Get to the Point, or . . . “I Don’t Want to Read the Whole Thing”

Note:   If you are a newly floxed person, you are probably still in shock and fear, to put it mildly, about what has happened to you, as well as being in the throes of all the physical symptoms.   This website has a lot of information in it, and for that reason alone, probably may be quite difficult to understand right now.  Just read this page and keep it in mind for the future.   The other thing I do recommend all newly or acutely floxed patients do is to get all the thyroid tests done as soon as possible.   Show this website to your physician or naturopath, or work with another flox victim familiar with the thyroid testing recommended on this site to help you.

Additionally, if you’ve never thought about your thyroid gland, haven’t ever had a thyroid problem, or are not a medical professional, this document and website may seem too complex and may not make much sense to you.  Even if you did have a thyroid problem and were on meds before being floxed, if you’ve never studied or researched much about your condition, this document may be beyond your understanding.  The best advice I can give for those of you in the above categories:   just be aware that for some – not all – but some flox victims, thyroid problems can contribute to floxing problems, and floxing problems can contribute to thyroid problems, both acutely and in longer term delayed reactions.  I believe that once a person has been floxed, they may always be at greater risk for thyroid problems.  I also believe that people with existing thyroid problems may also be at greater risk of being floxed.  So if you get nothing else out of this website, just be aware that if you’ve been floxed, at some point in time you should probably try and learn more about the thyroid overall, either on your own or with your physician, naturopath, or holistic practitioner.

I also would like to say that I am not selling anything on this website: no supplements, drugs, “the answer” , or any definitive treatments, cures, or “detox” for FQ toxicity or thyroid pathology.  There are no ads on this site, and for the most part, it’s a pretty boring format:   lots of writing.  This information was written in the spirit of “take what you want and leave the rest”.   I hope that those who choose to read through this information will find at least something useful to them in their own journeys of FQ toxicity and thyroid pathology.


OK, for those who just want to “get to the point”, here are the key points:

1.  I believe that both Tyrosine and Iodine metabolism and homeostasis were severely affected in me as a result of taking the fluoroquinolone antibiotic Ciprofloxacin.   Thyroid Hormone (TH) is nothing more than Iodine attached to Tyrosine, so in that way, anything that affects either Tyrosine or Iodine metabolism or homeostasis, will probably affect Thyroid Hormone metabolism and homeostasis as well.

2.  Post floxing, my cells appeared to utilize Iodine much as it would T3.   Post floxing, Iodine appeared to function as T3 in my cells.   Just like T3, taking too little – or too much – of iodine, gave me the same symptoms and made my floxing symptoms worse, as when I would take too little, or too much, of T3.

3.  Iodine when I was ON – and NOT on – thyroid hormone replacement medication (T4/T3):

  1. When I was taking thyroid hormone replacement medication:   if I wanted to increase my Iodine intake, I had to decrease my medication dosage, in order to avoid symptoms of “hyperthyroidism”.  This is similar to when people start taking T3, they usually need to decrease their dosage of T4, to avoid becoming too “hyperthyroid”.
  1. When I was NOT taking thyroid hormone replacement medication:   even the slightest amounts (MICROgrams) of Iodine would “shut off” my thyroid axis temporarily, as the rest of my cells in my body utilized that Iodine directly.   In other words, my thyroid gland would naturally decrease thyroid hormone production as long as Iodine was supplied.  The more Iodine I supplied, the more my thyroid gland would “shut off” (The “Wolff-Chaikoff” effect), to the point of almost being permanent.   Note that this was a natural consequence of me taking Iodine, whereas in example “3.1” above, I had to manually decrease my dose of thyroid hormone if my iodine intake increased.
  1. This will be a difficult concept to grasp unless you understand the thyroid axis and have read most of this document:   The only time that most, if not all, of my floxing/thyroid symptoms cleared up, was when serum/cellular iodine levels were high, and serum thyroid hormones (protein component of thyroid hormones) was very low.  This implied two things to me: 1) the protein component of thyroid hormones (tyrosine/carriers) was causing a problem in me (most likely autoimmune in nature, but it could have been anywhere in the chain of events of metabolism and homeostasis of tyrosine or other factors), and 2) confirmed the controversial proposal that extra-thyroidal cells of the body are capable of utilizing iodine directly for energy and/or creating intracellular T3.

4.  Because of the above mechanisms in #2 and #3.1 and #3.2 above, this created severe dietary implications and limitations for me.   Post flox, I became exquisitely sensitive to Iodine in any form, as my cells now appeared to “preferentially” utilize this iodine as it would T3 in me.   Iodine, in MICROgram amounts, is ubiquitous in most foods, and I now had to severely limit those foods in order to limit my iodine intake.

5.  For the first fifty years of my life, prior to taking the Cipro, I did not have this Iodine metabolism and/or homeostasis problem, or any known Thyroid Gland or endocrine problems.   In fact, I grew up on a rather high Iodine diet, and thrived on this.  Ultimately, I believe that my post flox body and cells desperately needed Iodine – but were unable to get it or utilize it properly due to this metabolism and homeostasis problem after being floxed.

6.  However, I do suspect that I had a predisposition to thyroid problems, genomically and phenotypically.   I suspect I had one or more subclinical or “silent” unknown thyroid autoimmune conditions prior to my first FQ exposure, which was triggered with my first FQ exposure, and then exploded into severe symptomatology with my second FQ exposure.   I strongly suspect that at least part of my acute, severe reaction to Ciprofloxacin included a “thyrotoxic” reaction.   I also believe my longer term and delayed symptoms are very “Thyroid hormone/Iodine”- related.

7.  I do NOT believe that Iodine itself is toxic to the thyroid gland or any other cells of the body (except for people who have a true iodine allergy).   However, I do believe that the floxing caused something similar to “Amiodarone Toxicity” in me in the acute phase, and Autoimmune Thyroiditis overall.   This may be due to FQ’s potentially having structural or conformational homology to thyroid hormones, thyroglobulin, or other protein components of thyroid hormone metabolism and homeostasis.   Or it may also be due to fluoride, an iodine-displacer, attached to the FQ’s, affecting iodine metabolism and homeostasis.   Attachment of a fluorine to pharmaceuticals helps with intracellular penetration, and this may be via means of iodine receptors located systemically (NIS, hSMVT).   The quinolone pharmacore, and piperazine addition along with fluoride, may damage these receptors.   Autoimmunity to any of these, as well as to the peroxidases/haloperoxidases, or any number of iodinated intermediates, may also be occurring.

8.  I believe that once a person has been floxed, they may always be at greater risk for thyroid problems.  As such, I do recommend a thorough thyroid panel, in particular the autoimmune component, be tested for in the acute phase and monitored for several years post flox.  This is true for people already on thyroid hormone medication as well (continual monitoring of the autoimmune antibodies despite being on thyroid hormone medication).  Current clinically available anti-thyroid antibody testing includes:   TPO, TgAb, TSI, TrAb, and TBII.   The TSI, TrAb, and TBII are every bit as important as the TPO and TgAb, and possibly more so during the acute phase.  It is not enough to only test TSH, T4, or maybe TPO.    I also recommend a traditional spot urine iodine test during the acute phase of FQT, as well as continual monitoring.    I highly suspect that people with low iodine status are susceptible to FQ reactions.    For those so inclined, testing for minerals during the acute phase would be a good idea; I would include Selenium, Zinc, and Copper in this testing.  Monitoring calcium, along with associated PTH (parathyroid hormone) is also very important and potentially very relevant for flox victims.   Elevated PTH can cause a host of flox symptoms, including tendon ruptures (secondary to bone breakdown at tendon insertion sites) and tooth decay and loss.   For information on comprehensive tests for flox victims, including Thyroid and Parathyroid Related Testing, also see:   Why Test? and “Dear Doctor” Letters, Testing On Your Own — When the Docs Refuse, and Comparing Your Own Lab Results Across Different Labs Or To Other Patients: Convert Your Numbers To A Percentage.

9.  If you feel you have, or developed a thyroid-related problem as a result of being floxed, learn as much as you can about the thyroid axis and how it works before initiating any supplementation or treatment.   Understand that having the autoimmune component complicates everything, and taking a thoughtful approach is prudent.   This is particularly true in the case with iodine supplementation.   Hashimoto’s Thyroiditis, is, in fact, considered to be an end stage “iodine organification” problem, and I suspect any Autoimmune Thyroid Disease, such as Grave’s, is as well.

10.   Most of this website focuses on the possible associations between Ciprofloxacin and TH/Iodine issues I developed as part of my severe FQT/FQAD reaction.   As the years went on (I’m almost on Year 7 of this ordeal), it became apparent that my thyroid problems were only a part of my bigger FQT/FQAD problems.   Consequently, I ended up exploring and researching topics under “TH/Iodine Problems Were Not The Only Issues” and “Additional Mechanisms to Consider”, which could affect TH/Iodine metabolism, but were more fundamental to a number of processes.   This was extended considerably as I learned more and researched even more mechanisms in “Additional Targets of Fluoroquinolone Antibiotics:  Examples and Research” (Part 1 and Part 2)”.   In these last links (Part 1 and 2), I provided numerous FQ-related scientific references organized by topic directly on the webpage for people to copy and paste and provide to medical professionals and others who may not understand (as I initially didn’t) just how dangerous these drugs really are.   For people researching these FQT/FQAD reactions, some of the ideas I present along with these references may be helpful in helping to elucidate or spur further ideas and mechanisms for consideration.

11.  Lastly, I’d like to bring up the concept of “promiscuous binding” of drugs such as the FQ’s.   Promiscuous binding means that the FQ’s are not only binding to their intended target of Topoisomerase enzymes in bacteria, but that they are in fact, most likely binding to other unintended targets as well, such as other enzymes, receptors, or transporters in human cells, including within our intracellular mitochondria.  FQ’s are not natural substances, finely evolved over millions of years to target only bacterial TOPO II.   In my opinion, it would be naïve to believe they are not promiscuously binding to other enzymes.    In the paper The Promiscuous Binding of Pharmaceutical Drugs and Their Transporter Mediated Uptake into Cells: What we need to know and how we can do so” author Douglas B. Kell says:   “There is abundant evidence that both drugs and proteins are highly promiscuous.   Most proteins bind to many drugs and most drugs bind to multiple proteins (on average more than six), including transporters . . . proteins and drugs are rather promiscuous with regard to their interactions with each other . . . some enzymes are comparatively specific while many are exceedingly catholic (nonspecific) with respect to their substrate choice.   Well-known examples of substrate non-specificity in the world of pharmaceutical drugs and xenobiotics include the drug-metabolising enzymes cytochromes P450 and carboxylesterase 1, influx transporters such as the organic anion and cation SLC (solute carrier) transporters, and efflux pumps such as the Multidrug And Toxin Extrusion (MATE) proteins and P-glycoprotein (and with promiscuous efflux transporters also being important in antiparasitic and bacterial antibiotic resistance and pharmacokinetics).   Many of these have exceptionally wide substrate specificities . . . While we have cited many papers and reviews showing examples of the exploitation of known BBB solute transport carriers in assisting CNS uptake, we can add a few other reviews and papers, such as ones exploiting the large amino acid transporter, the neutral/cationic amino acid transporter, the glucose transporter, the ascorbate transporter, and the organic cation , anion, choline and monocarboxylate transporters, a monoamine transporter, and a H+-amine antiporter. . . A straightforward analysis of the literature shows that it is becoming increasingly clear that individual drugs, and even intermediary metabolites, do experimentally bind to very many more entities than just the single ‘target’ via which they were typically discovered.”

Of course, if you’re a flox victim, you already know this is true, due to your own experience.   It’s quite obvious to those of us who are floxed that the FQ’s bound to and affected much more than “just the bacterial enzyme”.     Researchers and pharma know it too.  And what would be really decent is if researchers like this would spend as much time and energy figuring out the underlying mechanisms of the adverse effects of FQ antibiotics as they do towards developing and marketing any other drug, this problem, along with numerous other “chronic invisible illnesses” with similar underlying mechanisms, would  be solved.   Pharma, more than anyone, has the capability, resources, knowledge, power, and funding to learn from these adverse reactions right now (which they would actually profit from in the long run, given this is what seems to be their only motivation).  The only things they seem to lack are morals, ethics, and compassion.

But my point in quoting this paper is to show that the FQ’s are most likely affecting multiple targets within human cells and mitochondrial cells, targets such as enzymes, receptors, transporters, or signal transduction processes.   Additionally and more importantly, as a result of this binding and because of their mechanisms of action, FQ’s also have the potential to be highly mutagenic and clastogenic as well as create epigenetic changes, all of which can contribute to or cause the long term and permanent adverse effects (Topoisomerase Poisons: Harnessing the Dark Side of Enzyme Mechanism, The DNA cleavage reaction of topoisomerase II: wolf in sheep’s clothing, Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology, Non-antibiotic effects of fluoroquinolones in mammalian cells).    For those of us with some kind of susceptibility factor, most likely at the genomic /epigenomic level, possibly at the phenotypic expression level (a “subclinical” or “silent” reduced function of enzyme, receptor or transporter), there are devastating consequences for us when the FQ wipes out and trashes whatever enzymatic or receptor function is available to us.   But we are just the “canaries in the coal mine”.   FQ’s are no doubt targeting these same entities in the rest of the population as well.   Because of the genotoxic mechanism of action of these drugs, with continued use, it may very well be only a matter of time before a “toxic threshold” is reached for every individual exposed to these drugs.


Fluoroquinolone Antibiotics and Thyroid Problems: Is There A Connection?  Here is another summary of what this website is about, for people who want the “abstract” version.

Responsible Use of Fluoroquinolone Antibiotics   My recommendations for the responsible use of FQ’s.

A Public Policy Plan to Utilize the Pharmaceutical Industry and Pharmacogenomics to Reduce Serious Adverse Drug Reactions, Develop Personalized and Individualized Therapy, and Provide a Functional Map of the Human Genome   My hope and intention here is to simply provide some thought provoking ideas for change.

FQ Adverse Effects In Their Own Words from Physicians:  Medical professionals are not exempt from these reactions.  These are just a few of the stories taken from the internet.   If your physician doesn’t believe this can happen, perhaps they will believe the words of their colleagues.

FQ Adverse Effects BMJ 2015 Case Reports   Fluoroquinolone-Induced Serious, Persistent, Multisymptom Adverse Effects.   Golomb BA, et al. BMJ Case Rep 2015. doi:10.1136/bcr-2015-209821

Musculoskeletal Complications of Fluoroquinolones   2011 Mayo Clinic paper which lists the endocrine conditions of hypothyroidism, hyperparathyroidism, and diabetes mellitus as part of numerous “Potential Risk Factors” for adverse effects when taking a fluoroquinolone antibiotic.    Although this paper downplays the number, duration, and severity of these adverse effects the way they all do, this is the first paper I’m aware of that clearly states an “at risk” population who should not take this drug on Table 3, Page 136.   Usually this information is buried in obscure research papers no one, including your doctor, will ever read. (Note the at risk population includes people and related family members with autoimmune or endocrine disorders (diabetes, thyroid, parathyroid, etc.), steroid usage (ie, Prednisone, inhalers), low magnesium (how many of you know what your magnesium status is?) and “participation in a sport”(almost everyone else at some point in time in life).


In this announcement for one of the new FQs to be added to the market, Aleksandra Vlajnic, vice president of medical affairs at Bayer, is quoted as saying in a press release:   “Our data reflects Bayer’s commitment to advancing the scientific research in diseases of high unmet need, particularly pulmonary arterial hypertension and non-cystic fibrosis bronchiectasis.”    Too bad we’ll never see him (or any other Pharma exec) saying:   “Our data reflects Bayer’s commitment to advancing the scientific research in diseases of high unmet need, particularly those who suffer severe, lifelong, permanent disability called FQT/FQAD as a result of using our fluoroquinolone antibiotic products”.   Now that would be newsworthy.



Table Of Contents