Update: June 2015

Update:  June 2015

Update Summary:  I started taking thyroid hormone (TH) medication again, and some of my symptoms improved again.   In particular, I no longer have vertigo, the other CNS symptoms improved substantially (but not 100%), the cardiac arrhythmias improved, the eye pain and dryness improved, and my moods stabilized considerably.   Unfortunately, it’s become apparent I have progressing neuromuscular symptoms, and the TH is not going to solve that problem.   So although taking TH again has helped me again, I’ve gone as far as I can with the TH.   At this point in time, it looks like I’ve developed permanent and progressive neuromuscular issues from being floxed.

The rest of this update goes into a little more detail about the above.   It may be hard to follow or understand if you haven’t read the rest of this website or don’t have a good understanding of some of the topics I addressed in this website.   So you may want to skip it for that reason.


Starting Thyroid Hormone Medication Again

It’s now been seven months since I started thyroid hormone (TH) replacement therapy again (started Dec 16, 2014).    As I predicted, it was a much harder transition this time.   The first time I took TH in 2011, I started improving within days, and within a couple of weeks was walking, riding my bike, and swimming again.    Looking back, it feels like it was simply a matter of starting the meds, and improvement occurred.   I really didn’t experience any fatigue or muscle weakness with the addition of TH (T4/T3 combo).   At that point in time, I would say TH was definitely a large answer to my problems, even if not the entire answer I wanted.

This time, the entire transition was an entirely different experience, fraught with difficulty.   I had been off all TH meds for about two years, and there is no doubt that I had declined quite a bit during that time.    As I slowly increased the TH dose, it became quite apparent that some type of underlying severe neuromuscular condition was now being “unmasked” and had been progressing within me.   “Pushing” the TH, meant “pushing” energy requirements in me, that couldn’t be met due to this underlying condition.   I discussed this in several places throughout this website, using Addison’s, Myasthenia Gravis, or Mitochondrial Depletion/Damage as examples.    All of these have close interrelationships with thyroid disorders, and are affected greatly by TH.   Of course, FQ’s are known to have neuromuscular blocking activity, and there could be any number of mechanisms for that as well.  Because these neuromuscular mechanisms are unknown, there is no biomarker or definitive diagnosis available yet.

I took about 4-6 weeks to increase my TH dose slowly up to full replacement dose.   It was indeed, a “rough ride up”.    During that time, I was constantly walking the “tightrope” of trying not to get “too high” or “too low”, as I discuss here in “It Felt Like a Homeostasis Problem”.    “Too low” was easy for me – avoiding vertigo and some of the more severe CNS symptoms, including the severe depression and mood swings that are part of those symptoms – made sure I kept going, and slowly increasing my dose.   “Too high” became a constant struggle, because I was walking such a fine line on the “homeostasis tightrope”.    A few micrograms ahead of myself, and all the symptoms I wrote about in “How My Flox Symptoms Were Affected By TH and Iodine” worsened.   In particular, the neuromuscular symptoms and severe weakness were now coming to the forefront.   In addition, I developed neurological symptoms that were newer versions of my other ones, or more severe in nature.     During these times, I either waited it out and adjusted my dose accordingly, or, on a very few occasions, took a small dose of supplement titrated to effect when desperate.   If I hadn’t known what to expect, and been so familiar with my symptoms at that point in time, I don’t know that I would have kept going.   It’s not a journey for the faint of heart.

Since starting on TH, I’ve only experienced one more major “flare”, presumably hormonal in nature, on Jan 20, 2015.   This was only about 4 weeks into slowly raising the medication, so my thyroid axis was not yet fully “shut off”.   I went back through my notes and found this description here.   The “substance” I am talking about is presumably a hormonal dump, which felt like someone literally injecting an IV bolus into me, and I could literally feel it coursing through my veins:

HORRIBLE flare at about 4:30-5:00 am – basically, it was the “dying” feeling, except a little different because of the T4 on board.  Woke up DRENCHED in sweat, breathing hard, tachycardic and pounding heart, SEVERE thymus/LN/chest pain, was groaning – could feel the “substance” flowing through my veins, literally traversing down into my feet and legs, which developed severe burning and cold feeling, increasing with each pulse/flare, thighs felt like “menthol legs” as when acutely floxed again, horrifically cold, nausea and chills, whole body became neurologic with “electric fence” feeling.  Really thought this was it again, figured I was going to die; hard to feel like this isn’t a heart attack occurring or the agonal throes of death.  Unfortunately, I didn’t die – I laid there feeling several “waves” of this flare before it finally stopped; I guess going through it once wasn’t enough. 

Unbelievably, I was then able to get to sleep again, but felt terrible when I woke up – out of it, with “hyperhead” CNS symptoms, hard to breathe, the diaphragm muscles feel weak (as in when I get too much T4/T3/iodine), leg muscles weak as in the aftermath of too much T3/iodine, bloated and like digestion has stopped, feeling very full as a result of that; salivary glands or LN hurt and thyroid feels swollen and painful, jaw muscles severely painful with shooting neuro pains, tendons hurt.  Chest pain really prominent, presumably thymus, possibly perihilar lymph nodes.  The weakness is so severe in this aftermath that I cannot walk more than a few steps, I tremble and shake when attempting to stand, and even holding my head up is hard.  My eyes are painful and bone dry again until the T3 wears off.

The “substance” could be any number of things, which is why I describe it that way, but I do discuss throughout this website why TH is at the top of my list and why I believe this was probably a T4/T3 dump.   Other considerations could be a catecholamine dump (pheochromocytoma, which I tested negative for / paraganglioma), a ‘mild’ form of serotonin syndrome (tryptophan, serotonin and/or MAO metabolism problem; Carcinoid Syndrome), Mast Cell Activation/Cytokine Storm (hypersensitivity/immune responses), or very possibly a cholinergic crisis (some kind of ACh dump or accumulation.  I’m also going to throw Acute Intermittent Porphyria on the list, as TPO function, and iodine metabolism, is obviously questionable in me; CYP P450’s and some mitochondrial cytochromes are also hemoproteins, as well as TDO/IDO in tryptophan metabolism [note relationship of TDO/IDO to serotonin]).    Given the close relationship between TH and all of these, I suppose a TH flare could cause a flare of any of these or vice versa.   TH was within my control, whereas the other substances were not, and gaining control of TH does seem to help.   Since then I have not experienced these flares again, presumably because my TH axis is shut off, and the gland has atrophied/follicular contents emptied.   But they were a regular occurrence before I developed some kind of interpretation as to what was going on in me and before I was on TH.   Both times I was on TH these flares stopped, as long as I was on a full replacement dose of TH and kept the gland shut off.


Approaching Steady State Status with TH

It takes a long time for TH to reach “steady state” status; in general, about 6 months minimum.  I thought it might take even longer in me, but despite my other issues, I entered a somewhat quiet period after about Month 4, with slow, but steady improvement.   Please note that the key word here is “improvement”; none of the symptoms went away entirely, but they did improve and become much more tolerable.  The vertigo never returned, there was considerable improvement in the CNS symptoms, the eye pain and dryness improved a lot, and my moods stabilized greatly.   The thyroid axis shut off, flaring stopped, and the gland stopped swelling and being painful, so at least that area of my neck was pain free.   As long as I kept to the same schedule, eating the same foods, taking the same supplements, moving the same amount, never varying my routine, I could feel – well – not “good” compared to my pre-flox state – but certainly good in comparison to what I’d just been through.   So even though I was constantly walking that tightrope, it was a huge relief, and gave me a much needed break.   I didn’t feel like I was dying anymore, which had been an ongoing feeling for most of the time I was not on TH.   I didn’t try to exercise or do anything to cause a change in energy status; I just needed the break.

One of the things that may have helped my improvement was that I stopped taking any magnesium supplementation around the four month mark.   Toward the latter years, as my symptoms continued to progress, I could feel that magnesium would often make me feel worse, in particular, with weakness (And for anyone wondering, that’s all forms of magnesium, because whatever form I took, had a common component in it – magnesium).   I had been taking 250 mg twice a day, and sometimes more, since being floxed.   Once I started on TH again in Dec 2014, this negative effect of magnesium became increasingly clear, and I dropped down to 250 mg per day.   Somewhere around Month Four I stopped it altogether.   I then entered my “quiet period” where I continued to slowly improve.   As long as I walked my “tightrope” I could almost feel normal at times.   Until I decided to try magnesium again.


Magnesium Unmasked the Neuromuscular Problem

I took one 250 mg tablet, the same one I’d taken for the past five years, and it had a pretty immediate and dramatic effect.   The only way to describe it is that it felt like it literally “knocked the TH off the receptors”.   In other words, it felt like suddenly my “TH homeostasis” was gone.   For a few hours, for the first time in 6 months, I felt like I could develop vertigo again.   It also increased my weakness greatly – in particular, of the diaphragm, which made taking a full breath hard, and my thigh muscles.   I didn’t take any more, and recovered over the next week.   After another week, I decided to try magnesium again, but at a much lower dose.   The idea being here, that my “magnesium receptors”, or any enzymes depending on magnesium, would have to slowly upregulate or downregulate (depending on what was being affected).   Since “It’s a Homeostasis Problem” for me, perhaps I simply needed to go slower.

I started on about 20 mg twice a day.   The first few days were rough, with severe headaches, increased peripheral neuropathy, increased muscle cramps in calves, increased eye dryness, increased muscle twitching, increased eye pain, increased insomnia, and return of the laryngopharangeal pain and burning tongue and esophagus (which had developed during my Kombu experience, here).   The next few days most all these symptoms improved and actually went away for the most part, except for the muscle weakness, which continued to get worse.   The muscle weakness was also accompanied with severe “burning” in my thigh muscles and legs, and they also became “cold from the inside”.   This severe burning reminds me of when I hear of flox victims who develop this burning right away with IV’s of FQs, or who develop it over time, saying it feels like “acid in the veins” – a good description.   My CNS/head symptoms, however, improved even more, so I felt better about that.   I thought I could maybe work through the muscle weakness and burning, but by the end of the week, I couldn’t take it anymore.   The burning was severely painful, and the weakness was getting to the point I could no longer get up and walk.   I also had to be concerned with increasing diaphragmatic muscle weakness, and fear of going into some kind of Myasthenia-like crisis.   The very base of my tongue felt painful and “thick”, making swallowing difficult again.   My TH metabolism was changing in response to this newfound little bit of Mg as well, creating additional familiar symptoms, and I could tell I was going to have to make dosage adjustments if I continued with the Mg.    I couldn’t take the symptoms, and stopped the Mg after a week.   I felt very disappointed about this, because after the first few days, it did feel like magnesium was really helping in an overall way to make me feel better, and if it hadn’t been for the severe muscle weakness and burning, I certainly would have continued.  That was three weeks ago, and once I fell off that tightrope, I fell hard.   I haven’t recovered yet, and am still trying to regain the homeostasis I worked so hard for since starting TH again.   It took about a week for the severe burning to dissipate, but the severe muscle weakness remains.   I’m really not able to walk more than a few steps as a result, and any stress on the muscles makes the burning return again.  And all because of 20 mg Mg twice a day for one week.


Acetylcholine (ACh) Transmission Problems

This experience highlighted a few things for me.   Calcium made me feel better, while Magnesium made me feel worse.   Ca stimulates ACh release, while Mg inhibits pre-synaptic ACh release.   Magnesium is contraindicated for people with Myasthenia Gravis for this reason.   I had long suspected acetylcholine-related pathology and possible Myasthenia Gravis-like symptoms in me, and in my mind, this experience helped confirm that.   I have tested negative for most of the Myasthenia antibodies (see here); however, as with all autoimmune conditions, plenty of people who have been diagnosed with Myasthenia Gravis don’t have the antibodies.   There are also additional neurological antibodies available that I was unable to test, so perhaps those would have turned up positive.   Additionally, I originally thought of my symptoms as more muscarinic in nature, and there are no good tests for that; at this point in time, nicotinic symptoms appear to be progressing as well, so perhaps I might develop diagnostic antibodies over time.   On the other hand, I have no doubt that the FQ’s can cause a novel type of neuromuscular disorder, and there simply is no biomarker for it yet (which works out very well for Pharma, actually).    As just one example,  from an FQ-Induced collagen/connective tissue damage point of view, appropriate collagen formation is also very necessary for AChE function and ACh transmission, and lack of it can result in Myasthenia Gravis like symptoms, as these COL Q studies confirm: 1, 2, 3, 4  (and suppression of collagen prolylhydroxylation as in this FQ study here can affect COL Q; also scroll to “collagenous domains as substrates”, AChE, in this “Prolyl 4-hydroxylase” paper here).    To see an example of how Mg is used for its muscle relaxant and anti-convulsant properties, and potential side effects to watch for, see here.   Search on “Magnesium + Acetylcholine” or “Magnesium + Myasthenia Gravis” to see further information.   Also do a search on “Magnesium + NMDA receptor” to see its action here and how that may potentially be playing into flox symptoms.

I discuss in several places in this website why I suspected Myasthenia Gravis, or some type of variant of it, as part of my floxing syndrome.   For starters, there is a Black Box Warning stating that “FQ’s have neuromuscular blocking activity”, and are contraindicated for people with known Myasthenia as a result.   FDA is literally giving us a big clue as to mechanism of action here.   I developed weakness and neuromuscular symptoms right from the start, although these improved over time and with TH the first time I took it.   Myasthenia is associated with thyroid disorders, AITD and Graves in particular.   Symptom wise, once my thyroid gland started swelling and becoming painful, my “chest pain” – which I interpreted as “thymus pain” – literally waxed and waned in intensity right along with my thyroid gland.   It was this repeated and predictable correlation that made me suspect this “chest pain” was really thymus gland hyperplasia waxing and waning, and research articles helped to support this suspicion.   Taking iodine, TH, and estrogen/testosterone all seemed to worsen this thymus gland pain and presumed swelling of the thymus along with my thyroid gland.   “Hyperthyroidism” can cause hyperplasia of the thymus gland cells, and iodine, TH and sex hormones all produced “hyper” signs in me as part of my dosage symptoms as well as longer term symptoms if I got too “high” overall.    Interestingly enough, I know of at least one flox case where TH replacement therapy was started, “chest pain” subsequently developed, and a benign thymic mass was found and then surgically removed.   The thymus gland is heavily involved in developing central immune tolerance, and I had all the antibodies for autoimmune thyroid disease, which again, is closely associated with myasthenia in some people.   The pain along my jaw, down my neck, and across my collar bones, I came to believe were painful lymph nodes, as the pain essentially followed the road map of lymph nodes in this area.   I could also palpate the painful lymph nodes under my jaw line, although there was never any obvious swelling.   I believe the perihilar lymph nodes were also affected, along with the thymus gland, leading to that dry, burning feeling in my central chest along with the pain.    This “lymph node” pain was substantial at times, despite the lack of swelling, and also waxed and waned with my thyroid gland and “thymus” gland pain.   The location of these affected lymph nodes literally surround the thyroid and thymus glands, further indicating that both my thyroid gland and thymus gland were now highly antigenic.   Research also shows how FQ’s damage immune cells themselves; this may be another consideration for the initiation of these autoimmune processes that developed in me and the problems with my thymus gland.   Lastly, this latest “neuromuscular crisis” developed after only one variable was changed:  I started taking magnesium again.  Case studies exist confirming myasthenia crises developing after taking magnesium due to the acetylcholine blocking effects of magnesium.   I believe this happened in me, albeit with a much lower dose of magnesium than would occur with most people.   My symptoms were basically severe muscle weakness of the thighs and legs, weakness of the diaphragm making breathing difficult, and pain and weakness at the very base of my tongue and what felt like my upper esophagus, accounting for the swallowing difficulties.   My eyes, as ever, waxed and waned with pain, drooping, and double vision as well.   My heart muscle was unaffected in terms of “weakness”, although plenty of compensatory pounding and tachycardia is occurring with any movement or energy requests of skeletal muscles.   A trial of cortisol ruled out Addison’s.   And my “Kombu” experience took on yet another meaning as it turns out Kombu is very high in Mg as well as Iodine and glutamic acid, so I might have gotten a triple whammy there.    All the above confirms for me, to my own satisfaction, that the FQ’s damaged my acetylcholine-related system, as well as my thyroid system.   References supporting the relationship between Myasthenia Gravis, Thyroid Disorders, and FQ’s are scattered throughout the PDF’s I provide in the “References” section.   This includes some of the following references showing the links between TG and AChE here:  1, 2, 3, 4 for starters.

Acetylcholinesterase inhibitors (AChEi’s)are one standard treatment for Myasthenia Gravis.   In my case, a trial of AChEi might help differentiate between true Myasthenia (ACh transmission blockage) versus a cholinergic crisis (ACh receptor tolerance and “weariness”).    Cholinergic crisis is a greater threat to myasthenics with especially weak pharyngeal and respiratory muscles, and to severe cases with a fluctuating course.   So it’s a pretty serious consideration for a trial or treatment of myasthenia, and nothing to casually fool around with.    I often felt that many of my symptoms and acute flox reaction could be described as “cholinergic/anti-cholinergic” in nature , as if I were fluctuating between a “nerve gas toxicity” and a “good shot of atropine”.    These shifts could occur pretty rapidly, within minutes sometimes, as well as over much longer cycles (like months).    For these ‘fast switches”, it literally felt like “on/off’ switches were occurring, or sometimes I pictured potential antibodies acting like ‘ball valves’ in receptors, popping on and off.     So I do have a fear that taking an AChEi could “flip that switch”, with one mechanism being possibly due to post-synaptic ACh receptor problems.   Additionally, I feel that whatever is going on with me is very much of a ‘homeostasis’ issue in general, which is why taking any medication or supplement is fraught with difficulty all around.     In “Thyrotoxicosis and ‘Iodine Toxicosis’” I discuss how my severe acute flox reaction could have included a thyrotoxic reaction, followed by a longer term residual shift to hypothyroidism 6-12 months later.    In the same way, I question if my acute flox reaction also included an initial cholinergic crisis, with acute ACh receptor bombardment and non-responsiveness, transitioning to more of a myasthenia-like syndrome (ACh transmission loss) 6-12 months later.   There could easily be an interplay between these two as well, ie, TH issues exacerbating ACh issues and vice versa.   Based on my own experiences, I question if iodine itself is necessary for adequate ACh-related mechanisms to function.

There is a lot of information on the internet, including YouTube, about ACh synthesis, transmission, and metabolism which demonstrate the various places ACh-related problems could arise, as well as pharmacological drugs and supplements attempting to target specific areas.   Also see “Organophosphate Poisoning” to see the similarities between many of my cholinergic symptoms, those of other flox victims, and those of OP Toxicity — note discussions on Gulf War Syndrome, OPIDP, the delayed effects of COPIND without cholinergic symptoms, the wide range in variability of enzyme levels determine the sensitivity of humans to various OPs, and how OP residues on fruits and vegetables, and other examples of OP exposure from the environment, can act as triggers or contribute to causation in susceptible individuals.    Any movement at all, or any energy expenditure at all, will involve ACh, so if something is damaged in this system, the effects would be significant.    The neuropsych ramifications of ACh are substantial as well.    Even something as simple as the smell and taste of food can cause the vagus nerve to release ACh, which binds to receptors on parietal cells, causing an influx of calcium ions, and from there, a few more reactions results in producing hydrochloric acid required for the digestion of food in the stomach.   In fact, it was my immediate reaction to many foods (within seconds or minutes), long before digestion even occurred, that was one of my first clues to think that perhaps ACh was involved in the first place.

OPT can be acute or delayed, have a waxing and waning nature, a long recovery if at all, and severe neuropathy without obvious nerve damage on punch biopsies, for example.   Post synaptic ACh damage or “fatigue” could easily explain why there is only a certain amount of tolerance to anything from exercise to exposure of small amounts of OP’s (and possibly FQ’s) on food or in the environment.    This might include re-exposure to FQ’s for susceptible people or those who have been damaged “subclinically” previously by FQ’s.   FDA states that FQ’s have neuromuscular blocking activity, but don’t define how that happens (ie, blocking ACh transmission versus ACh post synaptic ‘shut down’ due to cholinergic overstimulation).   OPT might be a possible model of FQT.   If this were the case, relapses that occur long term or over time would not be because FQ residues remain in the body, but more because of an ACh transmission problem somewhere, for example, with post synaptic ACh receptors that have a limited tolerance for ACh.   Once this threshold is exceeded (which could occur with simple exercise, for example), symptoms similar to a cholinergic crisis could result again.


Minerals and Trace Minerals

Another pattern was beginning to develop when it became apparent that I was very sensitive to Iodine, Selenium, Magnesium, Calcium, Iron, and Potassium.   My sensitivity to Iodine, and the symptoms it caused, are discussed throughout this website.   I didn’t spend a lot of time writing about my experiences with Selenium, but it became apparent that I was as sensitive to Selenium as I was to Iodine, and that many of my responses were similar (like a stronger, but shorter duration type of response – and selenium is important for iodine metabolism).   I’ve discussed how Magnesium made me feel worse in this section, and how I felt much better once I increased my Calcium (Ca is needed for ACh release, and may act as a regulator of ACh receptor synthesis).    Iron made me feel better.   And once I took a 2 mEq potassium tablet, equivalent to about 80 mg potassium that might be found in 1/5 of a banana, and literally instantaneously dropped to the floor almost passed out (Hyperkalemic Periodic Paralysis is on the differential list).   The pattern here is FQ’s affecting minerals and trace minerals, which I discuss a little bit here (Additional Mechanisms), and certainly there is plenty of research to support this.   I question whether the FQ’s are damaging homeostasis of minerals and trace minerals by any number of mechanisms; for example, if receptors or transporters for these are damaged directly in somatic cells or mitochondria, cellular or mitochondrial membranes are damaged, genomic damage/mutations for these occurs, or if allergenic or autoimmune responses could develop to metal cofactors, alone or in specific proteins.


“Can’t Live Without It; Can’t Live With It Now Either”

One of the things I found out for myself was that I could no longer metabolize iodine properly, and that was something that appeared to acutely and dramatically change due to the FQ’s.    With iodine, it became apparent I was caught between a rock and hard place, which I describe in various places in this website and in “Iodine: Can’t Live Without It; Can’t Live With It Now Either”.   Now, it appears I am in that same situation with Magnesium.   And that’s a problem.   A BIG ONE.   I know I am not taking in even the minimum RDA of about 320 mg Magnesium through my diet.    Adding in 20 mg twice a day, for a total of 40 mg magnesium per day, for one week, put me in another “Myasthenia-like” crisis, and just about did me in.    Magnesium homeostasis and metabolism is absolutely necessary for life, every bit as important as iodine or more so.   At this point in time, it looks like I will have to severely limit my Magnesium intake in order to limit the neuromuscular blockage that occurs in me with it.   Yet, limiting Magnesium brings on all kinds of other problems, and eventually, I will simply get too low on Mg stores as well.   For all I know, the same is occurring with any number of other minerals and trace minerals necessary for life in me.


Be Careful With Magnesium and Iodine

I think my problems with Iodine are substantial, and are contributing to my much lower quality of life.   This is because I don’t think my problem with Iodine is “just a thyroid gland problem”, but in fact, is a systemic problem with extrathyroidal cellular metabolism of iodine.   Now, I’ve got a systemic problem utilizing magnesium too.   I think my case is a good example of how both magnesium and iodine can affect individual flox victims differently.   In my case, iodine shut off my TH production, leading to hypothyroidism.   In my case, Mg probably blocked much needed ACh transmission, leading to severe muscle weakness.   Both of these are well known phenomena within the research and medical communities, substantiated by research, and experienced by other patients, so although it may be rare, it’s not like I’m the only case.   Magnesium has taken on almost mythical proportions within the flox community, with some people recommending magnesium for everyone, the more the better.   The same is true with iodine within some factions of the thyroid community.   Both iodine and magnesium are incredibly important for survival and quality of life, and under normal circumstances, for people who metabolize and utilize these normally, “the more the better” probably applies.   But if you have a thyroid problem (in particular AITD) – or a neuromuscular condition (in particular MG/ACh-related) –or have been floxed – I think a thoughtful approach to using iodine, magnesium, or any supplement is warranted.   Regarding Mg, and based on the knowledge I have so far, if I had to take a guess, I would think that flox victims with too much neurological excitation could probably benefit from Mg, whereas someone like myself, with severe weakness and leaning more towards Myasthenia/decreased ACh production, Mg could make things worse.   For example, for people with an unknown underlying ACh transmission problem, the combination of two neuromuscular blocking agents – FQ’s + Magnesium – could be a double whammy in the acute phase, leading to extreme weakness.   I also wouldn’t be surprised if there’s a fluctuation going on between these two states over time, with differences in the acute phase vs. longer term.   Myasthenia, as with Grave’s Disease and many other autoimmune conditions, can wax and wane, and flare and dissipate over time by themselves, much like flox reactions.     When I took TH (T4/T3 combo) the first time, it helped me immensely, and I didn’t really experience signs of skeletal muscle weakness, except under extreme duress of T3-only dosing.   However, that severe weakness, that “funny weird kind of fatigue” was my very first symptom on Day 5 of my March 2010 reaction, and I now question whether that was the FQ’s blocking my ACh hard, which over time, I appeared to recover from.    I think careful experimentation, along with appropriate testing, could probably help each person determine what their sensitivities are, if any, to iodine and magnesium.   Using iodine and magnesium in this way might help determine if you’ve got a thyroid or ACh related problem as well.


Thyroid and ACh Are Probably Not The Only Issues

Is there a possibility that my neuromuscular problems could be due to something other than ACh-related or MG-related conditions?   Yes, of course.   I’d say it’s highly probable right now.   I don’t believe I have “just” a thyroid problem, or even “just” a “Myasthenia Gravis” problem.   I think the FQ’s did multiple damage in me, which is making itself evident over time.   If the FQ targeted my own topoisomerases, leading to direct DNA damage and preventing repair of that damage, this alone can account for the severity, long term progression, and permanence of my particular reaction.   Mitochondria can be affected by innumerable extra-mitochondrial mechanisms of damage, as well as be directly damaged by FQ’s.    And mitochondria, normally present in large numbers in nerve endings, synthesize a precursor to ACh, so along with all the other issues that can occur with damaged or depleted mitochondria, this would be one more.    The sad fact is, no one really knows exactly what the mechanism(s) of FQ-induced damage are, and until or unless that happens, there could be innumerable suspected known and unknown targets.   At this point in time, anything that increases energy production in me – such as TH, cortisol, iodine, Mg, CoQ10, D-ribose, and other supplements I’ve tried, now make my symptoms worse.   Exercise does the same, as this obviously increases energy requirements and energy production by all sorts of proteins.  This worsening of symptoms could be due to mitochondrial damage or depletion issues, or ACh-related issues, or any other common pathway mechanism, which means my cells and mitochondria can’t respond to these increased energy “pushes”.   Unfortunately, I think ALS is on the list as well, another condition the FDA has acknowledged, or some other neurodegenerative condition.   I would really like to test for mitochondrial disorders, but I was denied mitochondrial DNA and associated nuclear DNA testing by my insurance company, so it’s looking unlikely I’ll be able to test for that any time soon.

Looking back, if I had been appropriately diagnosed with the thyroid problems, and started and stayed on the thyroid meds . . .would I be OK today?   Would it have made any difference in where I am now?    Would dealing with the thyroid problem have prevented further progression?   Or was my progression inevitable?   I don’t know the answer to that.   No one does.   I only know the route I took.   I do believe now that had I gotten and stayed on TH early on, I would have stabilized the TH component of all this for myself, and probably lived a much better quality of life in the past five years.    Stabilizing the TH axis, in particular antibody production, may have prevented the attempted compensatory responses and cascading effects of interrelated systems, which ultimately may have created more damage in the long run without that TH correction.    AITD itself seems to be a part of or a precursor or post diagnosis to so many other autoimmune as well as “chronic invisible illness” conditions.   And I do know that some flox victims have gotten on TH +/- cortisol and basically recovered without relapses.   So that’s a possibility.   But I know it’s also a possibility that TH hormone might have helped for a while, but only delayed the inevitable.   Plenty of people experience “flox relapses” over time, which appears to substantiate this.    Unfortunately, FQ’s can damage some pretty important cellular and enzymatic processes, which can progress over time.

One thing I am quite certain of, is that not treating the TH issues only made my symptoms worse.   I was not going to recover by not doing anything, and simply “waiting to recover”.   Both times I was off TH I was miserable, and declining rapidly.  The first time, TH gave me back some quality of life, and had I remained on it, perhaps that would have been the extent of my “recovery”, for better or worse.   The second time, TH also improved some pretty major symptoms I could not live with, although it will definitely not solve some other major problems I now have.   It’s not for me to say whether other people should try TH or not, because each person’s TH status is different.   If anything is to be learned from this website, it’s how complicated TH issues really can be.  But I hope that some of the information in this website can be useful none the less, whether for patients, doctors, or researchers.