Prominent Activist Notes Possible Connections Between Fluoroquinolones and ME/CFS

I’m a big fan of Jennifer Brea–an activist and advocate for those with ME (Myalgic Encephalomyelitis – also known as Chronic Fatigue Syndrome or CFS), and the filmmaker behind the wonderful documentary Unrest. She is also heavily involved with the ME Action Network, “A global, grassroots network for people with Myalgic Encephalomyelitis and Chronic Fatigue Syndrome,” and a blogger on Medium. She is powerful, thoughtful, interesting, insightful, an amazing leader, and she has helped thousands (maybe millions) of people with ME to live with, and maintain hope through, a horrible and debilitating disease. She has brought understanding of the horror of ME to people in a way that is empathetic and thought provoking. She is a wonderful advocate for her community.

AND, I’m excited to tell the “floxed” community…

Fluoroquinolones are on her radar as a possible cause of connective tissue disorders that may lead to ME.

In her July 10, 2019 post, “Onset: Part III (Connections),” she notes that antibiotics are a potential cause of collagen and connective tissue disorders:

Antibiotics: doxycycline, which anecdotally some patients have benefited from, inhibits MMPs. Fluroquinolone antiobiotics, which can produce an ME/CFS-like illness, increases MMPs and in December 2018, the FDA issued a warning against its use in patients with Ehlers-Danlos Syndrome and Marfan Syndrome.”

Indeed, fluoroquinolones increase production of MMPs–a category of enzymes that are capable of degrading all kinds of extracellular matrix proteins including, but not limited to, the structural proteins of the aortic wall.

The article, “Ciprofloxacin enhances the stimulation of matrix metalloproteinase 3 expression by interleukin‐1β in human tendon‐derived cells” notes the following:

In this study, we have shown that the antibiotic ciprofloxacin, which induces tendon pain in some patients (1) and tendon pathology in rodents (3, 4), can increase MMP expression in human tendon‐derived fibroblasts. Specifically, ciprofloxacin potentiated IL‐1β–stimulated expression of MMP‐3 at both the mRNA and protein level.

Tendon pain and degeneration have been associated with an increase in the normal turnover of matrix proteins (9, 10, 12). MMP‐3 has a broad substrate specificity; it is able to degrade matrix components including type III collagen and the proteoglycans aggrecan and versican, and is capable of activating a variety of other MMPs and pro–tumor necrosis factor (11). However, its role in tendon physiology and pathology has not been clearly defined.

Our results raise the possibility that a combination of fluoroquinolone and (fluoroquinolone‐induced) inflammatory mediators might result in the inappropriate or unbalanced expression of MMPs.

Changes in expression of matrix components such as collagen and proteoglycans have also been reported in response to various fluoroquinolones.

The increase in MMP expression may not be the only way that fluoroquinolones damage and destroy connective tissues, but it’s almost certainly one way.

More information about the increase of MMP expression caused by fluoroquinolone antibiotics can be found in the post, “Fluoroquinolones Increase Expression of MMPs” as well as these links:

In a couple posts on this site, I have noted that ME/CFS caused by connective tissue disorders may be proceeded (even caused by) fluoroquinolone exposure. You can read about these theories in the posts Are Fluoroquinolones Causing Connective Tissue Disorders that are Leading to ME/CFS? and Do Fluoroquinolones Cause Cerebrospinal Fluid Leaks?

In Jen Brea’s post she note that there are many causes of collagen and connective tissue disorders, including viral infections, bacterial infections, mold, pregnancy, surgery, car accident, concussion, Ehlers-Danlos Syndrome and other connective tissue disorders, and sex hormones.

It is likely that many people who suffer from ME/CFS, as well as many “floxies,” have been exposed to several of these triggers. Personally, I was exposed to both fluoroquinolone antibiotics and changes in sex hormones (my period) when the flox bomb went off in me. I don’t think I had an actual infection, but most people also have a concurrent bacterial or viral infection when they take fluoroquinolones. I have also surmised in the past that perhaps floxies (as well as people with ME/CFS) have a yet-to-be-discovered form of Ehlers-Danlos syndrome. I also think that there are genetic predispositions to both fluoroquinolone toxicity and ME/CFS, and that the RCCX theory by Dr. Sharon Meglathery is a good place to start when looking at genetic predispositions for all sorts of mysterious illnesses. On the site https://www.rccxandillness.com/ Dr. Meglathery states:

“I believe that the RCCX Theory solves some of medicine and psychiatry’s greatest mysteries. The RCCX Theory explains the co-inheritance of a wide range of overlapping chronic medical conditions in individuals and families (EDS/hypermobility, autoimmune diseases, chronic fatiguing illness, psychiatric conditions, autism, etc.). It explains the underlying pathophysiology of chronic fatiguing illnesses with so many overlapping features (EDS-HT, CFS, Chronic Lyme Disease, Fibromyalgia, toxic mold, Epstein Barr Infection, MCAS, POTS, etc.). And finally, it reveals the gene which I believe confers a predisposition toward brilliance, gender fluidity, autistic features, and stress vulnerability, as well as the entire spectrum of psychiatric conditions (other than schizophrenia which can be co-inherited).”

Though there is significant overlap between fluoroquinolone toxicity and ME/CFS they are not the same, and there are many people suffering from ME/CFS who had other triggers set off their illness. With that said, the evidence that ME/CFS is a connective tissue disorder is mounting, and if a debilitating disease like ME/CFS is caused by disordered connective tissues, perhaps drugs that are known to cause connective tissue disorders (fluoroquinolones) shouldn’t be prescribed by the millions each year.

I appreciate that a leader like Jennifer Brea has the fluoroquinolone connection on her radar, and I hope that those in the ME/CFS community that are floxies as well are able to gain insight and support from both our communities.

I also suggest that everyone watch her wonderful film, Unrest. As a recent floxie hope commenter said, “It’s a good window of what it’s like to live with a chronic illness and I think a great example of what it’s like to have a supportive partner (her husband Omar).” Here’s the trailer:

At the risk of sounding too much like a fan-girl, I’m pretty stoked that fluoroquinolone toxicity is on Jen Brea’s radar, because I think she’s amazing. Read and watch her work, and I think you’ll agree. Much of it will likely resonate with many “floxies” as well.

*****

 

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4 thoughts on “Prominent Activist Notes Possible Connections Between Fluoroquinolones and ME/CFS

  1. Patrick Jordan July 29, 2019 at 11:44 am Reply

    Hey Everybody,

    I was really impressed by this article and by Sharon Meglathery’s work. I wrote an email to her that I will post here because I think that all of our collective brains might be able to work out an answer for all of the people all of the time instead of some of the people some of the time.

    =======================================================

    Hi Sharon,

    Your work was referenced in a recent article of Floxie Hope.

    I found your associations very compelling.

    Would you please expand on what you mean by these conditions being ‘inherited’?

    The reason I ask is because when I was studying the work of Hulda Clark (former Canadian government scientist) who was echoing the work of Robert Hegner from 1936 regarding hyperparasitism, she said that the allopathic blame of disease running in families could be laid at the feet of families sharing the same environment so they will be exposed to the same infectious agents. Simple enough, but I am fully aware of your implication of genetic mutation regarding your theory, so, we add Lida Mattman to the mix:

    mattman

    where Cell Wall Deficient stealth organisms can cause acute disease yet be totally undetectable, so that it appears that genetic mutation is at the heart of the condition yet the raging infection beyond immune surveillance could actually be driving the gene mutations.

    Don Mau is uncredentialed, however, we are looking into the veracity of his claims of remedies for lyme. His most compelling argument is that borellia is a sideshow to Bartonella. Bartonella, according to some of the more prominents speakers (but still wrong) on the subject literally eats connective tissue – which, falls very much into the range of Fluoroquinolone damage if that antibiotic pushed the lyme coinfections into CWD states. FQs could either facilitate the Bartonella and/or cause its own damage chemically.

    bayer presentation

    Horowitz
    Co infections Presentation, Diagnosis and Treatment HD

    novect Breitschwerdt

    I use the material listed above with caution because both Breitschwerdt and Horowitz know that antibiotics cause CWD organisms yet they still use the drugs. They acknowlege that Bartonella can get into the CD34 progenitor cells to zombify the WBC stem cells before they differentiate but NO ONE is working on solving what I consider the SOLE problem. If our immune system is offline then NOTHING will work.

    So the Don Mau material citing that Bartonella as a nanobacteria in the same group as Agrobacterium that is used for ***GENETICALLY MODIFYING ORGANISMS*** seems to me to be the smoking gun that sews together your entire narrative as presented on your home page. With lyme coinfections alone, you get the borellia inducing mast cell degranulation, you get the bartonella doing genetic rewrites and eating collagen, you get all of the viruses, bartonella and babesia in red blood cells giving chronic fatigue, H. pylori another spirochete leading to sympathetic insufficiency via vagus nerve infection, and… unfortunately my ‘favorite’….

    Alan MacDonald fetal autopsies

    you get the filarial worms that penetrate the cerebrospinal system and get into the brain to deliver the payload of the borellia = neuroborelliosis that can account for the ‘psychiatric’ manifestations since I do not accept psychosomatic manifestations as being valid but rather somatopsycho causation of disease whether it is mental or physical.

    The Floxie Hope article cited MMPs running rampant which brought to mind a posting on an autism site where the MMPs ‘should’ be able to be quieted by the proper balance of zinc and copper. Which brings us to your references on your home page to copper and recent claims that copper niacin remediates spirochetes. What I am trying to do is harmonize everyone’s findings within a Continuum.

    I concur that such conditions CAN be inherited once they have been established in the germline cells, but it is also highly probable that just living in the same family being exposed to the CWD contagion can cause acute mutations without the need for generational transfer.

    Best wishes

    Patrick Jordan

  2. diana July 29, 2019 at 1:37 pm Reply

    Pathogens that often cause ME/CFS symptoms are often “stealth bacteria”…..the diagnosis of the origins of ME/CFS is very difficult to make. Since accurate diagnostic technology is kept purposely away and illegal for obvious profiteering reasons, now we are left with a lot of unanswered questions . And…… since NOT everyone was/is exposed to fluroquinolones it might be possible to add another reason that perhaps fluoroquinolones could be an additional element. However I strongly believe Bartonella, is the culprit of many ME/CYF symptoms. Overlapping of Bartonella infection with several other stealth pathogens probably can make the symptoms even worse.

    • Patrick Jordan July 29, 2019 at 3:35 pm Reply

      Like the serpent asking Eve if god said that she wasn’t supposed to eat that fruit… let me ask;
      How do any of us know that we haven’t been floxed by vaccines that have antibiotics on their label? Because the Corvelva report out of Italy analyzed vaccines that didn’t even have the labeled ingredients in them but around 80 unidentified compounds. Word on the street is that out here in Pharm Country that Cipro is being investigated as a herbicide for agricultural crops. It was just a few years ago that the FDA finally banned ANTIBIOTICS being used on ORGANIC APPLES AND PEARS to control bacterial fireblight. If I may be allowed to be Uber Gross, I just heard story that cities have long been lacking in freshwater supplies to keep their operations going so they RECYCLE SEWER WATER so it is impossible to know if, shall we say: Previously Used Cipro might not be in the tap water. Just keepin’ it real. And don’t worry: I depress me.

  3. Lukasz July 30, 2019 at 2:24 pm Reply

    UNREST is a great documentary. It’s one I, and I’m sure just about anyone here, can closely relate to. The only other documentaries that hit me as hard as this one was Gleason (2016) and True Stories (2017). What all of these documentaries have in common besides tragedy is human willpower. It amazes me how much perseverance people can possess.

    As for CFS, there’s no question in my mind that fluoroquinolones and macrolides cause this debilitating disease. Sure there may be other triggers out there, but in my case, the above antibiotics were 100% the culprit for the onset of CFS. No ifs and buts about it. I was healthy before I took them so there would not have been any other trigger but the abx themselves. I’m willing to bet the great majority of CFS cases out there are also as a result of antibiotics or other pharmaceuticals. Again, I’m not ruling out other triggers, but antibiotics are for sure a leading cause of ME/CFS.

    What these recent years have taught us is that it doesn’t take long for the truth to manifest itself. The pharmaceutical cover-up that was deliberately created has worked to perfection. Hundreds of thousands killed, millions left badly injured. Luckily, sites like this have opened up many eyes and prevented more deaths/injuries. For some, too little too late.

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