Were My Problems With TH/Iodine a Primary or Secondary Problem?

I don’t know.  And I think this is an important point to recognize.

Throughout this website I am focusing on how changing levels of thyroid hormones (T3 and T4) and Iodine affected all my symptoms.  But were my thyroid problems directly due to FQ’s damaging some aspect of my thyroid axis? (ie, a primary problem).  Or was my thyroid axis, in fact, normal, and the extreme sensitivity I felt with changing levels of thyroid hormone was actually due to other factors? (ie, a secondary problem).

I think in my case, the answer is:  both.    I think I suffered from both a primary and secondary (and probably tertiary and more . . . .) problem when it came to my thyroid-related problems.  I tend to think that the Cipro did cause direct damage to my Thyroid Hormone(TH)/Iodine metabolism and homeostasis mechanism somewhere.   I feel that I have a lot of evidence for myself that this is the case.   But there’s almost no published research – only a few studies – implicating some kind of correlation of FQ’s with thyroid hormones or the thyroid axis.  Hopefully, in the future this will change.  But for now, there’s just not a lot of traditionally published data linking the two, although I believe plenty of anecdotal stories exist.

As an example of this, I think there’s a good chance I already had the autoimmune component – the antibodies – when I took the FQ, and that this contributed to my severe reaction in March 2010.  There’s no way to know for sure simply because, like most people, I was never tested for the antibodies before taking my first FQ in Jan 2009.  (I had taken Cipro twice in my life – the first time for 2.5 days in Jan 2009 and the second time for 9 days in March 2010).   I had had a few TSH screens before that, and they were in the 1-2 range.  And in fact, I didn’t test for the antibodies until about 15- 16 months post my March 2010 Cipro reaction.  So there’s always the question as to whether or not I already had the antibodies prior to any FQ exposure, or whether the 2009 Cipro literally caused, and started me on the road to antibody production.

From an autoimmune perspective, this mechanism makes sense when I think of how immediate, swift, and severe my March 2010 reaction was.  And in hindsight, I also now know there were some much milder delayed reactions, that could be thyroid related, after my first Jan 2009 exposure. I also just happened to have a TSH “wellness screen” done on Day 3 of my March 2010 Cipro reaction – this was 2 days before my actual symptoms started – and my TSH was around 3.8 or so – higher than it had ever been.  Twenty days later, after symptoms were starting to peak, my TSH was about 6.8 or so.  So something was probably going on with my thyroid.  I believe that my thyroid axis was in fact, directly and negatively affected due to the Cipro, and my TSH was responding accordingly.

Given the fact that I have all the common thyroid antibodies (TPO, TgAb, TSI, TrAb) and even my TSH has gone as high as 12 while not on thyroid hormone replacement medication post flox, I think it’s pretty safe to say that I’ve got some kind of thyroid pathology going on post flox.  And in my opinion, this pathology is now contributing greatly to my floxing symptoms, and probably contributed greatly to my severe systemic March 2010 floxing reaction as well.

However, it could also be that the fundamental primary problem was elsewhere or in addition to my thyroid pathology, such as with mitochondrial damage, or acetylcholine-related damage, or any other hormonal or neurotransmitter damage (GABA/Glutamate).   For example, in some circumstances, when I would increase Iodine or T3 by just a few micrograms, many of my floxing symptoms would dramatically worsen.  If thyroid hormone or iodine is giving a signal for increased energy demands, and my mitochondria were damaged or depleted and couldn’t meet those demands, perhaps that could be why my symptoms worsened.  In the same way, if acetylcholine-related problems were an underlying issue, such as with Myasthenia Gravis, then pushing the thyroid hormone/Iodine might have been placing energy demands on muscles that couldn’t be met due to this underlying condition.

And yet another take on this same concept is that I have Hashimoto’s Thyroiditis, which, for the most part, is considered a “thyroid” problem.   Yet the diagnosis of Hashi’s is often dependent on finding specific antibodies or “immune cells” in the blood stream or in thyroid tissues.   So even within this one diagnosis, the question can be asked:   is it a “thyroid problem” first – with an “immune system” problem that develops secondarily?   Or is it an immune system problem first, with “immune cells” going haywire, and attacking the thyroid gland proteins, thereby creating “thyroid problems” secondarily?  (No one knows the answer to that yet).

I also suspect that a receptor problem or signal transduction problem involving thyroid hormones is a real possibility in me as well.  These receptors are located throughout the body, including the brain, so the extreme sensitivity I now have to thyroid hormone could be due to that.  These receptors share homology and belong to a “super family” of steroid receptors that include many of the steroid hormones, Vitamin D, and retinoic acid (Vitamin A) as well, which could explain my sensitivity to all the other hormones as well.  “Thyro-normal” and “Endocrine-normal” people (as I used to be) can withstand variations in thyroid and steroid hormones in their blood stream without feeling the effects, as there are multiple homeostatic mechanisms in place at cellular and intracellular levels along with the HPT axis.  This is no longer the case with me.   So there’s a good chance that the floxing caused one or more other disruptions as well, exacerbating or potentially causing my “TH/Iodine metabolism and homeostasis” problem.

Thyroid hormone is intricately, intimately, and systemically related to every other system in the body, in particular with other hormones, and neurotransmitters.  Thyroid hormone is considered to be responsible for regulation of energy metabolism, and therefore interacts with mitochondria as well.  TH is needed for mitochondriogenesis, so being low on TH means being low on mitochondria.  Being low on mitochondria means available TH can’t be utilized efficiently, setting up a rather unproductive cycle for people with long term chronic illnesses.  Each of these systems affects and is affected by the other, making it difficult to sort out what’s causing what or where the underlying insults may lie.

I’m not sure what other problems I developed as a result of being floxed with Cipro.  But I am 100% certain of a few things:  Iodine, and thyroid hormones, drastically and dramatically affected all my floxing symptoms.  And life without Iodine, or the ability to utilize it effectively, is hell.

 

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