TH/Iodine Problems Were Not The Only Issues

Over time, I also had to accept that something more, other than “only” TH/Iodine problems, was occurring in me.  There was no doubt that thyroid hormones and iodine drastically and profoundly affected all of my symptoms, capable of dramatically improving them as well as worsening them.  But whether TH/Iodine homeostasis and metabolism problems were the direct result of damage by FQ’s, versus secondary to something else or even tertiary or compensatory in nature, I can’t say.  Numerous hypotheses about an underlying, unifying mechanism of FQ damage exist, such as DNA, oxidative, mitochondrial, GABA receptor damage, etc.  Any or all of these, plus potentially millions of other targets for mechanisms of damage, could be the case, and are worthy of exploration. It’s also most likely the reason that TH medications could not resolve my symptoms 100%.

However, again, what I can say with 100% certainty is that changing levels of TH/Iodine dramatically and profoundly affected all my symptoms. And TH/Iodine is intricately, intimately, and systemically related to the normal functioning and even viability of every cell in our bodies, including mitochondria.  So it was a reasonable assumption to believe that the FQ’s did somehow negatively affect and target this system.  It also became clear over time that many other hormones I could control, such as estrogen, testosterone, progesterone, cortisol, and DHEA, as well as the minerals Selenium, Magnesium, Zinc, and even Calcium affected my symptoms as well.  I eventually branched out to include testing various amino acid supplements, and supplements targeting the ACh and glutamate systems, to see if or how they affected my symptoms.  All of these work synergistically with the thyroid axis and modulate effects of TH.

Based on symptoms alone, I narrowed down my search for potential mechanisms to 1) TH/Iodine related, 2) acetylcholine related, 3) glutamate related, and 4) mitochondrial related.

  1. Virtually all of my symptoms could be explained via some kind of TH/Iodine abnormality. I often felt like I was fluctuating between hyper and hypothyroidism. I could test oral tyrosine, iodine, T3, T4, Se, and Zn by ingesting them separately and feel how they affected my symptoms. I also could easily test a number of thyroid related serum/urine parameters on my own without a doctor, which made this an attractive set of symptoms to explore. I could test TSH, total and free T3/T4, rT3, TBG, Tg, TPO, TgAb, TSI, TrAb, Se, Zn, and Iodine on my own and see how the resultant values correlated with my symptoms and with what I was taking orally. There were many additional “thyroid related” parameters I would have loved to test for, but most of these were considered rather esoteric, were expensive, and some were used in research but not clinically yet. Consequently, I really wasn’t able to do all the testing I would have liked. But again, I could do the basic testing on my own, which gave me something to focus on.
  1. Many of my symptoms could be explained via some kind of ACh related abnormality. I often felt like I was fluctuating between a “nerve gas toxicity” and a “good shot of Atropine”. I couldn’t do the extensive testing on this system that I wanted to do. However, I could try ingesting oral supplements like choline and CDP Choline to feel if these had any affects on my symptoms, test for RBC Cholinesterase, and I could look for some clinically available antibodies such as nAChR blocking, binding and modulating antibodies, anti-Ganglionic, and Striated Muscle and MuSK antibodies. There were a number of additional antibodies I would have loved to test for, but most of these were considered rather esoteric, were expensive, and some were used in research but not clinically yet. Consequently, I really wasn’t able to do the testing I would have liked.
  1. Many of my symptoms could be explained via some kind of glutamate/GABA abnormality. I often felt like I was experiencing a huge “MSG (monosodium glutamate) toxicity” during flares. I couldn’t do the extensive testing on this system that I wanted to do. However, I could try ingesting some supplements such as glutamine, or supplements/meds that were GABA agonists to see if these had any affects on my symptoms. Again, there were a number of antibodies I would have loved to test for, but most of these were considered rather esoteric, were expensive, and some were used in research but not clinically yet. Consequently, I really wasn’t able to do the testing I would have liked.
  1. Many of my symptoms could be explained via some kind of mitochondrial damage, depletion, or genetic abnormality. Mitochondria are considered to be a natural target for FQ antibiotics, simply because of their early relationship to the bacteria the FQ’s target. Mitochondria also will utilize many of the same enzymes, transporters, proteins, amino acids and organic acids, minerals, and even steroid and thyroid hormones that other cells of the body utilize. So in this way too, they could easily be affected in the same way at the same time if any of these other mechanisms or pathways are disrupted. Testing for mitochondrial disorders is still in its infancy, and there really isn’t any affordable well-accepted definitive testing yet available that I know of. There were some mitochondrial tests I would have pursued, but most of these were considered rather esoteric, were expensive, and some were used in research but not clinically yet. Consequently, I really wasn’t able to do the testing I would have considered if I’d had the financial means to do so. However, I could try ingesting some supplements that target or are used by mitochondria to see if these had any affects on my symptoms.

 

The “thyroid related” issues were the easiest ones for me to explore on my own, and researching them and testing myself gave me something to do and focus on while I waited to heal.  As I continued my research into possible targets and mechanism of FQT damage, I remained open to all possible mechanisms.   I don’t cover a lot of these other mechanisms, as others are no doubt already doing that.  However, in the next couple of sections I’ll briefly discuss ACh, glutamate, and mitochondrial related issues because I feel they may also be playing a role in my flox reaction.   I also added discussions on the consideration of FQ’s acting as Tyrosine Kinase Inhibitors, and Collagen/Connective Tissue Inhibitors, questioning whether thyroid problems or other symptoms could possibly occur via these routes as well.   Topoisomerases are another obvious target, so I threw that under this section as well.

 

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