Are Fluoroquinolones Causing Connective Tissue Disorders that are Leading to ME/CFS?

The symptoms of fluoroquinolone toxicity often mimic those of ME/CFS (Myalgic encephalomyelitis/chronic fatigue syndrome). Many people suffering from fluoroquinolone toxicity experience debilitating fatigue, and some are bed-bound and permanently disabled from this symptom, along with all the others that come along with fluoroquinolone toxicity. Both fluoroquinolone toxicity and ME/CFS are multi-symptom, chronic syndromes that are poorly understood and often disregarded by those in the medical community. Research into the mechanisms behind both fluoroquinolone toxicity and ME/CFS show that mitochondria (the energy centers of our cells) are likely related to both diseases, and so is autonomic nervous system dysfunction, mast cell activation, metabolomics, epigenetics, immune system dysfunction, hormonal imbalances, and other areas of human biology. Both fluoroquinolone toxicity and ME/CFS also have significant overlap with other diseases such as Ehlers-Danlos syndromes (EDS), Postural orthostatic tachycardia syndrome (POTS), and fibromyalgia.

The similarities between fluoroquinolone toxicity and ME/CFS may mean that they have a similar root mechanism…. or they may not. The root cause of fluoroquinolone toxicity is, of course, fluoroquinolones. (The mechanism behind fluoroquinolone toxicity is much more complex and the answer to the question of HOW fluoroquinolones hurt people is still being uncovered.) Most people who have ME/CFS don’t report that their symptoms started with fluoroquinolone exposure (though there is almost certainly some overlap, and there are likely some people who have been diagnosed with ME/CFS whose disease started with a fluoroquinolone prescription). There seem to be a variety of triggers that set off ME/CFS in previously healthy individuals, including, but not limited to, mold exposure and sensitivity, and exposure to a viral infection that the body never fully recovers from.

While it is possible that there are many cases of ME/CFS that were brought on by fluoroquinolones, and thus are “actually” fluoroquinolone toxicity (labels, shmables), it is also possible that both diseases/syndromes have a similar underlying mechanism despite different causes, and it is also possible that though the symptoms and features of both diseases are similar, they are actually different on a mechanistic and/or cellular level.

Though the possibilities for differences between fluoroquinolone toxicity and ME/CFS are potentially significant, the similarities are obvious, and it is likely that research that helps ME/CFS sufferers will help fluoroquinolone toxicity sufferers.

There is a theory about the mechanism behind ME/CFS that has recently come to my attention that could, potentially, tie it more directly to fluoroquinolone toxicity. The theory, in a nutshell, is this:

Some people with ME/CFS have an underlying predisposition for EDS, and thus collagen synthesis is disordered and connective tissues are weakened. The ligaments of the craniocervical junction (where your skull meets your first vertebra) become weak and this leads to craniocervical instability (CCI) and atlantoaxial instability (AAI) (together, CCI/AAI). When people suffer from CCI/AAI their neck ligaments don’t sufficiently hold up their head and their brain stems are compressed into their spines. This causes many symptoms of ME/CFS. (I’m not sure exactly how – ask someone who has done far more research into ME/CFS and/or CCI/AAI than me.)

You can read about how CCI/AAI relates to ME/CFS in these two links:

  1. MEchanical Basis
  2. A new diagnosis to add to the list: I have craniocervical and atlantoaxial instability

How does this relate to fluoroquinlones?

It is well known that fluoroquinolone antibiotics (Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/ofloxacin, and a few others) damage connective tissues–including musculoskeletal connective tissues like tendons, cartilage, bone, and muscle, as well as other connective tissues such as ocular tissue (including the retina)eardrums, and cardiac/heart tissue. Multiple studies have found that fluoroquinolones are toxic and damaging to connective tissues. Given the wide differences in tissues that fluoroquinolones have been shown to deleteriously affect–from cartilage to cardiac tissue–it is reasonable to assert that they damage all connective tissues throughout the body. (Read any of the articles in the citations listed below for information about how fluoroquinolones damage connective tissues.)

Given that fluoroquinolones damage connective tissues (probably all connective tissues – see links below), it is possible that they weaken the tendons of the neck and thus lead to CCI/AAI. CCI/AAI then leads to multi-symptom chronic illness including all the symptoms of ME/CFS (which are too numerous to count).

This weakening of tendons and subsequent CCI/AAI likely occurs more often in people with underlying connective tissue disorders like EDS. I suspect (though I have no proof of this) that there are many kinds of EDS that have not yet been identified, and that more people have the genes for a variation of EDS than those who can currently be diagnosed with the disease. It’s also possible that a genetic predisposition toward EDS is not necessary for fluoroquinolones to cause extensive connective tissue damage, and that they do so in everyone who is exposed to them (at varying levels, of course). Fluoroquinolones have been shown to damage dog and rat connective tissues, especially tendons, and human connective tissues exposed to fluoroquinolones have also shown extensive damage both in-vitro and through analysis of people exposed to fluoroquinolones. I have a hard time believing that all the rats, puppies, and people whose tissues were sampled all had underlying EDS prior to their tissues being destroyed by fluoroquinolones. However, it’s possible that underlying genetic predispositions, including those for EDS, determine how severely people are affected by fluoroquinolones. More research is, of course, needed.

Are fluoroquinolones causing CCI/AAI? And is CCI/AAI leading to ME/CFS? Given the large number of studies showing that fluoroquinolones destroy connective tissues and interfere with collagen synthesis, it’s quite plausible (even likely) that they cause CCI/AAI. How, and if, CCI/AAI is connected with ME/CFS is another question. But given the experiences of the authors of MEchanical Basis and A new diagnosis to add to the list: I have craniocervical and atlantoaxial instability, it’s a possibility that is certainly worth exploring.

 

Sources for the assertion that fluoroquinolones cause connective tissue destruction and disordered collagen synthesis:

Musculoskeletal Complications of Fluoroquinolones: Guidelines and Precautions for Usage in the Athletic Population. Hall, Mederic M. et al. PM&R , Volume 3 , Issue 2 , 132 – 142

Etminan M, Forooghian F, Brophy JM, Bird ST, Maberley D. Oral Fluoroquinolones and the Risk of Retinal Detachment. JAMA. 2012;307(13):1414-1419. doi:10.1001/jama.2012.383

Tsai WC, Hsu CC, Chen CP, et al. Ciprofloxacin up-regulates tendon cells to express matrix metalloproteinase-2 with degradation of type I collagen. J Orthop Res. 2011;29(1):67-73

Lee C, Lee MG, Chen Y, Lee S, Chen Y, Chen S, Chang S. Risk of Aortic Dissection and Aortic Aneurysm in Patients Taking Oral Fluoroquinolone. JAMA Intern Med. 2015;175(11):1839-1847. doi:10.1001/jamainternmed.2015.5389

Kaleagasioglu F, Olcay E. Fluoroquinolone-induced tendinopathy: etiology and preventive measures. Tohoku J Exp Med. 2012;226(4):251-258.

Adel Alrwisan, Patrick J. Antonelli, Almut G. Winterstein; Quinolone Ear Drops After Tympanostomy Tubes and the Risk of Eardrum Perforation: A Retrospective Cohort Study. Clin Infect Dis 2017; 64 (8): 1052-1058. doi: 10.1093/cid/cix032

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48 thoughts on “Are Fluoroquinolones Causing Connective Tissue Disorders that are Leading to ME/CFS?

  1. Patrick Jordan December 7, 2018 at 6:18 pm Reply

    Anyone want to speculate with me that the Flox chemical warfare agent might not have been developed in conjunction with the Lyme biological warfare agent to totally gut the connective tissue of everyone they touched? I was floored when I heard the words: Lyme eats collagen. If each are destructors on their own then it will be monstrous when they work together. The NIH will never link all of the diseases mentioned in this article to Lyme but the links between each of the named diseases is established in the article. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867488/
    see any overlap in the article above?

    • Tracy Whiteside December 7, 2018 at 7:42 pm Reply

      Shouldn’t the mass murdering monster, Margaret Hamburg be locked up in Prison, for the Securities fraud she has been committing for years, by earning billions of dollars from our hell, death, and, misery, The SEC met with her, and, her rotten AI expert, hedge fund owning husband, and, told them they could not own any pharmaceutical stocks, before she became head of the FDA# Funeral Directors Assn, so, they promptly invest 500 million into Johnson and Johnson, and, is still making billions off of her securities fraud, any civil rights attorneys want to help us ?

  2. Tracy Whiteside December 8, 2018 at 12:30 am Reply

    Why don’t we all put together paperwork,regarding Margaret HAMBURGS crimes against humanity, copies of her indictment for using Levaquin as her own personal eugenics program, copies of her being head of AAAS, a known eugenics organization, copies of her and Henry Schein poisoning children with mercury fillings, her massive securities fraud, stories of the horrors of floroquinolones, and, send them to FBIheadquarters and NYC FBI, and, see if they can’t lock this mass murdering monster up, we need to do it en masse, please, AAAS is her ninth eugenics organization, send stories about her parents both being former Presidents of The American Eugenics Society,we need to do this, her husband will be making the robots who are going to replace us, her massive securities fraud that the SEC refuses to do anything about, she’s a monstrous murderer, and, needs to be held accountable, please, let’s do this.

  3. Henk Noordhuizen December 8, 2018 at 4:30 am Reply

    Great information,again,Lisa.There is yet another link between FQ’s and ME:a magnesium defficiency.First supplement,advices on the (dutch) ME-website:magnesium. There is a growing list of medicines that cause a magnesium- and other vitamine and mineral defficiencies and I think the reason is that most of the synthetic/chemical medicines are seen and treated by the human bodies as a dangerous poison which has to be removed from the body as quick as possible.And therefore you need lots of magnesium and other minerals and vitamines.Orthodox medicines,by definitian,make you sick. They are a failed experiment to copy their sources;plants,bark and other natural sources.

    By the way: MAGNESIUM is,for good reasons,often called THE SECRET OF ORTHODOX MEDICINE.

    • Patrick Jordan December 8, 2018 at 5:03 am Reply

      ME and its analogs in the United States called fibromyalgia/CFS and a host of other things also has a connection with lyme. The organisms within that constellation of microbes like to EAT magnesium. So, we are back to the chicken or the egg of whether there was ever a deficiency of magnesium (how could that happen in the first place?) or if it was stolen from the host. Given that magnesium can be used as a food source by microbes in the same way that iron is, so supplementing with iron is contraindicated in anemia during an infection, then the question has to be examined if taking supplemental magnesium in the face of possibly cryptic infection might not do more harm. I know of many people who cannot tolerate magnesium supplementation. I took magnesium and got night sweats every time until I killed Babesia (northern malaria) with parasite herbs. Anyone with impaired kidney function can be harmed or killed by magnesium accumulation. I have moved from compartmentalized thinking to that of Continuum.

  4. Bronwen Duncan December 8, 2018 at 11:24 am Reply

    A book I came across helped me understand that there may be a connection between my fluoroquinilone symptoms and mitochondria (before I found your site): “Diagnosis and Treatment of Chronic Fatigue Syndrome – it’s mitochondria, not hypohondria” by Dr. Sarah Myhill. Interesting book with part of the puzzle.

  5. Steven L. Weyenberg December 9, 2018 at 12:59 pm Reply

    I have all these problems and often wondered why my neck is so messed up, sending weakness and pain throughout. I believe I have had some deformations with my skeletal system, (TOS syndrome X2), and those little irritating extra bones behind and outside of the knees causing problems already. Things of that nature among chronic fatigue/headaches already in-place, taking the fluoroquinolones really can and has upped the level of problems. I can no longer fight off oncoming allergie/sickness as well and with sleep disorder from those fluoroquinolones, it highly detrimental to quality of life. How many onset diseases and disorders are onset from these antibotics is surely astronomical.

    • Patrick Jordan December 9, 2018 at 1:19 pm Reply

      If someone could tell us the metabolic half-life/persistence of floxacillins it might go a long way to explaining persistence of symptoms. Liver cleansing and to the degree I have done will not be indicated for everyone (I’m not a doctor – not medical advice), however, I have been doing liver cleanses for nearly 4 years. All the way up to 2.75 years into it I was being poisoned by my own bile as it recirculated through my digestive tract until I broke that cycle. A lifetime of industrial chemicals were STILL ACTIVE in my bile so unless they were broken down and expelled from the body they could PERPETUALLY create the same poisoning symptoms everytime they passed the entero-hepatic circulation. So, if fluoroquinolones are not detoxified or have been run through Phase I re-dox and changed to even more toxic analogs yet have not been expelled through the bile and out the body, I wonder how many people are just auto-toxic after having stopped taking the chemical warfare agent?

  6. Mary December 11, 2018 at 11:08 am Reply

    I’ve been on this journey for two and a half years now along with cardiovascular problems.
    I have become very afraid of meds of any kind and have chosen more than once not to go for surgery.
    After my last visit with my cardiologist – who recommended surgery – I was so depressed and didn’t know what to do but pray for an answer.
    One night I was looking through youtube and I found a short piece by Dr. Raymond Francis, M.Sc.
    He gave me hope and I purchased three of his books.
    Please consider looking into all the information he offers. He knows first hand what it is to be poisoned by Big Pharm, a drug caused his liver to shut down.
    Blessings
    Mary

  7. Fermin December 15, 2018 at 4:03 pm Reply

    Hi,

    I’m from france. We are not looking at right direction. Fluoroquinolones are toxic, yes… The more quinolones you took, the biger the damage, but it’s not causing the chronic symptoms that people experience with relapses.. of course if you took too much quinolones, there is a direct damage from abx, but you have to take too much of that to end dissabillity. But what happen wen people took only one pill and end with permanent symptoms? Simple, it’s an autoinmune reaction, you can test what you want but it’ll show negative, because we don’t have test for that… In fact fluoroquinolone toxicity syndrome should be considered another autoinmune illnes, with it’s own test.. Of course IgG antiquinolone antibodys etc… It’s a chronic hypersensitivity type 3 reaction…. some people recover and other don’ts… Your body will create antibodys on the surface where quinolones penetrated… It penetrares deeplly into tendons and cartillage/tendon concentrations are much higher than blood, for that reason tendons, ligaments etc… are target places. It’s not mitochondrial dysfunction… Genotoxocity is not a concern on short term treatments and it shows low toxicity on human cells…

    We need to focus that on our inmune response like if it was another autoinmune illnes.

    • Patrick Jordan December 15, 2018 at 5:11 pm Reply

      You present a very refreshing alternative view to add to the whole. I say add to it because within Continuum there is never a single cause or single answer is it always: All Of The Above. Type 3 is serum sickness = Drug Fever. Implantation of Circulating Immune Complexes that then provoke an immune response that causes collateral damage to all of the tissue around it. This makes a lot of sense. So the implantation of the CICs could be addressed by enzymes but then the fallout from the release of the CICs that include the possibly still active drug would become a nightmare of what is falsely called the Herxheimer reaction. A fully integrated plan of how to degrade the CICs, capture and shuttle the fluoroquinolones out of the system, and repair the tissue damage would have to be thought out in advance before any action was taken. The starting point would be to find biocompatibe molecules that have an affinity for binding to FQ and then looking at the chemistry of supporting liver conjugates to make sure it is bound and taken out for delivery to the garbage haulers. We have found looking into Lupus (false label for Lyme disease) that there is no such thing as Anti-nuclear Antibodies as an ‘Autoimmune’ disease because the circulating antibodies can’t get into the host cell to attack the DNA or other components so this has been a purposeful Red Herring to keep people from looking at just what that foreign DNA might be that triggered the antibody response in the serum. Autoimmunity as a whole concept then falls into dispute because the Cell Mediated response that shows up to clear the embedded CIC with the FQ really isn’t autoimmunity to self, it was just collateral damage of a relatively simple and dumb system of the body trying to clear an invader the using the only tools that it has. Too bad it is the equivalent of a flamethrower in a paper house. Thank you for sending us in a new direction.

      • annspinwall4 December 16, 2018 at 11:42 am Reply

        Thank you so much for your outstanding comment and additional information!

      • Fermin December 17, 2018 at 4:01 pm Reply

        you are right patrick.

        I have done something that very few people did or maybe only me.

        I have neuroborreliosis, and unfortunately I made the mistake of taking a dose of levofloxacin. Take it together with doxycycline, amoxy and biaxin. I base my theory of autoimmunity in my personal experience, there are only three antibiotics that I can not tolerate under any circumstances and these are by surprise: doxy, amoxi, and biaxin …. A single dose and i experienced the initial symptoms of flox. But I can take, minocycline, azithro etc … that is, antibiotics that were not in “contact” with a quinolone. The immune system confuses these three antibiotics for the toxic … there is no other possible explanation .. it is all based on autoimmunity. Many lyme sufferers, have elher danlos.. chance? Or maybe it’s a genetic defect due to a congenital lyme … it’s all very complicated. What I am sure of is the first, this is all related to autoimmunity, or I prefer to call it an immune reaction … now, how can we detect this in the analytics? Is it a reaction based on antigens? A reaction mediated by cells? We must focus on this to find a cure and forget the mitochondrial dysfunction … to have a mitochondrial dysfunction, we should take extremely high doses for long periods …. Months or maybe years … Only then could we generate such destruction in our DNA , which would mean permanent damage forever.

        • Fermin December 19, 2018 at 11:10 pm

          So, my advice is… avoid all what you took the first week of poison…. and if there is hope things will be better. There is no cure.

    • Coletta December 29, 2018 at 12:55 pm Reply

      Fermin. I can barely understand all of this. But – I was found to have IgG Deficiency right before I was given Levaquin for pneumonia from the IgG Deficiency last year. It is believed that my late onset of IgG Immunoglobulin deficiency is related to damage from breast cancer treatment 8 yrs ago. I have felt that my Fluoroquinolone toxic damage might be related to my IgG deficiency. I also have wondered if Lyme disease has played a role. I was diagnosed with Lyme 25 years ago, treated for 4 months with Erythromycin and Tylenol and felt that I was cured. Now I wonder.

  8. Patrick Jordan December 20, 2018 at 4:32 am Reply

    The word: Cure can get you put in prison in the U.S. so I don’t use it. The AlterNOTive gurus use the word: reverse, as in Reversing Autism. The problem is that they worship at the epigenetic altar so they claim that they have corrected a problem when they simply switched off genes that were mutated therefore cause problems when they are active. If you switch off those genes the SYMPTOMS may not be as bad but the broken genes are still there. One point I was trying to make on this thread is the recirculation of poisons we have accrued during our lives in the enterohepatic circulation. If your bile is toxic then there can never be released from a circular hell. Avoidance is the first thing taught in Multiple Chemical Sensitivity, but I am proof that avoidance will correct NOTHING if the chemicals that you got when you were a child are still locked into your bile or fat. Writing that in real time made me do a serach for “fluroquinolones stored in fat”. Oddly the only return I got was:
    https://www.sciencedirect.com/science/article/pii/S0006349508704612/pdfft?md5=6912c875c6012a46c52df5d07187a887&pid=1-s2.0-S0006349508704612-main.pdf
    Not from France but amusingly from Belgium.
    I read many books and articles with dictionaries and medical texts at my feet because I admit most of the PDF was not written in Belgian, or English or any language I can recognize, but the gist of it is that fluoroquinolones can get INSIDE our white blood cells. This is considered a good thing to get rid of intracellular parasites but I have to study this material to see what the relationship is between flox lipophilic properties and the efflux pumps in human vs. bacterial cells. The one thing I am inferring from this is that these drugs have an affinity for fat, so we are back to my main premise. Therefore, as to ‘cure’ there can never be a cure if the drug is RECYCLING through our bodies.
    Another thought that came to me as I wrote is that they inferred that the fluroquinolones were hydrophobic. We cannot urinate out a poison unless it has been run through Phase I oxidation/reduction processes then passed on to Phase II. The absolute danger here is that some toxins can be made MORE TOXIC or even CARCINOGENIC after that process. The next step is to conjugate them in the liver for urinary excretion, but then we are back to the problem that they might resist transport in the urine that is water. If we go back to look at the danger of Phase I detoxification causing fluoroquinolones to perhaps be worse monsters than they already are then the secondary metabolites need to be studied to see if those might be causing the intractable problems people are experiencing while the unaltered drug is taking most of the blame. So, we will need to see what cytochromes are induced when this drug hits the liver and blood. There is a similar chemistry in the soil with glyphosate (Roundup) being toxic, yet its adjuvants in the pesticide and the metabolites of glyphosate are actually more toxic then the original poison.

    As to neuroborelliosis the single most important thing that needs to be clear is the relationship of filarial worms that crawl through humans like swiss cheese (I don’t know if there are french cheeses famous for holes) that carry borellia inside of them. The epic work of MacDonald explains this.
    this first one is highly disturbing:

    I use Hulda Clark’s parasite cleanse to keep all of those monsters at bay. Beware: I am not anyone else, therefore the depth of a person’s condition can determine if a parasite cleanse might increase symptoms which is NOT herxheimer but the lack of ability to deal with contingencies during a useful therapy.
    I really like sharing ideas with you because you inspire me to look deeper than I have previously. cheers.

  9. Patrick Jordan December 20, 2018 at 4:41 am Reply

    Neuroborelliosis

    I gave the wrong first link to MacDonald. That first one was really disturbing so don’t watch it if you can’t handle it.

    https://www.prnewswire.com/news-releases/lyme-bacteria-hides-inside-parasitic-worms-causing-chronic-brain-diseases-300270742.html

    I keep hammering this idea that the filarial worms are the key players here because everyone is taking ‘antibiotics’ for ‘bacteria’. It’s the equivalent of going elephant hunting with a toy water pistol.

  10. Patrick Jordan December 20, 2018 at 5:45 am Reply

    Different Drugs = Different interventions:
    https://www.ncbi.nlm.nih.gov/pubmed/2690618
    some detoxed by liver more than others. Glucuronidation is key.
    oxoquinolone metabolite should be a study focus.

    https://www.ncbi.nlm.nih.gov/pubmed/24548434
    The optimized conditions allowed picturing metabolites/transformation products formation and accumulation during the process, stating an incomplete mineralization, also shown by fluoride release.

    Most of the intermediates were already described as biodegradation and/or photodegradation products in different conditions; however unknown metabolites were also identified. The microbial consortium, even when exposed to high levels of FQ, presented high percentages of degradation, never reported before for these compounds.
    ———————————————–
    I don’t want anyone freaking out that Pandora’s Box has so many demons, because we can’t fight what we can’t see.

    Fluoride release? Fluoride is an enzyme disruptor, so that is a first start. Cytochromes are isoenzymes. Iodine is a fluorine antagonist.

    PHOTODEGREDATION? Does anyone have photosensitivity after floxing?

    ‘never reported before compounds’ now there’s a confidence builder….
    I’m working on getting the particulars.
    ————————————————–
    http://tmedweb.tulane.edu/pharmwiki/doku.php/fluoroquinolones
    “Penetrates in most tissues including prostate, however poor penetration into the CSF. ”

    pretty lame choice for neuroborelliosis.

    http://www.antimicrobe.org/d17.asp

    “The cerebrospinal fluid levels of ciprofloxacin and ofloxacin in patients with inflamed meninges are 40 to 90% of serum concentrations.”

    which of course flies in the face of the citation just above it, but none of these white coated assassins ever read each other’s publications.

    “As with most oxoquinolone metabolites, the oxo- metabolite of ciprofloxacin is active, although less so than ciprofloxacin. In urine, 36% of a 500-mg oral dose is recovered as unchanged ciprofloxacin, 9.6% as the oxo- metabolite, 2 to 4% as the dioxo- metabolite, and less than 2% as other metabolites

    Quinolones are eliminated by renal mechanisms, including glomerular filtration and tubular secretion, as well as by nonrenal routes, such as hepatic metabolism and transintestinal transport

    The potential for phototoxicity associated with ciprofloxacin, ofloxacin, trovafloxacin, levofloxacin, gatifloxacin, moxifloxacin, and gemifloxacin appears similar and are lower than that of clinafloxacin, lomefloxacin, and nalidixic acid, compounds that are substituted with an additional chlorine or fluorine moiety at the C-8 position.

    Clearance of theophylline and caffeine is inhibited by some of the quinolones, in approximately the rank order shown in Table 5. Given the different affinity for the cytochrome P-450 isozyme 1A-2, the fluoroquinolones vary in their relative degree of interaction with theophylline.”
    —————————————————-
    There’s one cytochrome to pay attention to. And with it comes warnings that I don’t know if everyone knows because I have not followed this blog before:
    ———————————————————
    “Caffeine, a chemical analogue of theophylline, interacts similarly when coadministered with quinolones. Patients receiving certain fluoroquinolones should be advised against excessive caffeine intake, and if CNS effects develop, they should be instructed to cease caffeine intake.”

    North Americans are addicted to zombie juice. I wonder how many floxies use caffiene not knowing they are making their symptoms worse?

    By the way: my questions are not rhetorical, I would really like some personal insights.

    “Fluoroquinolones form chelates with divalent cations, particularly aluminum and magnesium and, to a lesser degree, iron, zinc, and calcium.”

    This supports the notion that someone put out there to supplement with minerals but metal chelation is not conjugation and so there is no guarantee that the drug will be excreted. If there is circulating drugs that have never been cleared then perhaps a multi-step detox might be formulated.

  11. annspinwall4 December 20, 2018 at 11:12 am Reply

    Patrick, thank you so much for taking the time to educate on what we are up against in all this mess….you are exceptional and special…people take heed, this man is one of a kind and synthesizes data like no one else on the planet and I am happy to call him my friend and mentor!!

    • Fermin December 21, 2018 at 1:27 pm Reply

      Well.. I take large doses of caffeine and my symptoms don’t get worse…

      I don’t subscribe the theory of permanent fql particules in our body…

      We have biopsed muscle tissue of people suffering from flq toxicity… hair, nails etc… and there is not traces of abx.

      Fql make our inmune system crazy.. It’s permanent attacking our body… Of course if you took caffeine while on fql… you can have a worsening in tour symptoms.

      That’s easy… Test people for antiquinolone antibodys and if it’s positive you have that answer… It can persist for years…

      Magnesium can have a benefit in the acute phase to blind some quinolones, but after 48h i think it’s not going to help us, but it’s my opinion.

      • Patrick Jordan December 21, 2018 at 1:53 pm Reply

        Help me out with the ABX abbreviation: what does it stand for? Are most laboratories equipped to test for anti-quinolone antibodies? This is the most astounding thing I have heard of in a long time. In fact, the presence of these antibodies would support the idea that there isn’t such a thing as autoimmunity, but rather antibodies that target tissue that has implanted circulating immune complexes or were subject to antigenic mimickry. This stuff is HUGE.

  12. Debs December 21, 2018 at 5:24 pm Reply

    Yes many of us simply cannot tolerate caffeine Patrick. We are aware of this. I still cant handle it, many years after my last most damaging floxing

    • Patrick Jordan December 21, 2018 at 8:40 pm Reply

      I’m a thousand years behind in the biochemistry that needs to be done to get to the root of what is going on but it has to be done in a stepwise manner so that continuity is not lost. Morphine and its Opioid derivatives allow cell permissivity so that things like Herpes can enter. Nerve cells, white blood cells, somatic cells. Opioid epidemic indeed. The problem is that Herpesviridae family of viruses are mostly neurotrophic in their behavior, therefore they will cause pain. So what do people do? They seek out a pain killer. Enter Opioids. Enter: Herpes. More herpes means more pain means more opioids. Our next investigations were to be the other alkaloids like: nicotine, caffeine, and cannabinoids, and one I keep forgetting, to see if they have this same property of opening the door to viral infiltration. Therefore I cannot say at this point if caffiene is as bad as opioids for letting the alien in the airlock, but what we do know is that caffiene requires similiar cytochrome enzymes for detoxification as some fluoroquinolones. So we will pick up that line of thought to see if there is any way of supporting those enzyme systems to help clear the drug and/or the circulating immune complexes with the drug because if those cytochromes are exhausted then that will lead to symptoms as well. Which is to say that there is no simple single answer to what the symptoms are caused by, but one thing often shows to be true is that they are all related somehow back to the dominoe that got the rest to fall. CYP1A2 is the main player in caffiene (I always spell it wrong so I don’t bother after all these years) detoxification so this is where it gets tricky:

      IF you try a glass of grapefruit juice and you feel like total Hell then you didn’t need CYP1A2 disabled. This may indicate low Phase I detoxification and the need to support that oxidation process to get rid of the drug. If you feel better… that means that you were an OVER-oxidator and overwhelmed your Phase II conjugation pathways which either may be working at ‘normal’ capacity or need support. Cabbage, broccoli, brussels sprouts (YUK!) and all of the other cruciferates (Cauliflower is the most dangerous plant on the planet) can also inhibit CYP1A2, but, strangely increase the conjugation pathways. This would be useful if you were a fast oxidizer but a slow conjugator (no grammar jokes!).

      What needs to be determined is if this cytochrome works solely on the unmetabolized drug and/or its secondary metabolites and/or any circulating immune complexes with the drug.

      Next as our friend Fermin notes we also need to know if any of these cytochromes can help shuttle any anti-quinonlone antibodies out of the system, or if that is even a useful thing. This is the first I have heard of a xenobiotic agent having an antibody assigned to it that was not complexed with a protein, so then… we have to find out if those antibodies exist in freeform and circulate, or if they are complexed with antigens (whether those antigens are the target drug or not), and if they are implanted in tissue thus causing cell mediated responses to destroy the CIC and surrounding tissue. The last scenario might be a reason why you can biopsy muscle tissue yet find no flox there because the implanted CIC might have been broken up by the immune response that damaged the tissue. Heep bad medicine. So are anti-drug antibodies good or bad? Don’t know. If they are good to begin with then what caused them to go rogue?

      Sammy Hahnemann of homeopathic fame first thought that coffee was the cause of all chronic disease in mankind until he developed his Psora theory, so zombie juice is best avoided, however, it really wasn’t the problem with respect to not being able to tolerate it after being floxed. Caffiene indicates all of the downstream damage from the drug. It shows up as illness because you can’t detox that alkaloid. In a way: caffiene is a reality check.

  13. Patrick Jordan December 22, 2018 at 10:21 am Reply

    To the Floxie Flock:
    The next two postings will be covering material that one of our Little Red Hens provided. She is a data dog who likes to come home with a dinosaur bone so it is quite a bit to process. I will reserve comments for a separate post so that it doesn’t interrupt her flow.

    Be aware: I have not reviewed this material in detail yet therefore I cannot endorse anything presented. It is for informational purposes only to see if we can get a handle on the multi-systemic failures induced by a single chemical.

    Here is what she sent:
    ===========================================
    Sorry, I went a little mad……

    https://metabolichealing.com/extracellular-matrix-key-unravelling-chronic-disease/

    “The class of antibiotics known as Fluoroquinolones (such as Cipro) are known to cause changes to the extracellular matrix, increase metalloproteinases (which degrade the ECM), and can lead to degradation of collagen and tendon rupture (8, 9).”

    There seems to be a photosensitization process in the mitochondrial/fibroblast damage from fluoroquinolones.

    https://www.ncbi.nlm.nih.gov/pubmed/11195848

    https://journals.sagepub.com/doi/abs/10.1177/03635465000280031401

    https://fqresearch.org/dna-damage-fluoroquinolones/

    https://www.sciencedirect.com/science/article/pii/S0014483515300567?via%3Dihub

    https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1751-1097.1999.tb07979.x

    ???Digestive enzymes with protease would increase the damage.????

    https://www.researchgate.net/publication/12475442_The_effect_of_ciprofloxacin_on_tendon_paratenon_and_capsular_fibroblast_metabolism

    “This study demonstrates that ciprofloxacin stimulates matrix-degrading protease activity from fibroblasts and that it exerts an inhibitory effect on fibroblast metabolism. The increase in protease activity and the inhibition of both cell proliferation and the synthesis of matrix ground substance may contribute to the clinically described tendinopathies associated with ciprofloxacin therapy.”

    The following is really SICK!

    https://patents.google.com/patent/US6060474A/en

    OK? In light of the above link, the following makes no sense at all.

    https://res.mdpi.com/jfb/jfb-03-00361/article_deploy/jfb-03-00361.pdf?filename=&attachment=1

    Fluoroquinolones are iron chelators.

    http://www.jbc.org/content/290/36/22287.full

    “Here, we show that the FQ drugs norfloxacin, ciprofloxacin, and enrofloxacin are powerful iron chelators comparable with deferoxamine, a clinically useful iron-chelating agent.”

    https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1751-1097.1997.tb03160.x

    “The fluoroquinolone(FQ) antibiotics photosensitize human skin to solar UV radiation and are reported to photosensitize tumor formation in mouse skin.”

    Fluoroquinolones are Chemo Drugs!

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

    http://www.bioone.org/doi/abs/10.1562/0031-8655%282000%29072%3C0458%3AAOTEPB%3E2.0.CO%3B2

    Alteration of the Endocytotic Pathway by Photosensitization with Fluoroquinolones
    “Binding of LDL to their cell surface receptors is impaired by irradiation with 10 J cm−2 of UVA….”

    • annspinwall4 December 24, 2018 at 12:05 pm Reply

      Patrick, thank you so much for posting all the links and thanks so much for all your relevant, thoughtful comments. A lot of really good education here.

  14. Patrick Jordan December 22, 2018 at 10:56 am Reply

    My comments on the citations previously shared:

    For veterans of fluoroquinolone damage the notion of matrix metalloproteinases being activated is probably old news. MMPs are remodelers. They are not the enemy but they have been deranged so that they become harmful. I can’t figure out why it is so difficult to find a certain citation in my personal archives relating to a mom with an autistic child who addressed the MMP problem in that condition, where she said that MMPs are activated and deactivated by specific levels of zinc and copper. She made it clear that if you supplemented with zinc you might be able to shut down the cascade that leads to collateral damage of tissue, BUT if you took TOO MUCH ZINC you could make things worse. I call this concept: Booby Traps and Failsafes. Others might call it: damned if you do, damned if you don’t. I will look for that ancient citation and post it if I can find it.

    Right off you can see that well meaning people who get on boards or blogs and suggest that others try mineral supplements are not necessarily wrong, but if you don’t know the biochemistry then it could turn out like trying to blow out flame with gasoline on your breath.

    I would appreciate some feedback on experiences with photosensitivity. Current relationship to the sun after having been floxed for a long time will help, but what I am really looking for is: I took flox, then went to the beach…and….

    The Enzyme connection is going to be tricky as well. The editorial ??? that I put on the comments regarding digestive enzymes is to remind us that there are a full range of enzymes not just the gut enzymes that work within the somatic cell environment. One of our Red Hens experimented on himself with serrapeptidase (something that I would personally never touch) to see what it could do to scar tissues and adhesions. It diminished scar tissue but it also weakened the body to new injury. So he quit. The body healed but then the old scar tissue came back. Taking one for the team. Better him than me.

    This presents a problem, though, in that the Bartonella component of Lyme disease is a collagen eater. The infection might benefit from the use of digestive enzymes, but we are back to the Catch 22 of whether it helps or hurts. I bring up the lyme connection because nothing happens in isolation. Lyme is a worldwide epidemic so we can’t look at just flox or just lyme especially when connective tissue is at risk. In addition to that: autoimmune scurvy instigated by vaccine damage is probably a worldwide epidemic as well. We are trying to find a way to replenish the ascorbic acid without the insane use of I.V.s and to find a way to increase INTERCELLULAR LEVELS (NOT BLOOD LEVELS WHICH MEANS IT HASN’T GOTTEN TO THE CELLS) without the vitamin C or the tissue it serves being taken out before it can rebuild. Nothing happens in isolation.

    Iron chelation is problematic too in that would-be internet gurus will tell you how toxic iron is. Problem is iron is only toxic when the handling pathways of the body are deranged. Iron is of course essential for building blood, but its key function is to complex with vitamin C to make a lightening bolt that can kill invading microbes. In that sense it is highly toxic in a good way. Catch 22: supplementing with iron can feed existing infections. So, the question remains: is the iron a problem with existing infections (that could be taken out by an iron/vitamin C tag-team) because the handling pathways have been damaged?

    Before chemtrails I use to live out in the sun. I think that sunlight is beneficial, however, we can see from the links that UV has now become a booby trap. There is one tiny clue that needs to be followed up by me and the Red Hens regarding LDL and flox and UV. Put aside ALL of the internet and mainstream nonsense regarding low density lipoproteins. THEY ARE YOUR BEST FRIENDS. ONLY LDL can protect you against rampant PRION disease so that is why they were demonized. If anyone doesn’t mind sharing personal information on the Net then I would really like to hear what kinds of cholesterol levels folks have after being floxed.

    • Fermin December 22, 2018 at 7:37 pm Reply

      Patrick, your work is incredible!

      Yo talked about bartonella. I have Bartonella at high titers… it eat collagen hand to hand with lyme, and if you have fql toxicity… It’s a disaster.

      I’m taking roxithromycin for Bart. It’s better than clari, and azitro… It acumulates in high concentrations into macrophages… and it let the antibiotic travel to the site of infection.

      • Patrick Jordan December 24, 2018 at 10:17 am Reply

        Hi Fermin, thanks for your confirmation that at least as some level there is a crossover between fql use and its sequelae and the lyme epidemic, but once again you have forced me to consider if the average man and woman around the world doesn’t go into a doctor with some complaint that might be an unidentified infection where fql are the poisons of choice for a ‘doctor’ who is out of their depth, when the health condition/infection has such a high statistical probability that it was undiagnosed frank lyme & coinfection that as you note when lyme and fql hit headon there is a disaster of trainwreck proportions. I am against the use of drug antibiotics given that most of them take the cell wall off of organisms thus creating Cell Wall Deficient forms that literally has taken the human species (and all other life forms) to the depths of hell. However, there are ‘lyme literate’ (read: illiterate) doctors who actually use cipro, et. al. for things like Bartonella, because as you say these are among the rare few drugs that can get INSIDE host cells. The Devil’s Bargain is that the cop enters the bank to shoot everything in sight to get at the robbers. Two more posts below to show how much more you have revealed this complex problem to us (me and my team) to the point where I am questioning everything I was ever taught or taught myself since 1978. …and… Thank You.

        • annspinwall4 December 24, 2018 at 12:11 pm

          I think it absolutely criminal for a doctor to prescribe floxie drugs when there is a freaking “black box warning” about them being a drug of last choice….yeah, last choice all right….deadly to the patient. Here is a stupid article that explains that “black box warnings” can be easily overlooked by a doctor…total nonsense IMO
          https://www.peoplespharmacy.com/2014/10/06/black-box-warnings-are-easily-overlooked/

        • Patrick Jordan December 24, 2018 at 7:08 pm

          Hey, Annie. What you bring up is the question of: Intent. IF this is the drug of last resort then WHY is it given out freely for female bladder infections, etc? The question cannot be answered politically, or socially, or even within the bounds of medical ethics and it has NEVER been about money since they can print that funny paper at will. Therefore biology will be the only thing that can instruct us. Lida Mattman said that TB and Leprosy NEVER WENT AWAY, THEY ONLY WENT STEALTH DUE TO ANTIBIOTIC USE. So, we have to examine the mechanism of action of the available poisons and their intentional use. The Lyme Illiterate doctors throw doxycycline at everything as if it were holy water. But this poison is known to create Cell Wall Deficient organisms, and if memory serves is bacteriostatic NOT bacteriocidal. It was claimed on camera by one ‘doctor’ that he uses a combination of these ineffective chemicals orally while it is known that intravenous BACTERIOCIDALS have a shorter treatment duration and supposedly better outcomes. Not that I would endose even that madness. So, when dealing with liars you then have to question everything that is presented. ARE fluoroquinolones bacteriocidal? For how many organisms? If they are not bacteriocidal for ALL organisms, then what is their effect on bugs that they do not kill? These are research questions that demands an answer for all of us to know what the fallout is from using them even once. I can’t think of anything more horrific than to be given a FQL that are said to penetrate cell walls and thus exert more potent action against invaders like bartonella, just to have it cause the monster inside the cell morph into something else thus not die. The most important thing to keep in the forefront of our memories when researching this is that when an organism goes stealth it falls off of the radar of the immune system and diagnostic tests. So, on the face of it a physician can lie that they “got rid of” the organism because it no longer shows up on a test, but also the patient (victim) might even feel better because YOU ARE ONLY SICK WHEN YOUR IMMUNE SYSTEM IS WORKING. IF a bug goes CWD, then it can crawl through you like swiss cheese but you won’t be technically “ill” because there is no immune response to what cannot be seen for lack of surface antigens. Borellia alone with its cell wall competent form, CWD form called cysts in Europe, Blebs and according to Lida Mattman 5 other forms including virus-like particles has to either have these morphologies due to lifecycle stages and/or be provoked by host environment pressures like drugs. IF the FQLs don’t cause CWD forms but then induce any of Lyme & Company to adopt any of the other 7 forms then the INTENT of using such drugs was EXACTLY that end point NOT the false flag of calling it bacteriocidal and pretending that they shot the elephant while standing next to a cardboard cutout. I hope this makes sense to most people who read it because it is really Romper Room level of understanding of the problem. People smarter than me will have to come in to say that if these other variants are present all the way down to the viral forms then how do we clean up the mess all the way down to nuclease enzymes to break up the monster bug bits so that they can’t come back like Jason for another scary movie?

        • annspinwall4 December 25, 2018 at 2:16 pm

          Patrick, thank you again for your insight and added value to the comment section of this website. You have an amazing ability to cut through the BS and ask the hard questions that need valid answers. I’ve been prescribed flox drugs in the past without knowledge of their potential harm. Didn’t think I had been harmed, but at this point as a sufferer of Lyme and Company, who knows if taking this monster of a drug has potentially made my symptoms worse. Again, your knowledge and thoughtful comments are exceptional!!

        • Patrick Jordan December 26, 2018 at 8:23 am

          Thanks Annie; but now you’re freaking me out. I would like to hear from folks who had a casual brush with FQLs that then ended in disaster. We can presume that a long course of drugs would have devastating effects but what about the incidental eyedrops with flox in it? what about the women with bladder infections that got the drug of last resort as the first choice? Poison is in the dose but what might that dose be?

        • annspinwall4 December 26, 2018 at 1:32 pm

          Yes, good ‘ole floxie eye drops…had them for ocular rosacea (blepharitis) and now I have clogged tear ducts and may need surgery to repair…is the clogging caused by bleph or floxie? Will I ever know for sure? I hate all pharmaceuticals!! Thanks Patrick

        • Patrick Jordan December 26, 2018 at 5:41 pm

          Day Yam! Ye Olde Bait and Switch. What better way to have a patient forever than to pretend that you are treating someone for one condition but it creates another with time and plausible deniability that they weren’t related. It must be something new. Or in my favorite line from Aliens when Ellen Ripley says, “It must be something we haven’t seen before.”

  15. Patrick Jordan December 24, 2018 at 10:22 am Reply

    Hey Everybody,

    Here is an uneditorialized copy of an email that one of my top researchers sent me regarding one of our pet topics: cytochromes. I was so shocked by what I saw that it has me rethinking everything I learned or taught myself about biophysics. I will comment on the material in post right below it so that my ramblings do not interrupt the material presented. I will always empasize that just because I share information with citations it is NOT always an endorsement of content or conclusions. Cinch up your pantyhose… this is going to be rough.
    ===================================================

    https://www.pharmacytimes.com/publications/issue/2007/2007-11/2007-11-8279
    CYP1A2 Inducers
    Barbiturates
    Cruciferous vegetables
    Grilled meat
    Carbamazepine (eg, Tegretol)
    Primidone
    Rifampin (eg, Rifadin)
    Smoking

    Other drugs may stimulate CYP1A2, and they may reduce the efficacy of CYP1A2 substrates. Of particular note is cigarette smoking, which can substantially increase CYP1A2 activity.2 Thus, smoking may reduce the efficacy of any of the CYP1A2 substrates. For example, it has been known for many years that smoking substantially increases theophylline dosage requirements. More recently, smoking has been shown to reduce the serum concentrations and efficacy of the atypical antipsychotics, clozapine and olanzapine.

    CYP1A2 Inhibitors
    Artemisinin
    Atazanavir (Reyataz)
    Cimetidine (Tagamet)
    Ciprofloxacin (Cipro)
    Enoxacin
    Ethinyl Estradiol
    Fluvoxamine
    Mexiletine
    Tacrine (Cognex)
    Thiabendazole
    Zileuton (Zyflo)

    Drugs that inhibit CYP1A2 will predictably increase the plasma concentrations of the medications listed in Table 1, and in some cases adverse outcomes will occur. Of particular note is fluvoxamine, which is a potent CYP1A2 inhibitor and also inhibits other CYP450 enzymes, such as CYP2C19, CYP3A4, and to some extent CYP2C9. Thus, fluvoxamine may prevent other metabolic pathways from compensating for the CYP1A2 inhibition. The fluoroquinolone antibiotics, enoxacin and ciprofloxacin, also substantially inhibit CYP1A2.

    https://www.ncbi.nlm.nih.gov/pubmed/17214607

    Classic inducers were used as positive controls and herbal extracts were added in in vivo-relevant concentrations. Metabolites were determined by high performance liquid chromatography (HPLC). St. John’s wort and common valerian were the strongest inducing herbs. In addition to induction of CYP3A4 by St. John’s wort, common valerian and Ginkgo biloba increased the activity of CYP3A4 and 2D6 and CYP1A2 and 2D6, respectively.
    A general inhibitory potential was observed for horse chestnut, Echinacea purpurea and common sage. St. John’s wort inhibited CYP3A4 metabolism at the highest applied concentration. Horse chestnut might be a herb with high inhibition potentials in vivo and should be explored further at lower concentrations. We show for the first time that G. biloba may exert opposite and biphasic effects on CYP1A2 and CYP2D6 metabolism. Induction of CYP1A2 and inhibition of CYP2D6 were found at low concentrations; the opposite was observed at high concentrations. CYP2D6 activity, regarded generally as non-inducible, was increased by exposure to common valerian (linear to dose) and G. biloba (highest concentration). An allosteric activation is suggested. From the data obtained, G. biloba, common valerian and St. John’s wort are suggested as candidates for clinically significant CYP interactions in vivo.

    https://www.selfhacked.com/blog/cyp1a2/

    CYP1A2 metabolizes:
    Caffeine – CYP1A2 is the major caffeine-metabolizing enzyme (R).
    Hormones including melatonin, estrogens (estrone and estradiol), bilirubin, and uroporphyrinogen (R).
    Drugs such as theophylline, tacrine, clozapine, olanzapine, Tylenol (acetaminophen)(R, R), and MDMA (ecstasy) (R).
    Toxins such as aromatic heterocyclic amines, polycyclic aromatic hydrocarbons (PAHs), and aflatoxin B1 (R).

    This enzyme is activated via the aryl hydrocarbon receptor (Ahr) (R).

    CYP1A2 activity shows a remarkable degree of variation (up to 40-fold) between individuals based on their genes, ancestry, and environmental factors (e.g. smoking, coffee consumption, and diet).
    This enzyme is found mainly in the liver but has also been detected in the pancreas and lungs (R).

    It accounts for approximately 13% of total CYPs in the human liver (R).
    This enzyme is important for removing toxic chemicals from our body and processing hormones and other products of our metabolism.
    CYP1A2 activates cancer-causing agents such as aromatic heterocyclic amines, polycyclic aromatic hydrocarbons (PAHs), and aflatoxin B1 (R).

    Both increased and decreased enzyme activity have been linked to increased risk of cancer.

    Nonsmokers who are rapid CYP1A2 metabolizers (meaning they have increased CYP1A2 activity) have an increased risk of giving birth to infants with decreased birth size when consuming over 300 mg caffeine/day (R).
    These increase CYP1A2 activity:

    Cigarette smoke – dose dependently (R, R).
    Coffee consumption (R), 1.45-fold per liter of coffee drunk daily (R).
    Meat pan-fried at high temperatures – 1.4-fold (R).
    Chargrilled meat – 1.89-fold (R).
    Cruciferous vegetables, including broccoli, cabbage, brussel sprouts, and cauliflower (R, R). For example, 500g broccoli daily increases enzyme activity 1.19-fold (R).
    Diindolylmethane, found in cruciferous vegetables (R).
    Ginkgo biloba (R).
    Green and black tea (R).
    Higher BMI (R).
    Being female – 0.90-fold (R).
    Menstrual Cycle – 1.03-fold up to 1.10-fold (R).
    Insulin (R).
    Heavy exercise (R).
    Omeprazole (R).

    These decrease CYP1A2 activity:
    Curcumin (R).
    Cinnamon’s component o-methoxy cinnamaldehyde (R).
    Ginseng extract (R).
    Peppermint, chamomile, and dandelion tea (R).
    Grapefruit juice and its component naringenin (R).
    Starfruit juice (R).
    African lettuce L. taraxacifolia (R).
    Propolis (R).
    Echinacea purpurea (R).
    Licochalcone A, a major compound in traditional Chinese herbal licorice (R).
    Caffeic acid (R, R), found at a high level in thyme, sage, spearmint, Ceylon cinnamon, and star anise.
    Quercetin (R).
    Oleuropein, derived from olive oil (R).
    Kale ingestion, unlike that of other cruciferous vegetables (R).
    Apiaceous vegetables (carrots, parsnips, celery, and parsley) (R).
    Raspberry leaf (R).
    Antibiotic fluoroquinolones (R).
    Fluvoxamine (R).

    https://academic.oup.com/carcin/article/21/6/1157/2896318
    Brassica vegetables increase and apiaceous vegetables decrease cytochrome P450 1A2 activity in humans.

    Study diets
    During the four feeding periods participants consumed four different diets: a basal diet devoid of fruits and vegetables (Table I) and the basal diet supplemented with brassica (Cruciferae), allium (Liliaceae) and apiaceous (Apiaceae or Umbelliferae) vegetables. The brassica supplement comprised: 16 g (½ cup US household measure) fresh radish sprouts, 150 g (1 cup) frozen cauliflower [Food Services of America (FSA) Signature], 200 g (2 cups) frozen broccoli (FSA Signature) and 70 g (1 cup) fresh shredded cabbage. The allium supplement comprised: 10 g (3 tablespoons) fresh chopped chives, 100 g (1⅓ cups) fresh chopped leeks, 5 g (1 teaspoon) fresh minced garlic and 75 g (½ cup) fresh chopped onion. The apiaceous supplement comprised: 0.50 g (1 teaspoon) fresh dill weed, 50 g (½ cup) fresh celery, 5 g (3 tablespoons) fresh chopped parsley, 100 g (1¼ cups) fresh grated parsnips and 110 g (¾ cup) frozen carrot coins (FSA Signature).

    We have demonstrated that under controlled dietary conditions, at moderate levels of intake, brassica vegetables increased, apiaceous vegetables decreased and allium vegetables did not change CYP1A2 activity when compared with a basal, vegetable-free diet.

    Addition of selected apiaceous vegetables (namely carrots, parsnips, celery, dill and parsley) to the basal diet reduced mean CYP1A2 activity by ~13–25%.
    Certain apiaceous vegetables, including celery, parsnips and parsley, are significant sources of furanocoumarins (40), compounds which have been shown to inhibit several human P450s (41). Some Rutaceae (e.g. citrus fruits) also contain furanocoumarins and inhibition of CYP3A4 and CYP1A2 activity by grapefruit juice has been attributed in part to the presence of furanocoumarins (12,42,43). Direct supplementation of a specific furanocoumarin, 5-methoxypsoralen (1.2 mg/kg), in humans also resulted in a CYP1A2-dependent inhibition of caffeine N-demethylation (44), further supporting the inhibitory effects of this class of compounds.

  16. Patrick Jordan December 24, 2018 at 11:18 am Reply

    … and now… for the editorial portion of our show…

    The reason that cytochromes (redox isoenzymes found in several organs but also MITOCHRONDRIA) have been a focus of me and my homeys, is that oxidation/reduction transcends basic detoxification to functions like bile and hormone formation. Because I had MCS, I had focused on cytochromes for some kind of management of the condition until I learned that relentless cleaning of the liver was the key to fixing things not palliating. Being on this particular blog with the exceptional input from the posters has brought me to a point of questioning everything I thought I knew about the biophysics of detoxification as it relates to xenobiotics and substrates. The post immediately above this from Rooster (a Little Red Hen researcher) requires me to pose a series of questions, which implies that I have no answers. These questions, obviously are not rhetorical because someone (if not us) NEEDS to answer them because without those foundational concepts we will all be lost in a perpetual morass of illness with no clear way out.

    Induction of cytochromes means that there is some substance that causes them to be formed so that they can perform their fuction which would be to oxidize or reduce (remove or add an electron) to a substance so that it can be modified by conjugation in the liver to make it soluble in urine for excretion. Inhibition means that even though it has been made or circulating it is taken out of commission. THAT is where I got stumped. I was under the false impression that FQL simply bound to the CYP1A2 so that the drug could be detoxified and removed. Science is crap. It purposely uses vague or deceptive language within a practice that demands surgical precision, so now I am considering that there is an antagonist relationship with the CYP1A2 and FQL to the point where the cytochrome is NOT able to do its job in shuttling the drug out of the system. IF this is true then the mainstream medical literature that led me to the presumption that CYP1A2 got rid of FQLs was absolutely false. Somebody is lying, I’m stupid, or both.

    Therefore the material in the previous post is for archiving in your own files for future reference until we sort this out because the list of inducers vs. inhibitors is a mere curiousity until we know the mechanism of action. You can experiment with the list on yourselves at your own risk to see if they help or hurt (I did such things for 30 years) but be aware if they take you in the wrong direction it will hurt and you will need to know how to flip the switch in the other direction to get the process back on track.

    Adding to this confusion is the cult of epigenetics and the vague non-science nonsense that things like curcumin (that I use in the form of turmeric on a regular basis to feel halfway human) actually is a gene SILENCER. OK. WHICH GENES? Could it be that among any ones that it might affect that it could be our CYP1A2? one of the links above says that curcumin ‘decreases’ the activity of the cytochrome. WHAT DOES THAT MEAN? Imprecise language. Does it BIND with the cytochrome in such a way that it INHIBITS the action and/or in that binding takes it away from other substances like drugs or poisons that the body might benefit from getting them the hell out of Dodge City? Or is it that they imply wihtou saying that the gene was silenced so the cytochrome wasn’t even made? Like I said: these are SIMPLE questions that must be answered or I am at a total loss for knowing whether to take a breath or just hold it until I turn blue.

    But enough of the blah, blah science crap. Lettuce get to the stuff that people can relate to: Cigarette smoking (NICOTINE) and Coffee (Caffeine) are CYP1A2 INDUCERS!!!! So for the practical end of this: someone like Fermin said that drinking coffee is of no consequence yet Debs said that many floxies can’t handle it. What that tells us right away is that there might be a simplistic division between fast and slow Phase I detoxifiers. I can deal with this but it is not enough to give people a clear view on what to do.

    from a previous citation:
    “Clearance of theophylline and caffeine is inhibited by some of the quinolones, in approximately the rank order shown in Table 5. Given the different affinity for the cytochrome P-450 isozyme 1A-2, the fluoroquinolones vary in their relative degree of interaction with theophylline.”

    The kick in the cranium is that it MATTERS which flox you got floxed with. My false presumption was that if we simply supported the cytochrome that favored FQL detoxification then we could get an edge on getting it out of the body. This is FURTHER complicated with Fermin telling us that the FQL can form ciculating immune complexes and because it generated antibodies to itself so we are three layers deep in a biochemical problem that looks worse than an automatic transmission that a three year old has had-at with daddy’s tools.

    I know rare few people (civilians not necessarily floxies) who don’t use cancer sticks or zombie juice, so this makes me wonder if the bulk of mankind and floxies are simply hooked and suffer the consequences of the cytochrome fallout, or if they actually seek them out to modify the cytochrome response like a cat eating grass to feel better because it is sick to its stomach not because it knows the chemistry.

    There are dozens of more questions raised by the material in the previous post, but since there may be a significant connection between flox damage and lyme disease I will throw just a few more ideas out there for someone smarter than me to show us the way:

    Artemisinin that INHIBITS what I thought was going to be our flox-detox friend (the cytochrome) also has an odd habit of diminishing availablity of iron that serves a purpose of starving microbes and parasites that use iron as food as Wormwood acts as an anti-parasitic. Good stuff if you have lyme. Artemisinin can be detoxed quickly for those who are fast Phase I so it has been suggested to use grapefruit with the extract (I use whole wormwood) to increase its effectiveness. But apparently there will be floxies who could be hurt by ALL of this suppression of CYP1A2, so my entire concept of how to fight the forces of evil have been put into question.

    If you remember:
    https://res.mdpi.com/jfb/jfb-03-00361/article_deploy/jfb-03-00361.pdf?filename=&attachment=1

    Fluoroquinolones are iron chelators.

    http://www.jbc.org/content/290/36/22287.full

    “Here, we show that the FQ drugs norfloxacin, ciprofloxacin, and enrofloxacin are powerful iron chelators comparable with deferoxamine, a clinically useful iron-chelating agent.”

    I don’t even know what to do with that correlation at this point.

    Lastly (and they all sighed in relief) Caffeic acid is also a CYP1A2 inhibitor. I had no idea until today that it was found in thyme which is an ancient tapeworm remedy and Hulda Clark implicated parasites in cancer formation. Coffee enemas became popular for cancer treatment but I live only in mechanism of action so we find that caffeic acid causes apoptosis in cancer cells ONLY AS LONG AS IT IS AVAILABLE. Therefore you would have to continue with coffee enemas indefinitely unless you got rid of the SOURCE of the cancer. Thyme might be beneficial in that regard as the thymol paralyzes tapeworms (you still have to expell them). I bring all this up to emphasize that I am NOT looking for palliatives so that we can all just have a few good days by taking the edge off of SYMPTOMS. I’m talking about a stab at the heart of the Hydra so we don’t continually cut off heads that keep growing back. I would appreciate any input from floxies and their experiences with cancer. I live in a state called Continuum so I try to harmonize all factors into one continuous whole. Cheers.

  17. Patrick Jordan December 24, 2018 at 11:23 am Reply

    Me again. I thought it was EXTREMELY important to emphasize in a separate message that if you don’t understand any of the technical talk that within the chemistry of our bodies there are at least two kinds of responses so whenever you read a miracle cure by someone, then try it only to have it fail, it could be that it worked for them because of their specific physiology so it wouldn’t work for you, but doing the OPPOSITE might. Since this is FLOXIE HOPE, I just wanted to make sure that folks knew that simple biochemical principle so that they have HOPE that what worked for someone but didn’t work for them was EXPLANABLE BY SCIENCE if we simply apply mechanism of action and pay attention to individual variation. Cheers.

    • Fermin January 14, 2019 at 8:54 am Reply

      Hi Patrick

      I can afirm again that it’s an strong inmune response… I took 30 mg of prendnisone per day this weeks and i’m free symptoms… It’s a full autoinmune response prolonged in the time…

  18. Karen H. March 27, 2019 at 10:55 am Reply

    I just want to add today that I literally “got old” over night after taking Cipro. It literally “ate” my tissues and left sunken in “holes” in my muscles of my legs and arms and made my skin look like I was 80. Yes, almost overnight. I was so shocked that I kept telling people “I got old overnight”….but I didn’t connect the reason to it! Now I know. I am concerned 5 years later about my tendons acting up. I am afraid to bend them the wrong way or they feel like they will snap and break! And of course, as I said previously, I am now flat on my back with extreme pain when I stand. This all sucks, but perhaps by telling people they will stop taking these drugs and put the pharmaceutical out of business! Doctors don’t listen. Nurses don’t listen. No one listens except those who have experienced this Floxing and those near Floxie people. But I know women whose family still think its all in her head. I am worn out…..

  19. Oliver October 12, 2019 at 9:35 am Reply

    I can confirm that Cipro can lead to a CCI instability, which I was diagnosed with after pictures of an upright MRI here in Munich plus two doctors (who believe in it) are confinced that all my sympthoms are directly or indirectly related to CCI. I alos went to Regnexx in Belgium an the doctor also confirmed it plus knows about cases of Cipro causing problems in you c0 / c1 head connection. On doctor in Munich / Germaby is treating me at the minute but the outcome is open. I suffer from sleeping disorders, light and sound hypersenibility, low count in gut bacteria, paralysis, low blood pressure plus high puls etc. I should not have EDS but have got some kind of hypermobility. My herpes simplex I plús II values are much to high + EBV has got a low but to high count. Theres is defenitly a overlap of symptoms betweend CCI and CFS. If I do to much physically or menatally I will I have a full suffer phase for one day. I also got a little instability in my hip and the symptoms got worse step by step. The expert in Munich normallöy treats car crash victims very but is well aware of Ciprofloxacin causing ligament instabilities. If you can not sleep, try to sleep with a collar soft or hard plus find the ideal cussion. Avoid any noise and light at night (easier said than done). The radiologis told me that I have got brain stem contact if I move my head at night and I will defenetly wake up from this. It is like a shock to the body.
    I think that most of the symptoms of Ciprofloxacin regarding Tinnitus, sleep, depression, eye problems, balance, anxiety etc are linked to you neck as my doctor in Munich and the second doctor in the region of north east Bavaria can confirm that car crash victims have got the identical problems -> overstimulation of Sympaticus due to contact of the dens axis with the brain strem, followed by problems with yout lower deep neck muskles which are directly connected with your sympaticus. Due to the overstimulation of the sympaticus the body will have problems with digestion, taking in minerals etc. I found a second victim in North of Germany with matching sympthoms. Excuse some spelling problems, but got to finish due to overstimulation on computer screens.

    • Patrick Jordan October 12, 2019 at 12:43 pm Reply

      Hey, Everybody,
      I watch trends on the internet. This may not be news to the veterans but some recent information is coupling FQ damage with vitamin B1 deficiency. I never knew for decades that B1 requires phosphorylation for activation to a useable form, so I have been looking for pure Thiamine Pyrophosphate supplements outside of the UK. There is never any guarantee any one thing will work for any individual but the laundry list of what B1 deficiency can cause is nearly everything that Oliver wrote about.

  20. Bron November 1, 2019 at 1:56 am Reply

    Can I ask a question that may be answered in the lit. refs. but that I don’t have the stamina to read them atm…?
    Is damage done to connective tissue by fluoroquinolones permanent? If our tissues are constantly replacing themselves, would the damage done when taking fluoroquinolones be “overwritten” when the tissues are replaced while not taking fluoroquinolones?

    • Patrick Jordan November 1, 2019 at 5:02 pm Reply

      I will be curious to see what is offered. I have been working with a lot of folks with what would falsely be called Metabolic Disorders, but have been clinically been demonstrated to be mitochondrial damage at the genetic level. So, what has to be established is: Is the lack of healthy remodeling of damaged tissue due to genetic mutation? If so, then there is nothing short of gene repair that can remedy that. If it is genetic damage is it at the nuclear or mitochondrial level? One of our peeps did a search for drugs that cause mitochondrial damage. We looked at the lists: ALL OF THEM.
      So, my vote is for genetic mutation PLUS what people HAVE to be talking about during this Lyme Pandemic is Bartonella that eats connective tissue like ice cream.
      Specialize in FQ research to get the specifics and acute interventions.
      Generalize to get the big picture or nothing will be able to be repaired.

  21. Patrick Jordan November 1, 2019 at 5:05 pm Reply

    Whoopsie. And I forgot to add that I was doing serial liver cleanses every two weeks for three years before I stopped getting poisoned by my own bile. So, someone needs to come up with hard answers not on the supposed biological half-life of FQs but their ability to be sequestered and released (and not modified as metabolic intermediates) so that theoretically the same molecule could poison you ten times in ten months, be re-absorbed, therefore never excreted, and ready to play havoc again.

  22. Patrick Jordan November 3, 2019 at 7:40 pm Reply

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3816311/#R49

    anti-urease antibodies mimick connective tissue

  23. Tracy Whiteside November 3, 2019 at 9:16 pm Reply

    I have read that fog victims cannot undergo any kind of detox, that you will just flex yourself over again, I don’t think a full on detox benefits us, I’ve read that it harms us, I’m 11 years out, still horrifically injured and unable to fully function, we need to be compensated , can we collectively write and call certain senators and congressman, this is continuing to this day, 11 years of total hell, my son in laws dr just prescribed him levofloxacin, let’s get organized, WE NEED TO BE COMPENSATED.

    • Patrick Jordan November 3, 2019 at 9:40 pm Reply

      That’s the kind of thing that I wanted to get a handle on especially with the problem of connective tissue not being able to be remodeled. We can have sequestration of toxins (I’m the poster child for that) but if they get mobilized for any reason (autophagy, fat burning, etc.) then they will come out again only to do damage and then be sequestered again. Has anyone investigated the literal antidote or antagonist for FQs? If there was such a thing as detoxing after being floxed there would have to be a ‘chelator’ of sorts to get the molecule or its know metabolites out of the body. the reason why I posted the link above is because nothing happens in a vacuum so with the ‘auto-antibodies’ that can come from microbes and the fact that bartonella thinks connective tissue is tasty, that adds two more dimensions to a rather large problem.

  24. Michael November 15, 2019 at 12:00 am Reply

    From what I’ve been reading one I think it could be due to microvascular changes in the brain that are consequential to the disturbed regulation of flow and pressure in the microcirculation due to the dysautonomia brought about by FQ induced peripheral nervous system damage (including autonomic nervous system)

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