the two studies regardless of the presence or absence of diabetes.”

A more recent study, that looked at a larger population than the NEJM study, Risk of Severe Dysglycemia Among Diabetic Patients Receiving Levofloxacin, Ciprofloxacin, or Moxifloxacin in Taiwan, found that all of the fluoroquinolones on the market increased the likelihood of both hyper and hypo glycemia in diabetic patients:

“A total of 78 433 diabetic patients receiving the antibiotics of interest were included in the study. The absolute risk of hyperglycemia per 1000 persons was 6.9 for moxifloxacin and 1.6 for macrolides. In contrast, the risk of hypoglycemia was 10.0 for moxifloxacin and 3.7 for macrolides. The adjusted odds ratios (AORs) and 95% confidence intervals (CIs) of levofloxacin, ciprofloxacin, and moxifloxacin compared with macrolides were 1.75 (1.12–2.73), 1.87 (1.20–2.93), and 2.48 (1.50–4.12), respectively, for hyperglycemia and 1.79 (1.33–2.42), 1.46 (1.07–2.00), and 2.13 (1.44–3.14), respectively, for hypoglycemia. Patients taking moxifloxacin faced a significantly higher risk of hypoglycemia than those receiving ciprofloxacin. A significant increase in the risk of hypoglycemia was also observed among patients receiving moxifloxacin concomitantly with insulin (AOR, 2.28; 95% CI, 1.22–4.24).”

As mentioned in the Temafloxacin section of this post, fluoroquinolone use has been linked to development of diabetes. Given that all fluoroquinolones cause blood-sugar dysregulation, and two fluoroquinolones have been removed from the market because they caused severe blood-sugar fluctuations, perhaps fluoroquinolones are behind the dramatic increase in both type 1 and type 2 diabetes over the last 30 years. It is a hypothesis that should certainly be looked into.

Conclusion

I struggle with whether or not I think all fluoroquinolones should be taken off the market. Even though I know that they are all dangerous, and sometimes even deadly, drugs, I also know that we are running out of antibiotics in our arsenal and that sometimes dangerous drugs are necessary in order to save a person’s life. I tend to think that Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/ofloxacin, and the other fluoroquinolones, should be severely restricted, and that there should be strict procedures followed when they are prescribed so that it is ensured that they will only be used in life-or-death situations where informed consent is given.

When looking at the fluoroquinolones that have been removed from the market, it always strikes me that they were removed from the market quickly after just a few deaths or a few studies that showed that they are dangerous drugs. The fluoroquinolones that remain on the market (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/ofloxacin) have also killed people. According to an FDA review with the subject, “Pediatric Exclusivity Postmarketing Adverse Event Review,” between 12/20/1996 and 08/27/2008, 924 people were killed by Levaquin/levofloxacin, including three children. The figures for Cipro/ciprofloxacin, Avelox/moxifloxacin, and Floxin/ofloxacin are similar. So, why do Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/ofloxacin have such staying power? Why are they still on the market when Temafloxacin/Omniflox, Raxar/grepafloxacin, Zagam /Sparfloxacin, Trovan/Trovafloxacin, and Tequin/Gatifloxacin have been removed from the market? I don’t know the answers to those questions–I wish I did. It seems to me that the FDA used to be a stronger, more independent, more effective organization than it is today, and that it used to actually pull dangerous drugs from the market.

Rather than removing dangerous fluoroquinolones from the market, or even imposing meaningful restrictions on the fluoroquinolones that remain on the market, the FDA has instead chosen to increase the size of the fluoroquinolone warning labels. As I have noted before, changed warning labels open the door for lawsuits and that’s a good thing, but it is overall a useless move that is devoid of real change. Not enough doctors or patients read warning labels, and they are a lousy way to communicate the real risks of pharmaceuticals.

The fluoroquinolones that remain on the market are not significantly different from the fluoroquinolones that have been removed from the market. Updating warning labels isn’t keeping people from getting hurt by these dangerous drugs. I understand hesitation to remove them from the market completely, but there should be significant restrictions put on their use. Right now they are not being used prudently or appropriately. That must change. Too many people are being hurt by these dangerous drugs.

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Minor, but Strange, Post-Flox Health Issues

I wrote the following post about a couple minor, but strange, post-flox health issues I had four years after taking Cipro/ciprofloxacin. In 2015 I went through a period of pain in my pelvis, and in early 2016 I had an odd issue where I felt like I had a hot coal in my abdomen in the middle of the night, and that was waking me up. I got through both strange issues, and neither bother me currently. I wrote this post with the hope that it could help others to get through the same issues.

https://www.hormonesmatter.com/pelvic-pain-abdominal-heat-personal-story/

Please read and share it – thank you!

I’m on the fence about whether or not I think these minor issues have anything to do with fluoroquinolone toxicity.

The bulk of my fluoroquinolone toxicity reaction was so long ago–in late 2011 and through 2012, and I truly have fully recovered since. I live my life as I did before I got floxed–I exercise, travel, have relationships, work, and socialize approximately like I did before I took Cipro/ciprofloxacin. I have energy and I’m not in pain. I can read, write, and think like I could before I got floxed. I’m doing fine, and since I took the Cipro/ciprofloxacin so long ago, I hesitate to connect my recent strange health issues to my experience with fluoroquinolone toxicity.

However…. I suspect that both these issues, however minor and transient, have to do with adrenal and hormonal dysregulation, and it’s possible that both were caused by the Cipro/ciprofloxacin I took back in 2011.

I wonder if destruction of vital gut bacteria by fluoroquinolone antibiotics leads to an inability to process and get rid of estrogen (1), which leads to estrogen-dominance and low progesterone (2). Low progesterone may contribute to several fluoroquinolone toxicity symptoms including peripheral neuropathy (3), and it is also linked to cortisol production abnormalities and adrenal fatigue (4). Adrenal fatigue and cortisol dysregulation may lead to other endocrine system problems and health issues (5).

A discussion of the effects of fluoroquinolones on the endocrine system is better spelled out in the WONDERFUL web site http://fluoroquinolonethyroid.com/, and an overview of how fluoroquinolones affect the thyroid can be found on https://www.hormonesmatter.com/fluoroquinolone-antibiotics-thyroid-problems-connection/. The effects of fluoroquinolones on the endocrine system should be explored further, as it certainly seems that there are significant connections. (When I posted this article–https://www.hormonesmatter.com/progesterone-peripheral-neuropathy/–about the connection between progesterone and peripheral neuropathy, two floxies noted that their PN went away when they were given progesterone while pregnant.)

I’m honestly not sure what steps I should take to keep my adrenals healthy, or what anyone else should do to manage their hormonal balance post-flox. Our hormonal systems are incredibly delicate, and there are complex feedback and feed-forward loops that make adjusting them difficult. Hormones often don’t react in a linear, predictable way, and it is highly recommended that you see a doctor before supplementing progesterone or any other hormone.

Some things that may help, that are less drastic than hormonal supplementation, are: manage your stress (through lifestyle adjustments, meditation, and breathing exercises), avoid xenoestrogens (plastics, pesticides, and processed foods), take probiotic supplements that have a significant amount of lactobacillus, eat small meals throughout the day, take a rejuvenating vacation, and avoid sugar and gluten. I plan to do those things, as well as vagal nerve toning exercises (https://selfhacked.com/2015/07/30/28-ways-to-stimulate-your-vagus-nerve-and-all-you-need-to-know-about-it/), float-tank sessions (https://floxiehope.com/2016/04/25/floatation-therapy-for-fluoroquinolone-toxicity/), acupuncture, and gentle stretching. With those things, hopefully I can keep my adrenals functioning well, and hopefully I can keep strange health issues from popping up in the future.

******

(1) “The gut also plays an important role in estrogen elimination. Phase II detoxification in the liver (medical term for the process of eliminating many hormones including estrogen) utilizes conjugation of estrogen to other compounds so they can be excreted in bile.[iv] If the gut flora is unbalanced, certain bacteria secrete an enzyme called beta-glucuronidase, which cleaves the glucuronide molecule from estrogen, allowing estrogen to be reabsorbed into circulation vs excreted in the stool. Lactobacillus, a healthy bacteria, decreases the activity of B-glucoronidase.[v] If the activity of B-glucoronidase is increased, more estrogen will be reabsorbed and potentially worsen the endometriosis.” https://www.vitalhealth.com/endo-blog/endo-belly/

(2) http://www.johnleemd.com/estrogen-dominance.html

(3) https://www.hormonesmatter.com/progesterone-peripheral-neuropathy/

(4) http://www.livestrong.com/article/496026-adrenal-fatigue-low-progesterone/

(5) https://adrenalfatigue.org/cortisol-adrenal-function/

 

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A Full Recovery

Several of the recovery stories on floxiehope.com describe people who are mostly, but not fully, recovered. A lot of the recovery stories are from people who can see the light at the end of the fluoroquinolone toxicity tunnel, but they’re not completely out of the tunnel yet. Even though these recovery stories are not of complete recoveries, I think that they’re still valuable. The show that life can go on through and after fluoroquinolone toxicity, and they describe the physical, emotional, mental, and spiritual journey while it is still vivid and raw. Many of the people with partial recovery stories on floxiehope.com continue to improve. Life goes on–sometimes with bumps in the road/setbacks–but often toward continued recovery.

Some people who have read these partial recovery stories have asked, quite reasonably, if there are any people who FULLY recover, and return to their pre-flox capabilities. To this, I answer, “YES, I have fully recovered.” Me – Lisa – the author of the majority of the posts on this site. I have fully recovered.

When I wrote my recovery story in 2013 I was 90-something-percent recovered. I still had some autonomic nervous system issues and the fear and anger that came with getting poisoned by ciprofloxacin lingered. I wrote an update in 2014 that noted some features of my continued recovery.

Since 2014, I have continued to improve. I was physically completely healed in 2014, but the emotional journey has continued. I have worked through a lot of fear and anger since 2014. Both the fear, and most of the anger, have largely gone away.

I have healed.

I write this not to brag, or to diminish the experiences of those who don’t recover (there are some people who don’t recover, and they deserve our sympathy and support), but, as always, to give others hope. A full recovery is possible. I have fully recovered. I hope for the same for all who read this.

I recently (I got home day before yesterday at the time of writing this) visited Australia on vacation and was able to do all the things that I wanted to with ease. I went on a tour of Tasmania with a bunch of 20-something year olds and was able to keep up with them. We hiked to waterfalls and jumped off sand-dunes. It was fun! My feet didn’t hurt and I had plenty of energy to keep up with them. I was able to eat whatever I wanted. I slept decently–even on couches and in hostels. It was a good vacation. It was exactly what it would have been if I had never gotten floxed. I have recovered.

I hope that my recovery, and these pics of my vacation, give you hope that recovery, and a life that is full of activity and adventure, are possible. I posted these pictures, and others, on my facebook wall as I was touring Sydney, Melbourne and Tasmania. Several people thanked me for sharing the photos because they gave them hope that this type of travel is possible post-flox. It is possible. I had a fantastic time, and I hope that you are each able to take a similar journey, or whatever else you desire that indicates a full recovery.

All aspects of my journey through fluoroquinolone toxicity took time. I encourage you all to be patient with yourselves. I couldn’t have traveled through Australia like I did earlier this month when I was first floxed. I can do it now though, and that feels really, really, really good.

Cradle Mountain Tasmania Harbor Bridge Sydney Melbourne Montezuma Falls Tasmaia Sand Dunes Tasmania

 

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Mitigating Fluoroquinolone Damage

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?

Maybe.

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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 [25] 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).

It is also noted in Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population, that:

“A mitochondrial-targeted form of ubiquinone (MitoQ) demonstrated a larger protective effect than did untargeted ubiquinone. Oxidative stress frequently occurs in the mitochondria [22], and fluoroquinolone-induced oxidative damage to mitochondria in tenocytes and chondrocytes has been reported [26].”

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.

Russian Roulette

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.

 

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Dear Epidemiologists – Please Take a Look at Fluoroquinolones

FQWallofPain

This paragraph, in a 2013 New Yorker article entitled The Big Sleep, caught my attention:

“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.”

The drug featured in the article was a new sleeping pill called Suvorexant, and the quote is about Ambien, but it made me wonder–Can someone PLEASE do a similar epidemiological study for fluoroquinolones? I want to know how health outcomes are for those who take fluoroquinolones versus those who take other antibiotics.

The symptoms of fluoroquinolone toxicity are similar to the symptoms of autoimmune diseases like R.A., M.S., Lupus, scleroderma, and other autoimmune conditions–and several people have been diagnosed with those diseases after experiencing fluoroquinolone toxicity. Fluoroquinolone toxicity symptoms are also similar to those of fibromyalgia, M.E./C.F.S., P.O.T.S., and other “mysterious” diseases of modernity. Fluoroquinolone toxicity, like those diseases, features peripheral neuropathy and central nervous system disturbances (like brain-fog, intractable insomnia, etc.). Psychiatric disturbances have been commonly reported among those suffering from fluoroquinolone toxicity. Severe musculoskeletal problems among those taking fluoroquinolones have been reported (and actually studied). Frighteningly, some who have experienced fluoroquinolone toxicity have experienced symptoms of neurodegenerative diseases like A.L.S. and Parkinson’s.

The warning labels for fluoroquinolones are 43 pages long, and list many of the symptoms of fluoroquinolone toxicity. In the November 5, 2015 FDA meeting regarding fluoroquinolones, it was acknowledged that symptoms of fluoroquinolone toxicity are severe and that they resemble the symptoms of many diseases. Fluoroquinolones have also been noted as a source of permanent disability, and delayed adverse effects have been experience and documented. The FDA panel at the November 5th meeting noted that further studies of fluoroquinolones are needed.

YES, further studies are needed.

We need long-term studies that determine whether or not people who are given fluoroquinolones are more likely to be diagnosed with an autoimmune, neurodegenerative, psychiatric, or “mysterious” disease than those who don’t take fluoroquinolones.

I hope that someone takes a closer look at fluoroquinolones to see what the long-term health consequences of them are. Patients and physicians alike should know whether or not there are long-term consequences to taking a prescription drug–so they can adjust their actions accordingly.

Additional musings on this topic can be found in the December 14, 2015 post on Hormones Matter, “Dear Epidemiologists, Consider Fluoroquinolones.”

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Is Fluoroquinolone Toxicity “Real?”

What is required for fluoroquinolone toxicity to be “real?”

Most of the symptoms of fluoroquinolone toxicity are listed on the warning labels.

Tendinitis? Yup, listed on the warning label. Muscle weakness? Yup, that’s there too. Cardiovascular collapse, loss of consciousness, tingling, pharyngeal or facial edema, dyspnea, urticaria, and itching? They’re right there on the warning label. Liver failure is there too – that’s what “hepatic failure” means. “Convulsions, increased intracranial pressure (including pseudotumor cerebri), and toxic psychosis have been reported in patients receiving fluoroquinolones, including ciprofloxacin.” Serious central nervous system effects like, “dizziness, confusion, tremors, hallucinations, depression, and, rarely, psychotic reactions have progressed to suicidal ideations/thoughts and self-injurious behavior such as attempted or completed suicide” are also listed on the warning labels. Permanent peripheral neuropathy is listed too. So are musculoskeletal disorders—though the warning label only notes that those happen in pediatric patients—kids. Prolongation of the QT interval, renal impairment, phototoxicity and diarrhea are also listed.

Do the warning labels leave some symptoms of fluoroquinolone toxicity out? Sure. Even the FDA acknowledges that, “While most of the individual AEs (adverse effects) that exist within FQAD (fluoroquinolone associated disability) are currently described in fluoroquinolone labeling, the particular constellation of symptoms across organ systems is not.” The warning labels are a good place to start though.

If someone takes a drug, then develops side-effects that are listed on the drug warning label, it’s pretty reasonable to think that what they’re experiencing is an effect of the drug. It’s not only reasonable, it’s probable.

If thousands of people experience similar adverse effects after taking a drug, those adverse effects are likely caused by the drug.

Thousands of anecdotes certainly help to build a case, but they are still anecdotes, so scientific experimentation is needed to show that a drug is as damaging and dangerous as people claim it to be.

There are more than 200 peer-reviewed journal articles about fluoroquinolones in the Research section of the Links & Resources page on this site. There is PLENTY of evidence that fluoroquinolones do a massive amount of damage to the human body.

There is PLENTY of evidence that fluoroquinolones damage mitochondria, increase ROS, deplete antioxidants, deplete iron, deplete magnesium, damage the microbiome, downgrade GABA, are endocrine disrupters, cause lysosomal disorders, form poisonous metabolites in the liver, activate mast cells and release histamine, AND MORE.

Can any one of those things cause a multi-symptom illness? Yes, of course they can. And fluoroquinolones DO cause multi-symptom, often chronic, illness.

Despite all that, there is not a diagnostic code for fluoroquinolone toxicity, and fluoroquinolone toxicity is not taught in medical school. Many doctors do not recognize fluoroquinolone toxicity when they have a patient who is dealing with it. (Though that is changing—more and more doctors are recognizing fluoroquinolone toxicity, and that is a very good thing.) And, despite all the damage that fluoroquinolones do to cells, there is no test that shows fluoroquinolone toxicity.

A diagnostic code and a test will likely be required for some people to believe that fluoroquinolone toxicity is real. We should fight for those things, because they’re important in getting the problem recognized and the solution sought.

Even without the diagnostic code or adequate test, fluoroquinolone toxicity IS REAL. It is acknowledged in FDA documents and backed up by hundreds of peer-reviewed articles. If someone chooses to ignore that evidence, well, they’re operating on faith in their notions of infallible doctors, not the real, scientific evidence that shows the damage that fluoroquinolones do to cells.

Regardless of what anyone thinks, your pain and your experience are real. I know that it hurts when people assert that your pain isn’t real, or that you’re imagining what you know to be true. It sucks, to say the least. But you know your body, and you know what happened to you. Your truth, and your experience, matter. Other people’s beliefs about your condition don’t.

 

 

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Can Fluoroquinolones Activate Mast Cells?

What is the connection between fluoroquinolone toxicity and mast cell activation / histamine intolerance? Can fluoroquinolones trigger mast cell activation and histamine intolerance?

The symptoms of mast cell activation are similar to those of fluoroquinolone toxicity. According to Mastocytosis Society Canada, the symptoms of mast cell activation are:

skin lesions or sores, skin rash, spots, redness, hives, persistent fatigue, itching, flushing & severe sweating, joint, bone pain, headaches, tachycardia (racing heartrate), eyes tearing/dry, eye pain, persistent body/tissue pain, difficulty exercising, vertigo, episodes of low body temperature, unexplained Vitamin B12 deficiency, scents/odors/chemical reactions, difficult menses (females), numbness & tingling in face and extremities, skin feels on fire, unexplained anxiety, sudden drops in blood pressure, fainting, persistent diarrhea, vomiting, unexplained weight loss, cognitive impairment, sinus problems, chest pain, vision problems, hair loss, mouth sores, nausea, swelling & inflammation, odd reactions to insect stings, anesthesia difficulties, anemia, thyroid problems, decreased bone density, unexplained weakness, shortness of breath, sunlight sensitivity, temperature (hot/cold) sensitivity, difficulty with foods, drinks, anaphylactoid reactions, anaphylaxis, gastrointestinal pain, bloating, unexplained medication reactions, enlarged liver/spleen, liver/spleen/bladder/kidney pain, enlarged lymph nodes, frequent urination, recurring infections, neuropathic pain, constipation, iron deficiency, unexplained bruising, bleeding, malabsorption, intermittent tinnitus or hearing problems.

That’s a pretty comprehensive list of fluoroquinolone toxicity symptoms too. (Though, as I discussed with Dr. Wahls in episode 14 of The Floxie Hope Podcast, all of the multi-symptom, chronic diseases of modernity have more in common with each other than they don’t, and should probably all just be categorized as cellular dysfunction disorders and treated similarly.)

Several floxies who have been able to get a diagnosis from a doctor have come back with a diagnosis of mast cell activation, or a disease that is related to mast cells. For example, one floxie friend’s doctors have diagnosed him with eosinophilia, a disorder that is related to mast cells and histamine intolerance. Other floxies have been diagnosed as histamine intolerant, and instructed to go on a low-histamine diet. As noted above, many floxies have symptoms of mastocytosis, and it is possible that fluoroquinolones activate mast cells and trigger mastocytosis.

Mast cell disorders are considered to be rare, but, according to Mastocytosis Society Canada, “escalation in the prevalence of these patients worldwide has resulted in a flurry of medical research ongoing in numerous countries. This indicates that these disorders may not be rare, but rather have been commonly misidentified and unfortunately for patients worldwide, commonly undiagnosed. Since approximately 2005, every year there are new theories, classifications, and adjustments to the mastocytosis definitions due to escalation of patients presenting with these disorders worldwide.”

I found the following information connecting fluoroquinolones and mast cell activation / mastocytosis:

  • From the International Journal of Tissue Reaction’s article, Effect of levofloxacin and ciprofloxacin injection on permeability of the tail vein in mice and skin microvasculature in rats, “These results suggest that LVFX and CPFX increase vascular permeability through the induction of histamine release from mast cells in rodents.” (LVFX is levofloxacin and CPFX is ciprofloxacin.)
  • From the Journal of Pharmacy and Pharmacology’s article, Characterization of Histamine Release Induced by Fluoroquinolone Antibacterial Agents In-vivo and In-vitro, “Intravenous injection of levofloxacin and ciprofloxacin at 1–10 mg kg−1 produced dose-related elevations in plasma histamine level in anaesthetized dogs. In contrast, levofloxacin was devoid of plasma histamine increment in anaesthetized rats at 100 mg kg−1, whereas ciprofloxacin at the same dose caused endogenous histamine release. Levofloxacin and ciprofloxacin induced non-cytotoxic secretion of histamine from all mast cells tested in a concentration-dependent manner, whereas rat skin and peritoneal mast cells were thirty- to one-hundred-times less sensitive to the effect of fluoroquinolones as compared with the canine skin mast cells.” Note that in studies beagle puppies have been made lame by fluoroquinolones.
  • From the Archives of Toxicology’s article, Differential response of mast cells separated from various organs and basophils of dogs to the fluoroquinolone antimicrobial levofloxacin, “Histamine releases induced by the fluoroquinolone antimicrobial levofloxacin (LVFX) were investigated using mast cells separated from various organs and peripheral basophils of dogs, being the most susceptible species to quinolone derivatives, in both in vivo and in vitro systems. An intravenous infusion of LVFX at 30 mg/kg over a 30-min period produced endogenous histamine release from 5 min, and a maximum at 30 min, in which the plasma LVFX concentration was approximately 50 µM. A close correlation (r=0.87, n=20) between histamine and LVFX concentrations in plasma during the infusion was observed. In the in vitro study, LVFX at 30 µM or more caused histamine release from mast cells separated from the liver and skin, but not from the gastric mucosa, lung, and peripheral basophils. More exactly, the liver mast cells were most susceptible to LVFX among the organs tested. On the other hand, compound 48/80, a prototype histamine liberator, elicited the histamine release from the liver or skin mast cells at 10 µg/ml, and the calcium ionophore A23187 at 1 µM exhibited the histamine release from the mast cells derived from all organs examined. Histochemical analysis revealed that the liver and skin mast cells had positive reaction for both alcian blue and safranin staining, but the gastric mucosa and lung mast cells were only positive for alcian blue staining, indicating that LVFX preferably activated the connective tissue-type mast cells rather than the mucosal-type mast cells. The degranulation of the liver and skin mast cells brought about by either LVFX or compound 48/80, unlike the calcium ionophore A23187, was blocked by pretreatment with pertussis toxin, suggesting the involvement of pertussis toxin-sensitive G proteins. The results obtained from the canine experiments strongly suggest that LVFX induces histamine release from the connective tissue-type mast cells distributed mainly in the liver, somewhat in the cutaneous tissue, through the activation of pertussis toxin-sensitive G proteins.”

The articles noted above are all from animal studies, not human studies, but they show that fluoroquinolones can activate mast cells and histamine release in mammals, and it’s reasonable to think that they may do the same things to humans that they do to dogs. Also, the similarity between fluoroquinolone toxicity symptoms and mastocytosis symptoms, though not a smoking gun, indicate that further studies of the affects of fluoroquinolones on mast cells should be done.

A few good resources for people with mastocytosis, and it’s possible that floxies are in that category, are:

  1. Dr. Theoharides web site
  2. Mastocytosis Society Canada web site
  3. The Low Histamine Chef web site
  4. Alison Vickery’s web site

I suspect that mast cells are profoundly affected by fluoroquinolones and that mast cell activation is a big part of fluoroquinolone toxicity. The potential options, and mechanisms for fluoroquinolone toxicity, are mind-boggling. Add mast cell activation to the list.

 

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Healing is a Journey

One day I was doing Crossfit and the next I could barely walk.  The flox bomb went off in me quickly.  I had a slightly delayed reaction – my body exploded 2 weeks after I finished taking ciprofloxacin (when I started taking ibuprofen and when I got my period – both the contraindicated NSAID and the hormonal shifts probably played a role) – but once the fuse was lit, the bomb detonated quickly.  Suddenly I was unable to do the things I used to do with ease.  I was barely able to walk, much less hike up a mountain.  I was barely able to think, much less go to school while working full-time.  

In some ways I’m grateful that I didn’t fall apart gradually.  If my health had declined slowly I may have thought that I was just getting old, or I may have thought that I was coming down with one of the named mysterious diseases like fibromyalgia or CFS/ME.  I did think I had an autoimmune disease, not knowing whether or not they could strike a person suddenly.  All of the tests for autoimmune diseases came back negative though, and it wasn’t long before I realized that my symptoms were those of fluoroquinolone toxicity.  Because I went from well to sick so suddenly, it was not only plausible, it was clear that I was poisoned.  

But having my health suddenly stolen from me was terrifying, traumatic and, frankly, it felt unfair.  I had worked out regularly.  I had always eaten decently.  I was only 32.  I was healthy and strong.  How could I get poisoned?

The thing that felt most unfair about the situation was that there was no magic pill to put me back together again.  A pill could mess me up, but there wasn’t a pill to heal me.  I could suddenly be sickened, but I couldn’t suddenly get well.  Doctors could prescribe pills that could tear apart my cells, but they didn’t seem to have any advice for how to put my cells back together.  

It sucked.  

It sucks, and is unfair, that there isn’t a pill (whether it be a pharmaceutical or a supplement) that can reverse the damage done by fluoroquinolones.  It sucks, and is unfair, that the damage can be done suddenly, but the repair – the healing – takes time.  

As unfair and sucky as it is, the process of healing is not instantaneous – it takes time.  Healing is a process that requires patience, compassion, forgiveness, surrender, hard work, luck, nutrition, movement, tenacity, support, and love, among other things.  Perhaps the time healing takes is an opportunity to gain those things.  We all need more patience, compassion, forgiveness, surrender, hard work, luck, nutrition, movement, tenacity, support, and love in our lives.  Getting poisoned is a lousy way to come by those things.  But while you’re going through the trenches of fluoroquinolone toxicity, I encourage you to look around for those silver linings.

It took me a long time to get over anger about my health being stolen from me by Bayer/Cipro.  I’m still not completely over it and maybe I never will be.  But finding some appreciation for the journey has been helpful.  It has been healing.  

Healing is a journey, and the journey is healing.  They go hand in hand.  

I have learned that lesson.  Perhaps it’s what the storm is about.

“And once the storm is over, you won’t remember how you made it through, how you managed to survive. You won’t even be sure, whether the storm is really over. But one thing is certain. When you come out of the storm, you won’t be the same person who walked in. That’s what this storm’s all about.” -Haruki Murakami

 

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Fluoroquinolones and Mercury Poisoning

I recently received a message from a floxie friend that raised an interesting question. My friend asked:

Have you ever heard that FQ antibiotics can release stored toxins like mercury into the body? It has been two years since Cipro for me, and one month ago they found out I am highly mercury poisoned. But before I took Cipro, I was okay. The doctors are guessing that I have been mercury poisoned for a long time but somehow it is showing up in my blood now. Since the symptoms of Cipro toxicity and mercury poisoning are about the same, I’m wondering if they’re related.”

Over the years, several people have raised the question of whether or not fluoroquinolone toxicity is related to mercury poisoning, but I hadn’t heard of test-documented increases in mercury levels after taking fluoroquinolones until my friend sent me the message above.

The symptoms of mercury poisoning are similar to those of fluoroquinolone toxicity. The symptoms of mercury poisoning are:

skin rashes and dermatitis; mood swings; memory loss; mental disturbances; muscle weakness; nervousness, irritability, and other emotional changes; insomnia; headache; abnormal sensations; muscle twitching; tremors; decreased cognitive functions; peripheral neuropathy and more.

According to Dr. Thomas Nissen, “ Symptoms of mercury toxicity are many and varied, since mercury can both reach and affect nearly every cell in the body! Systemic (overall) effects can occur for this reason. The particular symptoms you experience first depend on your own genetic weakest links and on other toxic suppressors.”

Similarity of symptoms does not necessarily mean that two disorders are one in the same. For example, Chronic Lyme Disease and AIDS have similar symptoms, but that doesn’t mean they’re the same diseases. But it’s still interesting to explore the possibility of fluoroquinolone toxicity being related to mercury poisoning.

I searched for journal articles about the effects of quinolones on mercury. Unfortunately, I didn’t find much information. Most of the information I have is anecdotal and stems from me attempting to understand fluoroquinolone toxicity (with zero background in biochemistry), so please take this information for what it’s worth.

Fluoroquinolones have been documented to chelate magnesium and iron from cells. I wonder if mercury in the body is bound by these minerals, and then gets released into the body when the fluoroquinolone chelates the necessary mineral from the body (or when the quinolone binds to the mineral, stealing it from whatever it’s currently bound to).

Dr. Nissen points out that mercury can displace other minerals in the body, and that mineral displacement can cause serious health problems:

Replacement reactions, also called fight for site, occur when mercury (usually with a +2 charge) grabs the biological spaces which should be filled by necessary minerals. Symptoms that can be caused by a deficiency of minerals displaced by mercury include:

  • Magnesium: irregular heartbeat, receding gums
  • Iron: anemia
  • Copper: anemia, thyroid dysfunction, impaired digestion
  • Zinc: anorexia nervosa, loss of taste and smell, loss of appetite, low libido, PMS
  • Iodine: thyroid dysfunction”

For floxies, I wonder if the fluoroquinolone begins the cycle of mineral replacement. Fluoroquinolones chelate minerals, then mercury binds to the site that was vacated by the mineral, then mercury toxicity leads to chronic health conditions.

There are many “drug muggers” out there – drugs that deplete vital minerals and nutrients from the body. I wonder if all the drugs that deplete necessary minerals from the body are opening people up to mercury poisoning.

There are a variety of factors that determine how well one’s body can deal with mercury. Genetic factors such as MTHFR mutations (which play a role in determining how well a person deals with toxins) certainly play a role, as do an individual’s antioxidant levels. Many floxies have MTHFR mutations, and fluoroquinolones have also been shown to deplete glutathione and other antioxidants. Some floxies, including Richard and the author of Say Friend and Enter, have dealt with mercury poisoning issues as well as fluoroquinolone toxicity issues. Obviously, people who suffer from fluoroquinolone toxicity are less adept at metabolizing and clearing fluoroquinolones than those who take Cipro, Levaquin and Avelox without ill effects. Perhaps floxies are less able to handle other toxins, including heavy metals, as well.

There are a variety of mercury detoxification protocols that you can find online. Dr. Mercola’s protocol seems like a good place to start – http://www.mercola.com/article/mercury/detox_protocol.htm. He suggests:

  1. Avoid sugar, milk, grains and processed foods
  2. Eat foods that increase glutathione
  3. Take probiotics and eat probiotic rich foods
  4. Supplement magnesium
  5. Supplement chlorella
  6. Supplement MSM
  7. Eat garlic and cilantro
  8. Supplement minerals
  9. Make sure that you have sufficient hydrochloric acid levels to absorb minerals from your food
  10. Supplement vitamins C and E
  11. DMPS therapy

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Please note that chelation therapies (DMPS) can be dangerous and they should not be done without the direct supervision of a doctor. They can be hard on the kidneys, so they should also not be done unless absolutely necessary. Be careful, please!

As I noted earlier, this post is about possible connections, not established facts. Fluoroquinolones are not documented to have anything to do with mercury toxicity according to the journals I could find. The symptoms of fluoroquinolone toxicity and mercury poisoning are similar though, and given that fluoroquinolones have been documented to have profound effects on cellular mineral homeostasis, I think that it’s a hypothesis that’s worth exploring.

Post-script – If anyone reading this gets their mercury levels tested, please let me know what the tests say – I’m quite curious. Thank you!

Post-post-script – I wanted to point out some comments that Jason recently made on the floxie hope home-page about mercury. He has done extensive research on the topic and what he has to say is certainly valuable:

Toxic Metals and other Toxic substances (like Cipro…) are a HUGE issue, and as I guess you have gathered a mouth full of Mercury is bad situation to be in, and a major potential cause of Brain Fog and many many more issues for someone. This can be grossly exaggerated with someone with a MTHFR Gene issue, since they will NOT be able to detox Metals, Fluorides, Chlorine’s, and all the other Toxic Waste/Toxic Metals/Chemicals that we are subjected to on a daily basis properly, thus they will build up in the body and make the person more and more unwell. Since you are in the USA, for $99 the 23andme test is definitely a “no-brainer” in my opinion if you have not done it already, to find out if you do have these issues or not, on top of potentially being toxic in Mercury and other Metals.

Pretty much every living person has a toxic burden, Metals, Halides, and more; many people are able to keep it low enough to be healthy because their Methylation pathway works properly, actively detox, etc but others are not so lucky, and are even more unlucky if they do not realize this is the cause of most/all their issues. There was a whole bunch of discussion on Genes and the 23andme test last page starting from post 2 if you are interested in finding out more about this important part of someone’s health.

I would suggest to find a good ND, but be very careful with “Challenge Tests”. Many of them will want to give you a dose of DMSA or something else like DMPS, EDTA, etc and often the doses are VERY big, and quite dangerous (a big dose will ensure high levels show up on test, ensuring more money for them since you will “need” treatment = dangerous greed tactic). DMSA will mobilize several toxins in the body all at once, and if a person’s toxic load is large enough the body will not be able to handle all the poison being in the system at one time, and terrible damage can result. If you google Andy Cutler you will see he recommends not doing a challenge test at all, many people are following his advice and his Protocol for detoxing the body of Metals, he believes it needs to be done is slow safe fashion, which makes sense to me.

I myself am a little torn on the “testing issue”. I had a hair test done for Metals and Minerals which is what many people recommend you do to find out your toxic load. The things is it does NOT give you the whole picture, it is really telling you what the body is “expelling”, it is NOT telling you what your body is potentially harboring, since many of the Metals are hidden/stored in the body in Fat Cells, like the Brain, and if not mobilized they just sit there and screw you over, and will not come out in the hair, thus your hair test could say you are “low” in Uranium, or Nickel, but in fact you are not low, you are just not efficiently expelling/detoxing it at the time of the test. However, if the test shows you are high in something, there is a good chance you are actually too high and your body is trying to detox the excess of which some of it ends up in the hair. So these levels that show up, are somewhat dependent on if someone has a Methylation issue also, since poor Methylators are poor detoxer’s potentially skewing the results.

Having said all that, it is one of the best tests to do for this, and highly recommended to do regardless to find out what your Mineral profile looks like, though I still think there might be some viability of a “safe challenge test”, which would be as described above only with a smaller safer amount of a Chelator given right before a Urine test. Yet the reliability of the Hair test for Minerals is too somewhat questionable, out of the 100 or so labs around the USA that do these tests, 98 of them WASH the hair before doing the test. The trouble with this is many of the Minerals are water soluble, so washing the hair with a mild detergent and acetate like most do can skew the results of many of the Minerals. Google “Dr. Wilson Hair Test” and you will see more of what I am talking about. You will also find recommended ND’s on his site that use the one good lab in the USA that do not wash the hair.

This is all my opinion, one that is shared but none-the-less where I stand on the whole thing. I apologize for not giving a “Clear” solution, but this is frankly because in my opinion there isn’t one. As a result, for many years I did “nothing”, I now regret this and don’t recommend that course of action either. For yourself, my unprofessional recommendation is to “not” have a challenge test done, especially with Mercury still in your mouth, also do NOT take any chelators, and avoid Cilantro too, as this crosses the Blood Brain Barrier and taking this can bring Metal from the Mouth/Body right into the Brain. Doing the Hair test is a good idea, it will give you at least some idea on what is going on in your body, and if we are to believe Dr. Wilson, a VERY good idea, he has written a very long book on Hair Tests (his Mentor invented the idea) and how to interpret them, one I wish I had, but there is a lot of info on his website and ARL Labs website (the one he recommends) about how to interpret the results, and a good ND will hopefully be educated on these methodologies. Regardless of the results, if you can afford it if I was you I would find a good Huggins Dentist (trained in removing Mercury fillings safely) asap and start getting those removed. I had one that was “cracked”, and have no doubt it has caused me issues. Good luck, if you do have a heavy toxic load please be patient in its removal.

AND

I think the most popular is the Andy Cutler Protocol, which is a very slow/safe but PITA method, and uses synthetic Amino Acid Chelators DMSA, DMPS and also ALA all in small doses on a very strict time schedule due to their half lives. Lots of info on net about this you will see, chelators are bought from company out of Africa IIRC, there is a good Yahoo support group/forum where people answer questions etc (poorly organized unfortunately)

There are some others of note, and some are opposed to Cutler method such as Dr. Lawrence Wilson http://drlwilson.com/articles/chelation.htm (very good website with a TON of info on everything health). EDTA can be used, Dr. Mercola has made some suggestions like using Cilantro and others, funny enough Cutler warns against using EDTA and Cilantro, for potentially valid reasons, confusing the issue further. 😦

I think the best course of action for someone depends on many things. Do they still have Mercury fillings? Do they have the MTHFR & other mutations in their Genes? (found out with 23andme test) How big is their toxic load?

The first course of action is always to get fillings removed safely, and then getting a Hair metal/mineral test done. To me getting the 23andme test for $99 should be done too, for reasons I noted on FH. Then with that done, and with that information a suitable course of action can be recommended (I sound like a bluddy Naturopath here….) If someone has a huge toxin burden, I think the Cutler method makes sense, but the MTHFR could complicate this. If someone is moderately toxic, Cutler method might still be good, or a combination of ideas might be good enough, again depending on the MTHFR issue. If someone is only mildly toxic, they should for sure address the MTHFR issues first and foremost, which would help the body alleviate the burden on it’s own (of course with a MTHFR issue someone is likely NOT going to have small burden, depending on their age and exposures of course). Also with smaller toxic burden, things like Cilantro, Wheat Grass and regular exercise and Saunas should be enough to bring the burden down, assuming they limit their future exposures.

I hope that helps, unfortunately the waters are a little muddy on this, not unlike Cipro poisoning.

Just a final note that these are only my “untrained” opinions. Toxic load is a serious wide-spread issue, causes very serious health issues, and removal has to be taken very seriously and not “toyed” with, someone needs to put their trust in a professional or do a whole lot of research. There are many complicating factors, such as Candida overgrowth (something DMSA potentially stimulates), MTHFR & other Genes, current past/health problems of the person and things like condition of Liver/Kidney’s, Cancer, FQ toxicity, etc. (Emphasis added by Lisa.)

I also forgot to mention Spirulina & Chlorella, although I did mention Dr. Mercola, and this is 2 things he advocates. They are also something Dr. Sircus recommends (along with a few others, see link), here is a good article on the whole topic here: http://drsircus.com/medicine/essentials-natural-chelation

He actually gives a LOT of accurate advice in this article in my opinion, like his notes on ALA which are important, and note what he says about Magnesium too, which applies 10 fold to a Floxie with Heavy Metals. He notes that some studies found Chlorella on its own, did not seem to chelate anything effectively. However when used with Cilantro, it does, and this makes perfect sense to me because Cilantro is a “mobilizer”, it irritates the Metals stored and Chlorella is a “binder”, it is extremely absorbent and will bind to Metals to help them exit the body and not be “re-absorbed” once they are mobile, which is critical. Done wrong, the Metals from one area can mobilize and then be re-absorbed in other areas causing great oxidative damage like to the Brain.

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But Antibiotics Save Lives!!!

David Wolfe, a health, eco, nutrition and natural beauty expert (more information about him can be found HERE) posted the picture above on facebook.  He has more than 1,200,000 facebook followers and I greatly appreciate his help in spreading the word about the dangers of fluoroquinolones!  Many people commented on picture and told their story of how fluoroquinolones hurt them.  There are a lot of us out there, and the more the word gets spread, the more likely change is.

As always, there were some nay-sayers.  Honestly, there were a lot more people sharing their stories than there were nay-sayers, and I’m not suggesting that we all gang up on them, but I have some thoughts about the some of the nay-saying comments.  Here are some examples of the nay-saying comments:

“Want to go back to the dark ages before antibiotics?”

“If we didn’t have antibiotics…alot of people would die..”

“People who don’t believe in medicine should live on their own island of ignorance and watch their life expectancy drop to that of their intelligence.”

“Without antibiotics you can’t treat people with bacterial infections. Aka ur screwed. Pls don’t mislead the public. stick to quotes. My sincere request. Please.”

“Antibiotics have saved over 1 billion lives. Mr Wolfe’s irresponsible comments will cause deaths!!”

“WAIT! Are you trying to scare people off antibiotics now??? How many people would have to die of preventable illnesses before you retract this?”

Sigh.  Why do these people think that all antibiotics are the same?  Why do they think that all antibiotics are safe?  Why do they think that warning people about the dangers of fluoroquinolones equates to being anti-antibiotic?  Where is the grey area?  Can’t some antibiotics be appropriate for use in some circumstances but not others?  Can’t different antibiotics have different safety profiles?  Isn’t information about the dangers of drugs valuable so that people can make informed choices?  Doesn’t it matter that fluoroquinolones damage nerves, the musculoskeletal system, the eyes and kidneys?  Can’t that information lead to greater consumer knowledge and informed consent when fluoroquinolones are prescribed?  Can’t the dangers of fluoroquinolones be acknowledged without being “anti-antibiotic?”  Can’t we fight for prudent and appropriate use of all antibiotics (especially FQs) without negating the lives that have been saved by antibiotics (including FQs)?  GREY AREA, folks!  The world isn’t black and white.  Sigh.

A quote from my most recent post, “‘The 21st Century Cures Act’ Is On Its Way – Here’s Why You Haven’t Heard About It” seemed like an appropriate response to a lot of the nay-sayers.  Feel free to use this if you want it:

“A healthy and balanced microbiome (“the ecological community of commensal, symbiotic and pathogenic microorganisms that literally share our body space”) is crucial for all areas of health, and a disturbed microbiome has been linked to all of the diseases of modernity, including mental health disorders, neurodegenerative diseases like Parkinson’s and Alzheimer’s, autoimmune diseases, inflammatory bowel disease and Crohn’s disease, mysterious diseases like fibromyalgia, autism, etc. And while there is acknowledgement of the role that a healthy microbiome plays in these diseases, researchers and journalists alike have been loath to acknowledge the role antibiotics have played in contributing to these diseases of modernity. No one wants to be anti-antibiotic. Everyone knows that antibiotics have saved millions of lives, but that doesn’t mean they are without consequences. And the good that penicillin has done doesn’t mean that all antibiotics are equally safe or effective. I can make a pretty thorough argument that fluoroquinolone antibiotics, like Cipro/ciprofloxacin and Levaquin/levofloxacin, drugs that work by “inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination,” are at least partially responsible for many of the diseases of modernity (more information can be found HERE, HERE and HERE). Fluoroquinolone antibiotics do not have the same safety profile as amoxicillin, and to assume that they do because both are categorized as antibiotics, is foolish on multiple levels.”

That’s my two cents of a response to the people who say things like the quotes above.  Also, quit giving carte blanche to the pharmaceutical companies if they label their dangerous drug as an antibiotic, because that’s just stupid.

Now I’m done.  🙂

 

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Taking Career Opportunities

People who read and follow Floxie Hope are often surprised to hear that I have a day job.  Yes, I spend a lot of time on Fluoroquinolone Toxicity advocacy.  No, it does not pay the bills.  So, I have one of those job things.

Today, May 27, 2015, is my last day at the job I’ve had since March 1, 2011.  I’m moving on to a similar organization (I’m leaving the names of both my current and future employer out of this… just ‘cause) where I’ll be doing the same line of work, but the new job will give me more responsibility, opportunities, and money.  It’s a step up in my career and I’m excited for the future.

All change is bitter-sweet though….. and a little scary.

I got floxed in December, 2011 and there was a time when I thought that I wouldn’t be able to do my current job, much less move on to a job that required more of me – more work, more intellect, more problem-solving, more travel, more energy, etc.  My reading comprehension, concentration, memory and ability to relate to others were horrible after I got floxed.  I didn’t feel capable of doing my job for months after the flox-bomb went off in me.  Things that I did with ease before I got floxed suddenly became difficult.  I had trouble doing the most basic tasks.  I was scared that I no longer had the mental capacity to do the tasks that were required for the job, and that I was going to get fired.

My fears were largely unfounded, because my employer was incredibly patient with me.  My boss and co-workers saw me go from being strong and athletic to barely being able to walk a block, and they were concerned.  They let me take time off of work to go to appointments as necessary.  They saw that my mobility was hindered and did thoughtful things for me – like getting my print-outs from the copier and bringing them to me.  They believed me, and told their loved ones to stay away from the drugs that hurt me.  I am forever grateful to them for their support, sympathy and kindness.  They are wonderful people and it’s a good organization.

Around one year post-flox I had an annual performance review with my boss.  I thanked him profusely for putting up with my loss of mental capacity.  He seemed perplexed by my assertion that my brain had been fried for the last year.  As far as he was concerned, I was doing fine.  I’m glad that my memory loss and other cognitive deficits weren’t as apparent to him as they were to me.  (Floxie friends – know that you may perceive your cognitive issues to be worse than others see them.  I know what it’s like to feel stupid, but you’re not stupid, and other people will be more forgiving of any mental lapses that you have than you will be toward yourself – so try to be kind to yourself.)

I will always feel grateful for my employer for standing by me while I was sick.  They may not see it as a big burden, but I see it as a great blessing that I am thankful for.

It is time for me to move on from a very good organization though.  I have opportunities to pursue, and I’m hopeful that my new employer will be as good to me as my last employer.

There was a long period of time – years – when I truly didn’t think that I would be capable of furthering my career and taking a job that required more of me.  I was grateful for my position, but I was trying my hardest not to lose what I had, and moving onward and upward weren’t possibilities that I could even consider.  Now those possibilities are a reality, and I have the capacity to take new opportunities.  It’s nice, and I’m thankful for the support in my past that has allowed me to get to these opportunities to better my future.

I hope that all my Floxie friends recover.  May you all be blessed with opportunities and improving health.  Both happened for me, and I am hopeful that they will happen for you too!  Hang in there – it gets better.

Hugs,

Lisa

 

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What is Fluoroquinolone Toxicity? (Part 2)

 

The first post I wrote on Floxie Hope was a post entitled, What is Fluoroquinolone Toxicity???  It went over some theories that I had heard about FQ toxicity, and, more importantly, what FQ toxicity felt like.  It was a good start.

Since I wrote that post, I have done hundreds of hours of research on fluoroquinolones.  The research has resulted in this, updated post –

WHAT IS FLUOROQUINOLONE TOXICITY? on Hormones Matter.

It goes over some theories about the damage that fluoroquinolones do to the body.  It’s clear that fluoroquinolones do a lot of damage.  I wish that there were more researchers putting all the pieces together.

Luckily, understanding exactly what fluoroquinolone toxicity IS, isn’t required for healing.

 

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Post-Ebola Syndrome Emerges In West Africa – Links To Bayer Explored

 

Very sadly, “post-Ebola syndrome” looks a lot like fluoroquinolone toxicity syndrome. Bayer pumped 3 million euros of Cipro into West Africa during the crisis. Now people are chronically ill with a “mysterious disease.” It should be noted that Cipro has never been shown to be effective at treating VIRUSES like ebola. It is an unapproved use. Sending millions of euros of Cipro to West Africa was a medical experiment that was, and is, criminal.

A post about this horrible situation is in Collective Evolution.

Post-Ebola Syndrome Emerges In West Africa – Links To Bayer Explored

 

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The Floxie Hope Podcast Episode 12 – Elise

Elise Floxie Hope Podcast

 

I had the pleasure of interviewing Elise for Episode 12 of The Floxie Hope Podcast.

Elise shares a lot of valuable information in her podcast.  She goes over her long journey of fluoroquinolone toxicity, and things that she has done to heal, in the podcast.

You can listen to the podcast through these links –

http://www.floxiehopepodcast.com/episode-012-elise/

https://itunes.apple.com/us/podcast/floxie-hope-podcast/id945226010

Elise has generously offered to help anyone who wants to reach out to her –

Elise’s facebook info: https://www.facebook.com/elise.child.5

Email: elisedchild@gmail.com

In the podcast, Elise mentions that her naturopathic doctor, Dr. Cynthia Buxton, has helped her immensely.  Dr. Buxton can be found through this link – http://naturalhealthcarenw.com/?p=346

Elise was also helped by eating for her blood type.  Information about that can be found here – http://www.4yourtype.com/

The TQI diet also helped Elise – http://toquietinflammation.com/

Univera Xtra also helped Elise – https://www.newunivera.com/en-us/search?Text=xtra&Area=Products

Elise also found Cleansing/gut health options to be helpful: https://humaworm.com/, http://www.renewlife.com/herbal-cleansing/paragone.html

Liver support: Elise currently takes a tincture with milk thistle, dandelion, etc.

Elise noted, “I forgot to mention the value of amino acid therapy in my own healing, which can be extremely helpful with depression, anxiety, insomnia, getting off of antidepressants, etc. I feel it is very important to do this with one’s doctor for dosage, length of use and quality of supplements. Amino Acid Therapy Info: (some examples, lots of info out there) http://www.neurogistics.com/thescience/aminoacids.asp, http://www.antianxietyfoodsolution.com/wp/wp-content/uploads/2014/11/Anxiety-mood-emotional-eating-sugar-cravings-mood-quiz-by-Trudy-ScottV2.pdf

If you have any questions about any of these products, please contact Elise.

Thank you for listening to The Floxie Hope Podcast!  Stay hopeful, friends!

 

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FDA Testimony

Generic Fluoroquinolone Testimony FDA

Me practicing my speech. I won’t wear my fleece hoodie for the real thing. :p

I’m in Washington D.C. and will be testifying to the FDA at approximately 8:30 am EST on Friday March 27, 2015.  Rachel Brummert, President of the QVF will be testifying at approximately 3:50 pm EST the same day.

You can view our testimony through the webcast link noted in this FDA meeting announcement – http://www.fda.gov/Drugs/NewsEvents/ucm431265.htm

Rachel and I will do our best to tell stories of pain and suffering caused by fluoroquinolones, and to encourage the FDA to change the rules that are keeping people who are hurt by generic drugs from gaining recourse through the justice system.

A couple of notes – I wasn’t able to fit in all of the stories that were sent to me.  I had to cut many poignant stories because of time–I’m allowed to speak for 5 minutes.  Everyone who sent me your story – THANK YOU!  I wish that I could tell them all!

Also, this hearing is not about fluoroquinolones specifically.  It is about the fact that generic drug manufacturers cannot be held legally responsible for the damage done by their products.  Many people who have been hurt by various generic drugs will be testifying.  Generic drug manufacturers will also be testifying.  I can’t imagine what they’ll say though.  Are they actually going to argue that they shouldn’t be held responsible for the safety of their products?  Probably.  But if they can’t be held responsible for the damage done by their products, who will be held responsible?  The FDA?  Last I checked, suing government agencies wasn’t possible.  Generic drug manufacturers need to be held responsible for the damage caused by their drugs.  I hope that the FDA does what is in their power to make generic pharmaceutical companies liable for the drugs they make.

 

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The Ciprofloxacin Song

This is adorable and sad at the same time.  I hope that Ashley has improved.  She posted this in 2010.

She’s right – FIGURE IT OUT, BAYER!  Why is the list of adverse effects getting longer and longer each year?  How many people have to suffer from adverse effects of these drugs before VERY serious consideration goes into whether or not they should be on the market?  What is the mechanism by which fluoroquinolones downgrade GABA-A receptors?  How much damage do fluoroquinolones do to human DNA – both mitochondrial and nuclear?  What are the consequences of damaging the DNA replication cycle for bacterial DNA within a person?  What are the consequences of damaging nuclear DNA of human cells?  What are the consequences of damaging mitochondrial DNA of human cells?  What are the long-term consequences of using fluoroquinolones?  What are the intergenerational consequences of using fluoroquinolones?  These questions aren’t too much for us to demand answers to.  Bayer has the means to answer these questions, SO GET ON IT, BAYER.  And OF COURSE they won’t do it voluntarily, SO MAKE THEM STUDY IT, FDA!

Anyhow, here is Ashley singing The Ciprofloxacin Song:

 

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Testifying for Justice for Victims of Generic Drugs

Thousands of victims of generic ciprofloxacin, levofloxacin, moxifloxacin and ofloxacin have been unable to pursue legal recourse because of a couple of Supreme Court decisions that ruled that generic drug manufacturers cannot be held liable for harm caused by their products.

You can read more about these horrible Supreme Court decisions in this June, 2013 New York Times article, “In 5-4 Ruling, Justices Say Generic Makers Are Not Liable for Design of Drugs.

People are just as legitimately hurt by generic drugs as they are by name-brand drugs.  Arbitrarily taking justice away from a person because they were hurt by a generic drug is infuriating and wrong.

I have been given the opportunity to do something about this horribly unjust situation.

I have been invited by the American Association for Justice to speak at a Congressional Hearing on Capitol Hill on March 26th and to testify at a FDA hearing on March 27th regarding the lack of legal recourse for those hurt by generic pharmaceuticals.

This is a VERY exciting opportunity and I am honored to be able to tell Congress and the FDA about the harm that generic fluoroquinolones have done, and to encourage them to enact legislative changes that enable those who have been harmed by generic drugs to seek recourse and gain justice.

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Rachel Brummert, President of the Quinolone Vigilance Foundation, will also be presenting/testifying and you can learn more about what this opportunity will involve for both of us by reading the March 6th post on www.saferpills.org, “Executive Director Rachel Brummert speaking at Congressional Hearing and FDA Hearing.

It would be great if as many stories as possible about the pain caused by generic fluoroquinolones could be heard.  There are a couple of ways that you can share your story of pain caused by a generic fluoroquinolone, and the lack of justice available to you.

First, you can submit a comment to the FDA.  Instructions on how to do so can be found in the March 4th post on www.saferpills.org, “Generic Drug Victims: Share your story.”  I encourage EVERYONE to submit their story as a public comment.  Public comments really do make a difference!

Second, both Rachel and I would love to share some of your stories in our testimonies.  If you can please email either of us your stories, and what you would like us to say on your behalf to Congress and the FDA, we will appreciate it!  My email address is floxiehope@gmail.com and Rachel’s is Rachel@saferpills.org.  Rachel and I will coordinate so that we can tell as many stories as possible within the time allotted to us.  We can’t promise that we’ll be able to get to everyone’s story, and we will need to edit the stories for time and relevance, but we would love to share as many impactful stories as possible.  Please send either me or Rachel your stories / what you want us to say on your behalf, asap.  We need to get a drafts of what we are going to say to the American Association for Justice by the end of this week.  Sorry for the time crunch and thank you very much!

Thank you,

Lisa

 

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Study Finds that Ciprofloxacin Depletes Mitochondrial DNA

DNA replication fluoroquinolone Topoisomerase Interrupter

This post contains quotes from the article “Delayed Cytotoxicity and Cleavage of Mitochondrial DNA in Ciprofloxacin-Treated Mammalian Cells” that was published in Molecular Pharmacology in 1996.  It’s a good article.  It’s an interesting and damning article.  It’s a difficult article.  It would be nice if more people read it, and I wish that its implications were better understood and explored by research scientists and regular people alike.

Direct quotes from the article are in bold and italicized.  My commentary follows each quote.

“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.”

Ciprofloxacin depletes mitochondrial DNA in mammalian cells.  It’s right there in black and white.  I have no idea why it didn’t strike anyone as alarming when it was published in 1996.  It sure is alarming now.

It should be noted that, “There is indeed experimental evidence that prolonged injury to mitochondria, such as that which typifies oxidative injury to mitochondrial DNA or to components of the electron transport chain (ETC), has to cross a certain threshold (or a number of thresholds) before cell damage or cell death becomes manifest.” (source)  And that mitochondrial damage is linked to “symptoms such as fatigue, muscle pain, shortness of breath, and abdominal pain can easily be mistaken for collagen vascular disease, chronic fatigue syndrome, fibromyalgia, or psychosomatic illness.” (source)  Mitochondrial dysfunction has been linked to multiple diseases of modernity including autoimmune diseases, neurodegenerative diseases, autism and “mysterious” diseases such as fibromyalgia and ME/CFS.

Also, as I’ve pointed out before, the FDA has noted in their internal documents that fluoroquinolones are toxic to mitochondria, and that mitochondrial damage is linked to many diseases, including neurodegenerative diseases.  More information about that can be found in the post, “FLUOROQUINOLONE ANTIBIOTICS DAMAGE MITOCHONDRIA – FDA DOES LITTLE

“Resistance was not due to a decrease in cellular drug accumulation, suggesting that ciprofloxacin cytotoxicity is caused by the loss of mtDNA-encoded functions.  Analysis of mtDNA from ciprofloxacin-treated cells revealed the presence of site-specific, double-stranded DNA breaks.”

Consequences?  Implications?  What happens when cytotoxicity is induced by DNA breaks?

“These results suggest that ciprofloxacin may be causing cytotoxicity by interfering with a mitochondrial topoisomerase Il-like activity, resulting in a loss of mtDNA.”

Many assert that fluoroquinolones only affect bacterial topoisomerases.  It turns out that mitochondrial topoisomerases are affected too.  Fluoroquinolones should be used as prudently and cautiously as all other topoisomerase interrupting drugs.  All the other topoisomerase interrupting drugs are chemo drugs that are only used to treat cancers.  To prescribe a drug that depletes mitochondrial DNA and affects human topoisomerases in order to treat urinary tract infections and traveler’s diarrhea is absurd, short-sighted and wrong.

It should also be noted that, “Our data suggest that chemicals or genetic mutations that impair topoisomerases, and possibly other components of the transcription elongation machinery that interface with topoisomerases, have the potential to profoundly affect expression of long ASD (autism spectrum disorder) candidate genes. Length-dependent impairment of gene transcription, particularly in neurons and during critical periods of brain development, may thus represent a unifying cause of pathology in many individuals with ASD and other neurodevelopmental disorders.” (source)

The team of scientists who wrote that last quote are looking at whether or not fluoroquinolones turn on genes that are related to autism.  The results of their exploration have not yet been published.

What is known though, is that topoisomerases are really important.  Duh–they’re the enzymes responsible for proper DNA and RNA replication—did someone think they were optional?  Interrupting topoisomerases with drugs is a really, really, really bad idea.

“Studies have also suggested that 4-quinolones may interfere with cell growth by inhibiting mammalian mtDNA replication (6, 11). Castora et al. (11) 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.”

Naladixic acid is the backbone of all fluoroquinolone antibiotics.  The quote speaks for itself.

 “We recently demonstrated that the 4-quinolone drugs nalidixic acid and ciprofloxacin cause a selective loss of mtDNA in drug-treated mammalian cells (6). 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 a delayed cytotoxicity in cultured mammalian cells at concentrations that deplete cells of mtDNA.”

DELAYED CYTOTOXICITY!  When someone says that you “shouldn’t” be experiencing an adverse reaction to a fluoroquinolone weeks, months or even years after you took the drug, show them this.  Delayed cytotoxicity and mtDNA depletion–they’re right there.  Fluoroquinolones are NASTY drugs.  Why they are used frivolously is beyond my comprehension.

“We previously demonstrated that ciprofloxacin induces a selective depletion of mtDNA in mammalian cells. The depletion of mtDNA preceded a decrease in mitochondrial respiration and cell growth, suggesting that mtDNA was a primary target of drug action (6). Studies have recently shown that some cultured mammalian and avian cells can survive in the absence of mtDNA-encoded functions if the growth medium is supplemented with pyrimidines, pyruvate, and elevated concentrations of glucose (21-23). Cells deficient in mtDNA rely exclusively on glycolysis for energy.”

Hmmmmm…. So do our cells need/want more glucose??

And, again, I’d like to point out the clearly stated, “ciprofloxacin induces a selective depletion of mtDNA in mammalian cells.”

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“The apparent decrease in mtDNA cleavage at higher drug concentrations is reminiscent of the effect of DNA intercalating anticancer drugs on nuclear topoisomerase II enzymes (29, 30). Intercalating anticancer drugs such as 2-methyl-9-hydroxyellipticinium and Adriamycin have been shown to stimulate topoisomerase II cleavage at low concentrations but inhibit cleavage at high drug concentrations.”

Fluoroquinolones are chemo drugs.  All topoisomerase interrupters are chemo drugs.  Don’t give people chemo drugs to treat sinus infections.  It’s not a difficult notion.

http://www.collective-evolution.com/2014/10/15/fda-allows-chemo-drugs-prescribed-antibiotics/

http://www.hormonesmatter.com/cipro-levaquin-avelox-fluoroquinolones-chemo-drugs/

“The non-exonuclease-treated DNA contained both linear and nicked circular forms of mtDNA but did not contain closed circular supercoiled mtDNA (Fig. 8, lane A), suggesting that ciprofloxacin induces single- as well as double stranded protein-linked breaks in the mtDNA.”

Thanks for breaking my DNA, Bayer.

“The current results indicate that ciprofloxacin is not cytotoxic unless cells are continuously exposed to drug for a minimum of three or four cell doublings. In comparison, drugs that target nuclear topoisomerase II trigger an apoptotic type of cell killing, even after a short 2-hr drug exposure.”

Interesting.  What is the time-frame for cell doubling?  And I don’t think that the question has been definitively answered as to whether or not fluoroquinolones are stored in lipids, continuously exposing cells to damage, or not.

“Another possibility is that the growth inhibitory and cytotoxic effects of ciprofloxacin are caused by the inhibition of an essential mitochondrial function or functions. This is supported by the following observations: First, treatment of mammalian cells with ciprofloxacin results in a selective depletion of mtDNA, leading to a decrease in mitochondrial respiration (6). These mitochondrial events precede the drug induced loss in cell growth and viability (Ref. 6 and current results). Second, cells become resistant to ciprofloxacin when they are grown under conditions that do not require mtDNA encoded functions. Third, ciprofloxacin induces the formation of site-specific, protein-linked breaks in mtDNA, indicating the presence of a drug-sensitive mitochondrial topoisomerase Il-like activity.”

Given the connections between ciprofloxacin and mitochondrial damage–depleting mtDNA and decreasing mitochondrial respiration, and the connections between mitochondrial damage and multiple chronic, multi-symptom illnesses, it is not absurd to make the assertion that ciprofloxacin, and other fluoroquinolones, can cause those diseases (autoimmune diseases, neurodegenerative diseases, fibromyaligia, autism, ME/Chronic Fatigue Syndrome, etc.).

The article, “Mitochondria Resuscitation: The Key to Healing Every Disease” by Chris D. Meletis, N.D. is a succinct and illustrative look at how mitochondria are related to multiple areas of health.

It’s nice and dandy that “cells become resistant to ciprofloxacin when they are grown under conditions that do not require mtDNA encoded functions” but human beings don’t have a bunch of cells that live in petri dishes that can grow without requiring our mitochondrial DNA functions.  I wonder what happens when human cells attempt to adapt to resist ciprofloxacin and adapt by ceasing to require mtDNA encoded functions.  I bet you a buck that no one knows the answer to that question.

Cipro breaks mitochondrial DNA.  WHY WASN’T THIS REPORT PAID ATTENTION TO?  All of the results in it warrant fluoroquinolones being taken off of the market until further investigation can be done.  This is absurd.  I know that there are cases where fluoroquinolones can save lives, I get that, and I’m usually decently reasonable about not calling for their removal from the market.  But this article spooked me severely.  We, collectively, have NO CLUE what the consequences of depleting our mitochondrial DNA are.

“Neither cell growth nor viability seems to be affected until cells have undergone three or four cell doublings in the presence of ciprofloxacin (Ref. 6 and current results). During this time span, the content of mtDNA decreases >90%, suggesting that drug is causing a loss in cell growth and viability by interfering with mtDNA replication.”

Nasty drugs – but if you metabolize them fast enough, they’re less nasty – apparently.

“Ciprofloxacin, as well as several other 4-quinolone drugs, can cause significant unwinding of DNA”

It’s what they’re designed to do.  They’re topoisomerase interrupters.  The mechanism of action for ciprofloxacin is, “The bactericidal action of ciprofloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases), which are required for bacterial DNA replication, transcription, repair, and recombination.” (source)  It doesn’t take a rocket scientist to realize that drugs that inhibit the DNA and RNA replication, transcription, repair and recombination are dangerous.  I hate the FDA for allowing these dangerous drugs to be used as antibiotics.  It’s ludicrous.

Delayed Cytotoxicity and Cleavage of Mitochondrial DNA in Ciprofloxacin-Treated Mammalian Cells” is not a hopeful article.  It is, frankly, a terrifying article.  More than 20 million prescriptions for fluoroquinolones are given out in Americans each year for the last couple decades, and that’s only a small portion of the prescriptions given worldwide.  What have we done to our collective mitochondrial DNA??  What are the consequences of depleting our mitochondrial DNA?  No one knows the answers to those questions.

Anyone who thinks that people aren’t sick with the diseases related to mitochondrial poisoning, isn’t looking very hard.  People are sick.  They’re in pain (peripheral neuropathy is thought to be caused by mitochondrial malfunctions), they’re depressed and suffering from even worse psychiatric disorders, they have heart conditions and metabolic disorders (source), ME/Chronic Fatigue Syndrome, autism, and many other misunderstood, chronic illnesses.  There are many potential culprits for the sorry state of human health in the 21st century, but fluoroquinolones aren’t even on the list according to most people.

FLUOROQUINOLONES DEPLETE MITOCHONDRIAL DNA, LEAD TO MITOCHONDRIAL DYSFUNCTION AND ALSO OBLITERATE THE MICROBIOME!

I’ll keep screaming it until I’m heard.

Back in 1992 it was noted that, “the interaction (of fluoroquinolones) with DNA is still of great concern because of the possible long-term genotoxicity of quinolone compounds, which are increasingly adopted as first-choice antibiotics for the treatment of many infections, and because it addresses the real mechanism of action of this class of molecules.”  (source)

I really wish that these warnings had been heeded.  Sadly, they’ve been ignored.

Our poor mitochondrial DNA.  I hope that mtDNA recovers and that the situation isn’t as dire as I suspect.  But the truth is, no one knows.  No one has a clue what the consequences of depleting mtDNA through unnecessary use of topoisomerase interrupting drugs are.

Floxies certainly know that the consequences of fluoroquinolones can involve a massive amount of pain and suffering.  It’s not okay.

Bayer, Johnson & Johnson, the FDA and everyone else involved with frivolously prescribing these drugs should be ashamed of themselves for failing to protect our mitochondrial DNA.  Topoisomerase interrupters should never have been approved for use as antibiotics.  It’s simply absurd.

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The Floxie Hope Podcast Episode 10 – Ariel

Haruki Murakami Storm Quote

 

In Episode 10 of The Floxie Hope Podcast Ariel shares her journey through fluoroquinolone toxicity.  Ariel felt and looked like she had aged 15 years in a matter of just a couple months after she took ciprofloxacin to treat a urinary tract infection.  She also suffered from anxiety, insomnia, depersonalization and many areas of her life falling apart.  Though Ariel is still going through her fluoroquinolone toxicity journey, she has learned many life lessons along the way.  She has found her strength and joy has returned to her life.  Ariel brings beautiful perspective to the journey through fluoroquinolone toxicity.

You can listen to Episode 10 of The Floxie Hope Podcast featuring Ariel through these links:

http://www.floxiehopepodcast.com/episode-010-ariel/

https://itunes.apple.com/us/podcast/floxie-hope-podcast/id945226010

Reviews on iTunes are greatly appreciated!  Thank you very much for listening to The Floxie Hope Podcast!

 

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The Floxie Hope Podcast Episode 5 – Rose Casanova

Floxie.Hope.Podcast.1800.72.dpi

Rose joined me for Episode 005 of The Floxie Hope Podcast.  In this episode, Rose shares her journey through fluoroquiolone toxicity and discusses how getting floxed changed her perspective on medicine.

You can listen to Episode 005 of The Floxie Hope Podcast through iTunes –

https://itunes.apple.com/us/podcast/floxie-hope-podcast/id945226010

It will be greatly appreciated if you log into iTunes and leave a review of The Floxie Hope Podcast.  Subscriptions through iTunes (or any other podcatcher) are greatly appreciated too.  Thanks!!

You can also listen to the podcast directly through this link –

http://www.floxiehopepodcast.com/episode-005-rose-casanova/

Thank you very much for listening to The Floxie Hope Podcast!  Getting our voices out there, and telling our stories, is helpful.

Thank you, Rose, for sharing your story!!!!

 

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Off Label FQ Use – WTF are they thinking???

It has come to my attention that (some) doctors are prescribing Cipro to patients who are having adverse reactions to other drugs.

I am so flabbergasted by this that I’m close to speechless.

WHY would anyone think that it is appropriate to give a fluoroquinolone to someone who is experiencing an adverse reaction to a drug?!  NOWHERE in the literature for fluoroquinolones does it say that they should be used to treat adverse drug reactions.  It makes no sense.

I thoroughly disagree with fluoroquinolones being used as antibiotics in cases where there are other, safer, remedies that can be used.  They are too dangerous and it is a violation of the oath to “do no harm” to prescribe fluoroquinolones when there are safer antibiotics available.   But at least fluoroquinolones do kill bacteria.  Most doctors aren’t aware of how dangerous fluoroquinolones are, and they use them for the purposes for which they are indicated – urinary tract infections, prostatitis, sinusitis, typhoid, anthrax, and other bacterial infections.  There are even some articles that indicates that fluoroquinolones can be used as chemotherapeutic agents to kill cancer cells.  But there is NO REASON to think that they should be given to people who are experiencing adverse drug reactions.  It’s insane and it’s dangerous.  What in the world are these doctors thinking?!

Why would any doctor who has taken the Hippocratic Oath prescribe a drug that has a 43 PAGE warning label and a black box warning, for purposes other than those for which it is proven to be effective?  Why would a doctor who has taken a pharmacology class think that it is okay to give a topoisomerase interrupter to someone who doesn’t even have an infection (or cancer – topoisomerase interrupters are really only appropriate for use to treat cancer)?  Why are they ignoring the serious and severe adverse effects that are listed on the warning label?  Why are they handing out Cipro like it is candy?  Why are they giving drugs that deplete liver detoxification enzymes to people who are having an adverse reaction to another drug?  WHY?

Here is a video from a guy (a Veteran) who was given a prescription for Cipro after he went to the VA doctor’s office with an adverse reaction to Finasteride:

Another case is illustrated in this comment, which, frankly, broke my heart:

“The baby reacted badly to each vaccination, screaming throughout the night each time, and the doctor prescribed her cipro drops after each one. She can’t taste, and has many delays in speech, reading, learning, and physical development, even though she started off being very advanced in certain ways.”

WHY?

Why would a child (A CHILD) be given Cipro after she has had an adverse reaction to a vaccine?  To completely shut down her liver?  To shut down her kidneys?  To destroy her mitochondria?  To obliterate her microbiome?  To make sure that the microbial protection that her microbiome should give her blood-brain barrier is completely destroyed and the aluminum in the vaccines gets deep in there? (See post-script for sources.)

What kind of masochistic doctor does that to a child?

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There seems to be a strange and disturbing trend to give people Cipro for no justifiable reason – just ‘cause.  Bayer donated (aren’t they sweet?) 3.7 million Euros worth of Cipro to the countries of West Africa to help them deal with Ebola.  Ummm….. Ebola is a VIRUS.  In case it needs to be said, antibiotics do NOTHING to treat viral infections.  In fact, they can make viral infections worse by killing off the good bacteria in the microbiome that are fighting the virus.  If the doctors in West Africa are giving the people who are fighting Ebola Cipro, they are doing them no good.  Cipro can do plenty of harm too.  The warnings on the 43 page warning label aren’t a joke, and they’re not temporary.

The Western Medicine doctors in West Africa wonder why people don’t trust them and would rather go to a local Shaman.  Shoot, I’d rather go to a Shaman than be needlessly pumped full of Cipro.  The Cipro would definitely kill me, at least I’d have a chance of survival with the Shaman.

We’re in this bizarro world of Orwellian notions of drug safety.  The most dangerous drugs, like fluoroquinolones, are pushed as having “an excellent record of safety and efficacy.”  Just ignore the permanent peripheral neuropathy, severe psychiatric disturbances, mitochondrial dysfunction, cellular mineral chelation, antioxidant depletion, microbiome obliteration, etc. that they cause.  Those symptoms can happen weeks, months, or even years after administration of the drug, so it is pushed that fluoroquinolones are “safe” and that the multi-symptom, chronic illnesses that result from them are a “coincidence.”

Doctors are throwing Cipro at people who they don’t know how to deal with.  If you or your boyfriend/father/son is having bizarre psychiatric problems after taking Finasteride, or your child is reacting badly to a vaccine, they’ll be given Cipro.

Why?

I cannot for the life of me understand why.

Post Script – 

The findings published in Science Translational Medicine in the 2014 article, “The gut microbiota influences blood-brain barrier permeability in mice,” are fascinating and likely quite consequential.  The scientists/researchers found that gut microbiota influences blood brain barrier permeability.  Mice with a compromised (or nonexistent) microbiome showed more permeability in their blood brain barrier than mice with normal/healthy microbiomes.  Blood brain barrier permeability means that unwanted molecules and cells from the bloodstream can enter the brain.  Disturbing our microbiome with antibiotics, especially powerful chemotherapeutic antibiotics like fluoroquinolones, is quite consequential to the brain.

Here are some articles about the study:

Science Translational Medicine, “The gut microbiota influences blood-brain barrier permeability in mice

Translational Microbiome Research Forum, “Gut Microbiota Influences Blood Brain Barrier Permeability

NeuroScienceNews.com, “Gut Microbiota Influences Blood Brain Barrier Permeability

The Scientist, “Mother’s Microbes Protect Baby’s Brain: Bacteria in the gut of a pregnant mouse strengthen the blood-brain barrier of her developing fetus.

Karolinska Institute, “Gut microbiota influences blood-brain barrier permeability

 

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Antibiotic Resistance – Can We Please Stop Being Stupid?

Can I just complain about how ridiculously STUPID the over-use of antibiotics in agriculture is?  Antibiotics are regularly used prophylactically in livestock in order to fatten up the animals and to compensate for the abhorrently unsanitary conditions in commercial feedlots.   Neither of those things are okay in the least.  They are appalling in themselves.

But if you don’t care that pigs, cows, chickens and turkeys are dirty and fat, you may say, “so what?”

The “so what” is that pathogenic bacteria are QUICKLY adapting to antibiotics and are getting stronger.  This is speeding up the process of antibiotic resistance among bacteria that can not only make livestock sick, but can also make humans sick.  When YOU get sick with one of these bacterial infections that is resistant to antibiotics, well, you may be screwed, because even fluoroquinolones don’t touch some of these nasty, antibiotic resistant, bacteria.

According to the CDC:

“Each year in the United States, at least 2 million people become infected with bacteria that are resistant to antibiotics and at least 23,000 people die each year as a direct result of these infections. Many more people die from other conditions that were complicated by an antibiotic-resistant infection.”

For a while the CDC, FDA and others, led by the pharma and big-ag lobbies, tried to BS (lie to) us all by saying that antibiotic resistance in livestock had nothing to do with antibiotic resistance to humans.  The 2013 CDC Report on Antibiotic / Antibmicrobial Resistance settled that argument as it noted that:

“Antibiotics are widely used in food-producing animals, and according to data published by FDA, there are more kilograms of antibiotics sold in the United States for food-producing animals than for people… This use contributes to the emergence of antibiotic-resistant bacteria in food-producing animals. Resistant bacteria in food-producing animals are of particular concern because these animals serve as carriers. Resistant bacteria can contaminate the foods that come from those animals, and people who consume these foods can develop antibiotic-resistant infections. Antibiotics must be used judiciously in humans and animals because both uses contribute to not only the emergence, but also the persistence and spread of antibiotic-resistant bacteria.”

Here is a good article in Wired explaining the CDC report – “CDC Threat Report: Yes, Agricultural Antibiotics Play a Role in Drug Resistance.”

The reports are in.  The scientific consensus has been stated.  Over-use of antibiotics in agriculture is hurting humans.  So, perhaps we should stop over-using antibiotics in agriculture.  That seems like a good idea.  Too bad the big-ag and pharma pockets are deep and they control the hearts and minds of legislators.  More info on that can be found here – http://www.healthline.com/health/antibiotics/politics-pork-and-poultry-why-legislation-has-not-passed

As bacteria in livestock become resistant to penicillin and sulfa antibiotics, fluoroquinolones will be used more frequently.  Fluoroquinolones already are being used in livestock, just not as frequently as other, safer, antibiotics.  But as bacteria become resistant to safer antibiotics, fluoroquinolone use will surely increase.  For humans as well, as antibiotic resistance increases, fluoroquinolone use will increase.  Doctors will have to pull out the “big guns” because the smaller ones will no longer work.

Antibiotic resistant bacteria are not only harming livestock and people, they are harming the earth itself.  The animals that are given antibiotics excrete those antibiotics (everybody poops – and pees) and the antibiotics go onto the earth / the soil.  This messes up the microbiome of the soil (yes, soil has a microbiome) and more antibiotic resistant bacteria thrive in the soil.  That’s the topic of THIS POST.  Our earth is, literally, getting floxed.  It’s going to get worse too, as stronger and stronger antibiotics become preferred in agriculture, because the traditional ones are no longer doing the job.  The fluoroquinolones will hurt the animals that they are given to, destroy the microbiome of the soil, and leave us Floxies with nothing to eat.  Great.

I wish I didn’t think this was going to happen in my lifetime, but I fear that it will.

The antibiotic arms race will likely continue, with increasingly powerful antibiotics being developed to compensate for antibiotic resistance.  Those synthetic antibiotics will likely have the same, or worse, devastating “side-effects” as fluoroquinolones.  Destruction of the microbiome and destruction of mitochondria is consequential for human health, animal health, and the health of the earth itself – the soil.  Though the importance of the microbiome is starting to be recognized, it may be too late to stop destroying our microbiome with antibiotics.  (The alternative is to fight pathogenic bacteria with helpful bacteria.)  We are accustomed to turning to drugs, and to wantonly killing bacteria.  I don’t see us stopping any time soon.

The bacteria will die – because there isn’t any political will to stop being foolish with antibiotics.  The insects (pests) will die – because there isn’t any political will to protect them from pesticides.  The bees will die – because corporate profits are, apparently, more important than our food supply.  The frogs will die – because no one understands non-linear hormonal responses.

Perhaps, with a painful number of human deaths from this ridiculousness, we’ll, collectively, stop being so stupid.  Maybe.  Because 23,000 human deaths per year (from antibiotic resistant bacteria) haven’t made policy-makers do squat about the over-use of antibiotics in agriculture.  Recommendations for prudent antibiotic use are put into place, but no actual changes are made.  Recommendations.  Recommendations will do nothing to solve this problem – nothing.

P.S. – Sorry for not being hopeful.  Here’s something I hope – I hope that the canaries in the coal mine are listened to.  That’s what we are – canaries.  Is anyone listening?

 

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Fluoroquinolone Induced Gene Upregulation and ROS

The article, “The Fluoroquinolone Levofloxacin Triggers the Transcriptional Activation of Iron Transport Genes That Contribute to Cell Death in Streptococcus pneumonia” is difficult.  It’s not light reading.  I wish it was.  I wish the articles that have information about how fluoroquinolones affect cells were easy to understand and to read.  I wish that we had easy, simple answers about how fluoroquinolones lead to the myriad of adverse events that are listed on the FDA warning labels for them.  I wish that more was known about how fluoroquinolones work.  I wish that a list of definitions wasn’t necessary at the beginning of this blog post.  But this stuff is hard, and a list of definitions is necessary, so, hereyago (some definitions paraphrased from the Wikipedia article because it’s easiest and I’m not a biochemist – for more info, go to the wiki page, or elsewhere):

Reactive Oxygen Species (ROS):  “Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling and homeostasis.  However, during times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically. This may result in significant damage to cell structures. Cumulatively, this is known as oxidative stress. ROS are also generated by exogenous sources such as ionizing radiation.”  ROS can be incredibly nasty.  They can lead to cellular damage, including DNA damage, and are related to every chronic disease there is.  They’re also related to ageing.  As damage from ROS (also called oxidative stress and free radicals) accumulates, ageing and the diseases of old age occur.  Interestingly though, ROS are not all bad.  They serve as signaling mechanisms within cells and play a large role in turning genes on and off (epigenetics).  They need to be in balance.  If they’re not in balance, a whole lot of things can go wrong.  They’re kind of like tequila.  A shot of tequila mixed with lime juice and other goodies, is excellent in a margarita.  But if you drink the whole bottle, and then mix it with some whiskey, it’s really bad and destructive.  The ways that ROS work within cells is not linear and difficult to study.  Not a whole lot is known about ROS or how they affect human health.  The article, “Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production” has a really nice over-view of various ROS and their effects.  It’s easier to think of them as different  alcoholic drinks though.  Some are beer – pretty benign unless you have a ridiculous amount of them.  Others are potent – more like Everclear – and they can do a lot of damage to you quickly.

Fenton Reaction:  “Iron(II) is oxidized by hydrogen peroxide to iron(III), forming a hydroxyl radical and a hydroxide ion in the process. Iron(III) is then reduced back to iron(II) by another molecule of hydrogen peroxide, forming a hydroperoxyl radical and a proton. The net effect is a disproportionation of hydrogen peroxide to create two different oxygen-radical species, with water (H+ + OH–) as a byproduct.”  Basically, iron can “donate or accept free electrons via intracellular reactions and help in creating free radicals.”  Free radicals are ROS.  Some of the nastiest ROS are created in the Fenton Reaction – hydroxyl radicals and hydroperoxyl radicals.  (“Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production” has good info on both of those.)

Type II topoisomerases, gyrase and topoisomerase IV:  “Type II topoisomerases maintain DNA topology and solve the topological problems associated with DNA replication, transcription, and recombination (20). Gyrase introduces negative supercoils into DNA (21), whereas topo IV relaxes DNA and participates in chromosome partitioning (22). Chromosomal topology in Escherichia coli is maintained homeostatically by the opposing activities of topoisomerases that relax DNA (topo I and topo IV) and by gyrase.” (from “The Fluoroquinolone Levofloxacin Triggers the Transcriptional Activation of Iron Transport Genes That Contribute to Cell Death in Streptococcus pneumonia”)

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You got all that?  Even the definitions are difficult.  Now onto some highlights of the article, “The Fluoroquinolone Levofloxacin Triggers the Transcriptional Activation of Iron Transport Genes That Contribute to Cell Death in Streptococcus pneumonia.”

Basically, the researchers found that levofloxacin upregulated genes that are involved in iron uptake and triggered the Fenton reaction in certain bacteria.  The increase in reactive oxygen species that ensued contributed to the lethality of the levofloxacin.

There are a few interesting things that should be noted about this.  First, levofloxacin can upregulate genes.  How consequential is this?  Can eukaryotic genes be upregulated, or can only bacterial genes be upregulated?  What about mitochondrial genes?  What does upregulation of bacterial, mitochondrial and even eukaryotic nuclear genes do to the person who has taken levofloxacin?

Some interesting research is being conducted about the relationship between the microbiome and genetic, heritable traits.  This National Geographic article, “The Most Heritable Gut Bacterium is… Wait, What is That?” notes some of the relationships that are being explored.  Our genes can affect our microbiome, our microbiome can affect our genes, can the genes of our microbiome affect…. US?  Where does the microbiome stop and where do we begin?  Those are all questions that have not yet been answered.  Unfortunately, fluoroquinolones, like levofloxacin, are thoroughly messing up our microbiomes and even causing the upregulation/expression of certain genes.

The second thing of note from the article is that the upregulated genes caused the activation of the Fenton reaction in the bacterial cells.  Again, how does this affect our microbiome?  How does it affect US?  Hydroxyl radicals and superoxide anions are nasty ROS that damage everything in their wake.  What happens to the health of the microbiome, and the host (the person) when their gut is suddenly full of toxic ROS?  Leaky gut syndrome?  Autoimmune reactions?  The multi-symptom, chronic illness that is fluoroquinolone toxicity syndrome?

There is quite a bit of evidence that fluoroquinolones do to mitochondria what they do to bacteria – disrupt the process of DNA replication and reproduction and lead to destruction and cell death.  I think that mitochondrial destruction has a lot to do with fluoroquinolone toxicity.  However, I don’t think that the role of disruption of our microbiome and destruction of our gut bacteria should be overlooked.  The signaling that goes on within our microbiome, and between “us” and our microbiome, is critically important and poorly understood.  Triggering bacterial DNA destruction and death, upregulation of genes and the Fenton reaction – which leads to production of highly destructive ROS, is a very, very, very bad idea – even if it just stays within the microbiome.

The conclusion of “The Fluoroquinolone Levofloxacin Triggers the Transcriptional Activation of Iron Transport Genes That Contribute to Cell Death in Streptococcus pneumonia” is that:

“In conclusion, we have shown for the first time that fatDCEB transcription is regulated by the supercoiling level. The primary effect of the interaction of LVX-topo IV is the upregulation of the operon by local increase in DNA supercoiling. This upregulation would increase the intracellular level of iron, which activates the Fenton reaction, increasing the concentration of hydroxyl radicals. These effects were observed before the inhibition of protein synthesis mediated by LVX. All these effects, together with the DNA damage caused by the inhibition of topo IV, would account for LVX lethality. The possibility to increase FQs’ efficacy by elevating the levels of intracellular ferrous iron remains open.”

Because, apparently, seeing the big picture of the symbiotic relationship between the microbiome and the rest of the organism (the person), isn’t the goal.  The goal is to kill bacteria.  It’s ridiculously short sighted.  Sigh.

Because we’re in Floxieville, there has to be a paradox.  Supplementing iron helped me more than just about anything else.  Iron is one of the few supplements that made me feel markedly better immediately after taking it.  Other Floxies have reported that their ferritin levels are low post-flox.  The role of the Fenton reaction in fluoroquinolone toxicity would lead one to think that iron should be the last thing that a Floxie might need or want.  It helped me though.  I had more energy and even my tendons felt better when I started supplementing iron.  I don’t know if this has something to do with the kind of iron in my supplement/body – FE3 or FE2 – or if the iron had been converted to other chemical compounds and I needed to replace it, or what.  I do know that, as I said in the beginning of this post, this stuff is hard.

The Fluoroquinolone Levofloxacin Triggers the Transcriptional Activation of Iron Transport Genes That Contribute to Cell Death in Streptococcus pneumonia provides a good description of how fluoroquinolones work:

“The killing effect of FQs has been related to the resolution of reaction intermediates of DNA-FQ-topoisomerase complexes, which generates irreparable double-stranded DNA breaks (31). This could occur in E. coli by two pathways, one dependent on protein synthesis and the other independent of it. It has been shown that hydroxyl radical action contributes to FQ-mediated cell death occurring via a protein-dependent pathway (32). This result agrees with a recent proposal suggesting that, following gyrase poisoning, hydroxyl radical formation utilizing internal iron and the Fenton reaction (33) is generated and contributes to cell killing by FQs (34) as well as by other bactericidal antibiotics (35, 36). In this mechanism, proposed for Enterobacteriaceae (35, 37), the primary drug interactions stimulate oxidation of NADH via the electron transport chain that is dependent on the tricarboxylic acid cycle. Hyperactivation of the electron transport chain stimulates superoxide formation. Superoxide destabilizes the iron-sulfur clusters of enzymes, making Fe2+ available for oxidation by the Fenton reaction. The Fenton reaction leads to the formation of hydroxyl radicals that would damage DNA, proteins, and lipids (38), which results in cell death. Instead of a generalized oxidative damage, a recent study supports that the main action of hydroxyl radicals is the oxidation of guanine (to 8-oxo-guanine) of the nucleotide pool. The incomplete repair of closely spaced 8-oxo-deoxyguanosine lesions caused lethal double-strand DNA breaks, which would underlie much of the cell death caused by beta-lactams and FQs (39). However, recent investigations have questioned the role of hydroxyl radicals and intracellular iron levels in antibiotic-mediated lethality using antibiotic concentrations either similar to (40) or higher than (41) those used previously. The disparate results obtained using diverse antibiotic concentrations and times of treatment emphasize the complexity of the lethal stress response (42).”

Similar destruction happens in mitochondria.  As I mentioned though, even if it didn’t happen in mitochondria, and only happened in bacteria, that destruction and those reactions are horrible things to do to a person’s microbiome.  It is, after all, part of us.

All of the people at the FDA who think that it’s okay not to strictly regulate drugs that disrupt the process of DNA replication and reproduction, and lead to the upregulation of genes and induction of the Fenton reaction, which leads to high levels of highly reactive ROS, should be fired.  I’ve learned enough biochem in the last 3 years to know that induction of the Fenton reaction in any part of the body is a really bad idea.  The scientists at the FDA should be able to figure this out.

 

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Shades of Grey – The Good and Bad of Fluoroquinolones

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Here is a new post about fluoroquinolones on Hormones Matter –

Shades of Grey – The Good and Bad of Fluoroquinolones

From it –

“Fluoroquinolones can do good, but they can do harm too. Categorizing things in terms of good or bad is the natural inclination of most people, but it’s never that simple for drugs. All drugs can do good, but they can do harm too – hence the list of side-effects that comes with each prescription. We can’t yet ask for drugs to only do good, and never do harm – that’s not the way the world works. But we can ask for dangerous drugs to be used appropriately. It is ONLY appropriate for fluoroquinolones to be used in life-or-death situations when other antibiotics aren’t effective. To use them flippantly, and when they aren’t entirely necessary, is inappropriate and a violation of the Hippocratic Oath.”

I hate that cipro hurt me.  I hate that fluoroquinolones hurt any of us.  But I still don’t think that they should be banned entirely.  It is not unreasonable to demand that they be used sensibly though.  The amount of collateral damage done by FQs is unacceptable.  Collateral damage should be minimized.  It’s not too much to ask for.

 

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Antibiotics After Fluoroquinolone Toxicity

People often ask about what they should do to treat infections post-flox.  Here are my tips.

First, please INSIST on getting your infection cultured and confirmed before you take any antibiotics.  As anyone who has had an adverse reaction to an antibiotic can tell you, antibiotics are not benign drugs.  They have side-effects (HERE is the 43 PAGE warning label for Cipro/Ciprofloxacin).  Some of those side-effects are life-altering and/or life-threatening.  You don’t want to put any drugs into your body unless you absolutely need them.  A culture should be done to confirm that an infection is present before you take an antibiotic – no matter what.

Because antibiotics have been shown to wreak havoc on the microbiome and bactericidal antibiotics damage mitochondria – and because both microbiome disruptions and mitochondrial dysfunctions are linked with every chronic disease there is – I highly recommend looking into some non-pharmaceutical options first.  Garlic has been shown to have antibiotic qualities and to be more effective against biofilms than many antibiotics.  For urinary tract infections, D-mannose has effectively helped thousands of people get rid of their infection.  Some other non-pharmaceutical remedies for urinary tract infections can be found HERECoconut oil has been shown to have anti-bacterial qualities and it may be good for treating skin and GI infections.  Colloidal silver not only has anti-bacterial qualities on its own, it also has been shown to increase the effectiveness of pharmaceutical antibiotics when used in conjunction with them.  Andrographis is an herb that has antibiotic qualities.

If non-pharmaceutical options aren’t working and you need an antibiotic to get rid of your confirmed infection, here are the antibiotics that I recommend along with reasons as to why I recommend them (or not).

  1. Most Floxies seem to do well with doxycycline and other tetracyclines. Tetracyclines are bacteriostatic antibiotics that, “stops bacteria from multiplying but does not kill them.” (source)
  2. Several Floxies have taken Z-pack’s without incident
  3. Amoxicillin seems to be about as benign as antibiotics get. So, it’s not harmless, but it’s well tolerated generally.
  4. Penicillin seems to be well tolerated – unless you’re allergic to it.
  5. Cephalosporins seem to be well tolerated

There are probably some other antibiotics that are fine for Floxies, I just haven’t heard about them.  Please feel free to leave a comment below if there is an effective and relatively safe one that I’m missing.

Here are the antibiotics that I recommend avoiding because they have side-effects that are similar to those of fluoroquinolones, and because many Floxies react badly to them –

  1. Macrobid / Nitrofurantoin
  2. Flagyl / Metronidazole
  3. Bactrim / Trimethoprim / Sulfamethoxazole
  4. Augmentin

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Fluoroquinolones – Cipro/Ciprofloxacin, Levaquin/Levofloxacin, Avelox/Moxifloxacin, Floxin/Ofloxacin and a few others – should be avoided entirely unless you are dying and make the decision that getting “floxed” is preferred to death.  Every warning label for every fluoroquinolone says that people who have an existing hypersensitivity to a fluoroquinolone should not take them again.  “Ciprofloxacin is contraindicated in persons with a history of hypersensitivity to ciprofloxacin, any member of the quinolone class of antimicrobial agents, or any of the product components.” (Warning Label)

Before you take an antibiotic, or any pharmaceutical for that matter, I highly recommend that you look up the review for that drug on http://www.askapatient.com/ and look it up on http://www.peoplespharmacy.com/.  Also, look up the drug’s warning label.  Be informed.  Make an informed decision.

Here is a list of antibiotics – http://en.wikipedia.org/wiki/List_of_antibiotics  I didn’t get close to going through all of them.  But I hope that this post gives you some guidance when/if you are faced with an infection.

I’m not a doctor, so please take this advice for what it’s worth.  Doctors should be consulted when you have an infection.  The internet should be consulted too though, because doctors aren’t capable of knowing everything and informed consent is really important.

 

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Crowdfunding Floxie Hope

Floxie.Hope.1800.72.dpi

I’m asking for support of Floxie Hope.  Thank you very much for your consideration!

I’m trying crowd-funding.  The basic premise of crowd-funding is that many people each give a little money to support a cause or organization because they find value in it.

I’m a bit biased, but I think that a lot of value is offered through Floxie Hope.  The stories of healing and recovery offer hope and tips to those going through the horror of fluoroquinolone toxicity. The posts offer information that Floxies can share with their families and friends to help spread the word about the dangers of fluoroquinolones. The posts also help friends and family members to understand what is experienced when the fluoroquinolone toxicity bomb goes off in a Floxie’s body.  The Links & Resources page links to articles explaining the science behind fluoroquinolone toxicity – and gives Floxies something that they can show to their doctors to help them to understand what is happening in the Floxie’s body.  People have reached me through the “contact me” link and I hope that I have helped them through offering guidance and support.

I hope that everyone who visits Floxie Hope gains knowledge, strength, community, information, support, and even amusement.  I hope that it makes the journey through fluoroquinolone toxicity a little bit easier to bare.

If you would like to support Floxie Hope, here is a link to support Floxie Hope monetarily:

 

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Additionally, there are lots of non-monetary ways that you can support Floxie Hope.  I greatly appreciate everyone who:

  1. Shares posts and articles about fluoroquinolone toxicity on social media
  2. Comments on Floxie Hope (a huge THANK YOU to everyone who has helped to form a community of support on Floxie Hope)
  3. Talks to your friends and family about the dangers of fluoroquinolones

It’s a good site.  If you agree, please donate a few dollars through the link above, spread the warning to those you love, and/or spread the hope to those who are suffering.

Thank you for your time, consideration and support – in whatever form it takes!

Wishing you hope and healing,

Lisa

 

P.S. – If you are in a giving mood, here are some other organizations that are providing value to the Floxie community, who will also appreciate support/money:

 

 

Fluoroquinolones Surpass Vioxx and Thalidomide in Harm Done

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In a May, 2014 letter to the U.S. SenateDoctor Jay S. Cohen said of fluoroquinolones, “In my 40+ years in pharmacovigilance, FQs (fluoroquinolones) surpass Vioxx and Thalidomide in the degree of permanent harm done.”  Let that sink in for a bit.

Fluoroquinolones – cipro/ciprofloxacin, levaquin/levofloxacin, avelox/moxifloxacin and floxin/ofloxacin – drugs that are seen as simple antibiotics (though they do severe cellular harm and are more appropriate for use as chemotherapy drugs), that are prescribed more than 20 million times per year in the U.S. alone – are doing more harm than Vioxx – a drug that led to more than 140,000 American heart attacks, and Thalidomide – a drug that has caused birth-defects and deaths of thousands of children world-wide.

Vioxx has been removed from the market, and the use of Thalidomide is severely restricted.  Fluoroquinolones, on the other hand, are prescribed with abandon, despite the fact that hundreds of studies have shown that they do severe cellular damage and thousands of patients have filed reports with the FDA noting that a variety of severe health problems have been experienced after taking a fluoroquinolone.

Transgenerational Side-Effects

I have argued that fluoroquinolones have transgenerational ill effects and that children are suffering because of the epigenetic effects of fluoroquinolones (HERE and HERE).  I have never hoped to be wrong about anything more than my assertions that fluoroquinolones are related to autism, but the possibility exists – because we really don’t know what the transgenerational effects of microbiome destruction and depletion of mitochondrial DNA are – and fluoroquinolones do, indeed, both obliterate the microbiome and deplete the only non-redundant form of DNA that we have – mitochondrial DNA.  (1)………………………………..

READ MORE ON COLLECTIVE EVOLUTION

http://www.collective-evolution.com/2014/06/25/these-popular-antibiotics-are-prescribed-to-millions-every-year-they-have-detrimental-effects-everyone-needs-to-be-aware-of-this/

 

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Adverse Drug Reactions are Like Earthquakes

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Here is a post about how adverse drug reactions are like Earthquakes –

http://www.hormonesmatter.com/adverse-drug-reactions-like-earthquakes/

Drugs, just like earthquakes, can shake your world and cause damage and destruction.

 

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Epigenetics and Fluoroquinolones: Now What?

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Per Dr. Chandler Marrs (who runs www.hormonesmatter.com), “Above and around genetic codes reside the on/off switches to many processes (the switching of genes on and off is epigenetics). If common medications, including fluoroquinolones, up or downregulate these processes and create new diseases, what is someone who takes them supposed to do? Can epigenetic changes be reversed? What is the patient to do with all the recent research on epigenetics? The research is all well and good, but what does it mean to the patient?”

Indeed.

Here is a post about how fluoroquinolones, and other common pharmaceuticals, affect epigenetics. There are currently more questions than answers and the right path is far from clear.

https://www.hormonesmatter.com/epigenetics-common-medications/

 

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Articles About Fluoroquinolone Toxicity to Give to Your Doctor

People often ask for articles about fluoroquinolone toxicity to share with their doctors.  Following are a few articles that I recommend.

What you should share with your doctor depends on your doctor’s willingness to read what you give him or her.  Doctors are busy.  Most of them don’t have the time, energy or inclination to keep up with all of the latest drug research.  They depend on the FDA to regulate drugs and they assume that if a drug has been on the market for years, it must be safe.  They are wrong in those assumptions.  It would be more appropriate for them to assume that all of the mysterious diseases of modernity (fibromyalgia, chronic fatigue syndrome / M.E., autoimmune diseases, allergies, dietary intolerances, autism, etc.) are due to the damage that pharmaceuticals are doing to the mitochondria, microbiome, endocrine system, etc.; and the feedback loops between those delicate systems.  Unfortunately, most doctors haven’t had that epiphany quite yet.  Here are some articles that can at least introduce Fluoroquinolone Toxicity Syndrome to them:

Show your doctor this if 4 sentences is his/her limit:

I’m going to ruffle feathers, but I’ll tell you anyway” By Suzy Cohen

SuzyCohen

Here are more details on fluoroquinolones being chemo drugs, as Suzy Cohen notes: “ CIPRO, LEVAQUIN AND AVELOX ARE CHEMO DRUGS” by me (Lisa Bloomquist) on Hormones Matter.

For doctors who are willing to take the time to read a few articles, but aren’t going to spend a lot of time looking into FQ toxicity, I recommend that you show them these:

  1.  Dear Doctor letter written by Dr. Plumb, a doctor who was Floxed
  2. New York Times article by Jane Brody, “Popular Antibiotics May Carry Serious Side Effects
  3. PBS Frontline expose about fluoroquinolones
  4. Forbes article by Melanie Haiken, “Antibiotic Alert: The Drug the Doctor Ordered Could Cause Deadly Side Effects
  5. Fluoroquinolones 101” by me (Lisa Bloomquist) on Hormones Matter.

For doctors who are willing to read journal articles about fluoroquinolones, I recommend these:

  1. Physical Medicine and Rehabilitation (PM & R) “Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population
  2. Science Translational Medicine, “Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells
  3. Journal of Young Pharmacists, “Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients
  4. Molecular Pharmacology, “Delayed Cytotocicity and Cleavage of Mitochondrial DNA in Ciprofloxacin Treated Mammalian Cells

There are more than 100 other useful peer-reviewed research articles on the Links & Resources page of Floxie Hope.

Another thing that you can do is go over the FDA warning labels for the fluoroquinolones with your doctor:

  1. FDA Datasheet – Ciprofloxacin (Cipro)
  2. FDA Datasheet – Levofloxacin (Levaquin)
  3. FDA Datasheet – Moxifloxacin (Avelox)

The severity of adverse reactions to fluoroquinolones isn’t noted anywhere on the labels.  Nor is the fact that symptoms can be delayed.  It is assumed, by everyone, that adverse drug reactions are transient and that they will stop when administration of the drug has stopped.  This isn’t true for fluoroquinolones.  The adverse effects listed on the fluoroquinolone warning labels are multi-systemic and perhaps your doctor should wonder how and why fluoroquinolones cause multi-symptom, chronic illness.

Most people, doctors and patients alike, think that adverse reactions to fluoroquinolones are rare.  If you feel like going over this post with your doctor, I think that I make some good points in it:  “Is Fluoroquinolone Toxicity Rare?

Multi-symptom chronic illness brought on by a chemotherapy drug masquerading as an antibiotic is something to take seriously.  If your concerns are not taken seriously, I highly recommend finding another doctor.

And please thank the doctors who listen to you, read the articles that you give them and start being more prudent with their use of fluoroquinolones.  When a critical mass of doctors realize the dangers of these drugs, we’ll start seeing change.  I thank every one of you who takes the time to talk to your doctors about fluoroquinolone toxicity.  It does a lot of good.

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Don’t take Cipro, Levaquin or Avelox if….

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Post on Hormones Matter –

http://www.hormonesmatter.com/dont-take-cipro-levaquin-avelox-fluoroquinolone-toxicity/

In an ideal world, fluoroquinolones would be reserved for use in life-or-death situations. Until then, and until medicine can be completely customized and individualized, these groups of people should avoid fluoroquinolones:

1.  People who have reacted badly to a fluoroquinolone in the past.

2.  Athletes.

3.  People on steroids (corticosteroids).

4.  People who need to take NSAIDs regularly.

5.  Immunocompromised Individuals.

6.  People with Mitochondrial Dysfunction.

7.  Children.

 

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Gulf War Illness Tied to Cipro

The connection between Gulf War Illness and Fluoroquinolone Toxicity is well accepted among “Floxies,” but the connection hasn’t been made for most of the general population, or even most of the Gulf War Veteran population.  I wrote this post with the hope that the issue would be pushed in both the general and the Veteran populations.

http://www.collective-evolution.com/2014/01/06/gulf-war-illness-tied-to-cipro-antibiotics/

http://www.activistpost.com/2014/01/gulf-war-illness-tied-to-cipro.html

http://naturalwellnessreview.com/2014/01/gulf-war-illness-tied-to-cipro-antibiotics/

http://beforeitsnews.com/alternative/2014/01/gulf-war-illness-tied-to-cipro-antibiotics-2867166.html

http://banoosh.com/blog/2014/01/07/gulf-war-illness-tied-cipro-antibiotics/

http://polishgazette.com/?p=96735

http://thenwo.net/health-and-science/gulf-war-illness-tied-to-cipro-antibiotics/

There are definitely multiple factors at work in leading to the sickening of Gulf War Veterans. Many of the factors probably compound each other. I hope that the complexity of GWI isn’t used as an excuse to not get to the bottom of it. The Vets deserve answers. I wish that those who have officially been investigating GWI ($340 million invested into determining a cause and no resolution for the Vets) would look at Cipro. I don’t know why it hasn’t even made the list of compounding factors yet. I trust that it will soon.

 

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Conflicting Study Results: Do DNA Breaks Hold Answers?

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.

Sources:

  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 –

http://www.jimmunol.org/content/184/9/4827.full.pdf

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 –

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249743/?report=printable

http://link.springer.com/article/10.1007/s00284-012-0094-7#page-1

https://www.jstage.jst.go.jp/article/tjem/226/4/226_4_251/_pdf

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: http://psychrights.org/Research/Digest/NLPs/DrugsCauseMitochondrialDamage.pdf

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.” (http://www.mrc-mbu.cam.ac.uk/research/mitochondrial-complex-i) 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 http://www.ncbi.nlm.nih.gov/gene/51103, “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 (http://www.jbc.org/content/273/42/27668.full). 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. http://en.wikipedia.org/wiki/Rotenone 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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Doctor Referral List

Several people have asked me for referrals to doctors who specialize in Fluoroquinolone Toxicity.  Unfortunately, there are very few doctors who claim any expertise in Fluoroquinolone Toxicity (I say claim because even the most in-depth medical journals say that the mechanisms through which fluoroquinolones work, and sometimes don’t work, are unknown at this time).  But there are doctors who have read-up on fluoroquinolone toxicity, who are familiar with the issues of Floxies, who are willing and able to listen and to help, when possible.  Here is a list of the doctors who have been identified thus far –

 

https://docs.google.com/spreadsheets/d/10HdvKMTV1YGPyubf9KCYivtG8i2jo8w1kZjBDjNdt38/edit#gid=7

 

If you find a good doctor that you like who you would like to refer other Floxies to, please add the doctor, or other medical professional that helps you, to the referral list –

 

https://docs.google.com/forms/d/e/1FAIpQLSeSLS4uxb4P8g05Jo7MomnuLle9qGaIPValUL22v-AKwuXy6Q/viewform

 

I did not create these google documents.  I want to thank the person who did (I’m not sure who that person is, sorry).  Thank you for putting this together!

 

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Antioxidant Depletion by Fluoroquinolones

antioxidants

One of my favorite journal articles about the adverse effects of fluroquinolones is Oxidative Stress Induced by Fluoroquinolones on Treatment for Complicated Urinary Tract Infections in Indian Patients written by V. Talla and P.R. Veerareddy and published in the Journal of Young Pharmacists.  It’s a pretty damning article and it’s easy to read.  I highly recommend that you read it yourself.  Here is the link –

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249743/?report=printable

Even though it’s written at a level that most people can understand, there are a few terms that I’m assuming aren’t known by the average person reading this blog.  So, I have taken the main points from the study, as I see them, and explained them to the best of my ability.  Basically, I did the Google and Wiki look-ups so you don’t have to.

Here are the main points of the article:

1. “There is a significant and gradual elevation of lipid peroxide levels in patients on ciprofloxacin and levofloxacin dosage regimen but not with gatifloxacin.” What is lipid peroxide and do we want our levels to be high or low?  Wikipedia tells us that, “Lipid peroxidation refers to the oxidative degradation of lipids. It is the process in which free radicals “steal” electrons from the lipids in cell membranes, resulting in cell damage.”  (1)  Basically, lipid peroxidation is not something you want going on in your body.  You don’t want your lipids to be degraded via oxidation.  You don’t want cell damage.  Drugs that significantly increase levels of lipid peroxide are hurting you – at least on that level.


2. “There was substantial depletion in both SOD and glutathione levels particularly with ciprofloxacin.”  Superoxide dismutases (SODs) “are enzymes that catalyze the dismutation of superoxide (O2−) into oxygen and hydrogen peroxide. Thus, they are an important antioxidant defense in nearly all cells exposed to oxygen.” (2)  Additionally, “Within a cell, the superoxide dismutases (SODs) constitute the first line of defence against ROS.” (3)  SOD is “Present both inside and outside cell membranes, SOD is one of the body’s primary internal anti-oxidant defenses, and plays a critical role in reducing the oxidative stress implicated in atherosclerosis and other life-threatening diseases. Studies have shown that SOD can play a critical role in reducing internal inflammation and lessening pain associated with conditions such as arthritis.” (4) SODs are necessary for neutralizing the oxidative damage done by reactive oxygen species (ROS) (more on ROS below).

Glutathione is also depleted by fluoroquinolones.  Per Dr. Mark Hyman, Glutathione is “the most important molecule you need to stay healthy and prevent disease.”  (5)  Dr. Hyman notes that glutathione depletion “leaves you susceptible to unrestrained cell disintegration from oxidative stress, free radicals, infections and cancer.  And your liver gets overloaded and damaged, making it unable to do its job of detoxification.”  Glutathione is an extremely important antioxidant.

SOD and glutathione work together to neutralize oxidative damage done by ROS.  Here is a brief description of how SOD and glutathione work together:

SOD is responsible for catalyzing the conversion of superoxide to elemental oxygen and hydrogen peroxide. This transformation is called dismutation, hence the enzyme’s name. Although hydrogen peroxide is also a pro-oxidant compound, it is subsequently converted by the enzymes catalase and glutathione peroxidase to simple water and oxygen. (4)

Without the proper amount of SOD or glutathione in your body, ROS will wreak havoc on your system, causing oxidative stress and damage to every bodily system.   

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3. “On the 5th day of treatment, plasma antioxidant status decreased by 77.6%, 50.5%, 7.56% for ciprofloxacin, levofloxacin and gatifloxacin respectively.”  Antioxidants are molecules “that inhibit the oxidation of other molecules. Oxidation is a chemical reaction that transfers electrons or hydrogen from a substance to an oxidizing agent. Oxidation reactions can produce free radicals. In turn, these radicals can start chain reactions. When the chain reaction occurs in a cell, it can cause damage or death to the cell.” (6)  Oxidation is bad, antioxidants are good, cell death is bad – we want plasma antioxidant levels to be high, not low.  Decreasing plasma antioxidant status is bad for your health on a cellular level.

4. “In conclusion ciprofloxacin and levofloxacin induce more reactive oxygen species that lead to cell damage than gatifloxacin.”  The researchers also note that, “Several in vitro and in vivo study using animals revealed that fluoroquinolones induced oxidative stress by producing reactive oxygen species (ROS).”  ROS are described as follows:

Without oxygen, we could not exist. However, in the process of generating energy by “burning” nutrients with oxygen, certain “rogue” oxygen molecules are created as inevitable byproducts. Known as free radicals and reactive oxygen species, these unstable, highly reactive molecules play a role in cell signaling and other beneficial processes when they exist in benign concentrations.  But when their numbers climb, as may occur as a result of aging and other conditions, they may wreak havoc with other molecules with which they come into contact, such as DNA, proteins, and lipids. As such, these “pro-oxidant” molecules become especially toxic.

In fact, a prevailing theory of disease and aging states that the gradual accumulation of pro-oxidant molecules, and the harm they incur, is responsible for many of the adverse changes that eventually cause various diseases. These include cancer (possibly triggered by free radical-induced damage to cellular DNA) and inflammatory and degenerative diseases such as Alzheimer’s, arthritis, atherosclerosis, and diabetes. While scientists have not yet reached consensus on the topic, accumulated evidence overwhelmingly identifies increased oxidative stress with age as a source of damage to cellular structure and function.  (4)

Additionally, the wikipedia article on ROS does a nice job of explaining the damage that ROS can do – http://en.wikipedia.org/wiki/Reactive_oxygen_species

5. The authors of the study also note that, “The efforts of the endogenous antioxidant enzymes like SOD to remove the continuously generated free radicals initially increase due to an induction but later enzyme depletion occurs by 73.3% and 32.2% for ciprofloxacin and levofloxacin respectively, resulting in oxidative cell damage. Hence when the generation of reactive free radicals overwhelms the antioxidant defence, lipid peroxidation of the cell membrane occurs. This causes disturbances in cell integrity leading to cell damage/death. In the present study the repeated administration of CFX (ciprofloxacin) (recommended dosage regimen of CFX for UTI) resulted in increase free radical adduct generation by CYP450 mediated metabolism that cumulate and may result in increased ROS and substantial reduction in antioxidant defense.”

I think it’s a pretty damning article.  It’s easy to read and understand.  It doesn’t answer all questions about the damage done by fluoroquinolones, but it does a nice job at describing some of the issues that go on in the body when fluoroquinolones are ingested.  I suggest that you bring a copy to your next doctor’s appointment.

Sources:

  1. http://en.wikipedia.org/wiki/Lipid_peroxidation
  2. http://en.wikipedia.org/wiki/Superoxide_dismutase
  3. Alscher RGErturk NHeath LS., “Role of superoxide dismutases (SODs) in controlling oxidative stress in plants” Journal of Experimental Botany 2002 May; 53(372):1331-41. http://www.ncbi.nlm.nih.gov/pubmed/11997379
  4. Dale Keifer, “Superoxide Dismutase Boosting the Body’s Primary Antioxidant Defense” Life Extension Magazine.  June, 2006 http://www.lef.org/magazine/mag2006/jun2006_report_sod_01.htm
  5. Mark Hyman, MD, “Glutathione:  The Mother of All Antioxidants” 04/10/2010 http://www.huffingtonpost.com/dr-mark-hyman/glutathione-the-mother-of_b_530494.html
  6. http://en.wikipedia.org/wiki/Antioxidant

 

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Lessons Learned from Getting Floxed

1980-08 #15 - Version 2

I’m going to start this post with a disclaimer – when I say I “asked for” this, I don’t mean that I deserved to get sick.  It is not my fault that I got sick.  I have made plenty of mistakes in my life, and plenty of the mistakes that I’ve made have to do with taking those Cipro pills.  But still, the bomb that went off in my body as a result of taking Cipro was not my fault.  Those of you who are sick from fluoroquinolones or other Rx drugs, it is not your fault.  The disproportionately horrifying adverse reaction that you are going through makes any responsibility that you have in creating the problem miniscule in comparison to the responsibility of those who are at fault.  There are people who are to blame for your illness, but you are not one of them.  You are a victim.  So, when I say that I “asked for” the things that have come into my life after getting Floxed, I mean those words literally – I asked for them.

I’ve always wanted:

  1. Purpose
  2. Direction
  3. Passion
  4. Righteousness
  5. Something to say that was important/interesting
  6. To be heard/validated
  7. A spiritual outlet
  8. An identity
  9. To be a fighter – to be strong
  10. To lose 10 pounds

I asked for those things.  I sent those desires out into the universe in whatever form I sent them – vague thoughts, wishes, desires, prayers, etc.  If you had asked me at any point in my adult life if I wanted any of those things, I would have said yes.  There would have been no hesitation.  Without a doubt, I wanted each of those things to come into my life.  I didn’t have a plan of action for how I was going to obtain any of them, other than the most trivial of them – to lose 10 pounds – I always had a theory on how to do that.  I wanted all of the more important things too, but I had no idea how to get them.

I vaguely looked for purpose, direction, passion, righteousness and an identity through my education and career choices.  I got a Masters in Public Administration with the hope of finding a way to make the world a better place through public policy.  I had every intention of finding my purpose and passion through my Master’s program but when the program ended it was a struggle to pick a topic for my thesis because I hadn’t discovered anything that I really cared about.

I work for a non-profit.  The non-profit that is my employer does good work in the community by lending money to developers of affordable housing.  I like that I do something that is generally helpful, but I don’t feel passionate about what I do.  I admire the people who feel passionately about their careers and their lives.  I wished to live like them, to have something that got me riled up, something that I really cared about, something that made a difference in the world and that made me someone important.

I never thought that I was particularly tough or strong.  I have always been strong physically, but emotionally and mentally, I was sensitive and (I hate to admit it) weak.  I would sacrifice myself so that others could win, or not feel bad.  I needed validation and was torn down easily.  I never had much will-power, thus the fairly constant unfulfilled wish to lose ten pounds.

Despite not having passion, direction, etc. my life wasn’t bad.  In fact, it was quite good.  I had my health.  I had a family and friends who loved me immensely.  I had enough money (everyone wants more, of course, but I had enough to get by).  I had a job.  I owned a home.  Life was good, it just didn’t have the “oomph” that I wanted it to.  I wanted more “oomph” and, over time, never specifically consciously, I wished for the things listed above.  I wanted them.  I asked for them.

I got all of those things.  I survived getting poisoned by Cipro and in doing so I learned that I’m not only a survivor, I’m a fighter.  I gained passion, direction, righteousness, etc. through screaming that it is NOT OKAY for people to be poisoned by prescription antibiotics.  I found that I have something to say and a surprising number of people are listening to me.  I found spiritual outlets (you can read about that here http://www.collective-evolution.com/2013/09/14/a-journey-through-pharmaceutical-induced-illness/) and I found my soul.  I found my purpose.

I got exactly what I wanted.  Through getting sick.  Through recovering.  Through Cipro.  Out of all the things in the world, fucking Cipro, brought me those gifts.

I asked for them.  I asked and I received.  They just didn’t come in the packaging that I was looking for.

It’s kind of funny, isn’t it?  In a shoot-me, horrifying kind of way, it’s funny.  Be careful what you ask for, because you just might get it.

There are some other things that I gained from getting sick.  If I had been a more wise person, I probably would have wished for them ahead of time.  They are:

  1. Empathy
  2. Compassion
  3. Patience
  4. Tolerance

I gained those things from being knocked down, from being sick.  When I was healthy, I didn’t even realize that I was lacking those things for those who are not healthy.  I now see the world in a way that enables me to have empathy, compassion, patience and tolerance for those who are struggling and sick.  In gaining those things, I have become a better person.

To wonder if it was the right thing, to wonder if my health and longevity should have been sacrificed so that I can have a purposeful and passionate life, is futile.  That choice, if it was a choice, was not made on a conscious level.  I certainly know that I will never sign up to get poisoned again and that I will do everything in my power to keep others from going through what I went through.  But the experience of getting sick, the experience of recovering, and now the experience of fighting, have made me a better person.  It’s good to be empathetic, compassionate, patient, tolerant, passionate, determined, righteous and even skinny*.  These are not bad cards to be dealt.

* Do NOT even think about taking a fluoroquinolone for weight loss.  I could list the ways that that’s a stupid idea, but I’ll just leave it at – don’t be an idiot.

 

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Moving forward after Cipro knocked me down

When I realized that Cipro was the cause of my body going completely hay-wire (I didn’t know immediately because my reaction was delayed), and I saw stories on the internet of people getting worse and worse indefinitely, and/or living with pain and disability caused by fluoroquinolones, I thought that I had accidentally killed myself. I thought of writing letters to my family and friends to say goodbye, to let them know that I was gone and that I was so, so, so sorry that I had taken those pills.

In some ways, even though I survived, obviously, I think that I should have written those letters (even though they would have scared the crap out of my loved ones and probably gotten me locked in a psych ward). Because I am different now. The old Lisa is gone. I certainly didn’t die in the physical sense, but who I was changed in an instant, with those 6 pills.

……..

Apparently search engines don’t like it when there is duplicate content on the internet.  In order to appease Google, I will refer you to the other site, www.collective-evolution.com, where the story was published in full – http://www.collective-evolution.com/2013/09/14/a-journey-through-pharmaceutical-induced-illness/

 

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