T3/T4 Flares

For people who don’t understand what a “flare” is, I’m talking about the autoimmune flares that can occur when someone has an Autoimmune Thyroid Disease (AITD) such as Hashi’s.   The thyroid gland is made up of numerous little “sacs”, kind of like little balloons, or like individual grapes in a cluster of grapes.  These little “sacs”, called follicles, contain stored T4 and T3, waiting to be secreted into the bloodstream whenever the body needs them.   Normally, extremely tiny amounts of T4 and T3 are secreted into the bloodstream in a very controlled manner.    But in an autoimmune attack, the immune cells or white blood cells (WBC’s) “attack” these follicles, rupturing them, so that they spill their contents into the bloodstream suddenly.    The longer, more frequent, or more severe these attacks are, the more follicles are ruptured, and the more thyroid hormone is dumped into the blood stream.   This sudden “TH dump” can result in the “hyperthyroid symptoms” experienced, such as increased heart rate and palpitations/arrhythmias, anxiety, sweating, chest pressure, intracranial pressure, and more.    Of course, the more follicles are destroyed, the less capable the thyroid gland is of making more thyroid hormone too – which eventually can lead to chronic hypothyroidism.   See “Thyroid Damage Due to Collagen/Connective Tissue Damage” for a more detailed description of how this could happen.

Another scenario where something similar can occur is when someone has what’s called Autonomously Functioning Nodules – nodules of functional thyroid tissue that spit out thyroid hormone whenever they want, regardless of TSH or other feedback mechanisms.    It’s similar to thyroid cancer cells running amok, which can do the same thing, except Autonomously Functioning Nodules are typically benign.  The end result is the same as with autoimmune attacks though — sudden bursts of T3 and T4 in a very uncontrolled manner.    And Grave’s disease, which causes hyperthyroidism, works by yet an entirely different mechanism, but also causes flaring with the same end result.

If it’s just one flare one time, the T3 will metabolize off within a day or so, relieving these “hyper” symptoms, and T4 effects might be felt only minimally over time because of the longer half life and the fact it’s not as metabolically active as T3.  Unfortunately, it’s rarely “just one flare”.    More often, these flares are multiple in nature, occurring anywhere from every few minutes to daily, and lasting however long they’re going to last.   This accumulation of T3 and T4 then has much more serious repercussions, both immediately due to the T3, and longer term due to the T4.  These “thyrotoxic flares” can be dangerous and life threatening if they go on often enough and long enough.  When a person ends up in the hospital with life threatening hyperthyroid symptoms, with blood levels above the normal levels for T3 and T4, this is like an “end stage” situation.   Either flares have been developing enough over time, or an acute massive consistent flare has occurred, leading to this situation. (Or, it could also be due to Grave’s disease (“typical” hyperthyroidism), where the antibodies are keeping TSH turned “ON” all the time).

On the other hand, if these flares are sporadic enough, a person may feel symptoms of being “hyper”, even while the blood levels won’t show it, because there’s not enough chronic and consistent flaring going on.    T3 levels can spike well above normal during a flare – creating symptoms such as tachycardia, arrhythmias, sweating/hot flashing, tremoring, anxiety, headache, etc. — but metabolize off back into the normal range within a day or so quite easily because of the half life of 4-6 hours.    So a person could be flaring in the morning, with symptoms, but by the afternoon, T3 has decreased enough that the blood levels won’t indicate frank hyperthyroidism. This is always something to keep in mind with T3:  because of the short half life, the blood levels can actually go up and down quite a bit during the day and night.  This is especially true in people with thyroid disorders, particularly autoimmune ones.    There are a number of things influencing T3, and blood measurements of it are very fluid (changeable) as a result.  This is one reason why traditional medical practitioners often don’t utilize T3 as part of their thyroid blood testing or screening.

There are any number of “triggers”, or “toxic insults”, that many thyroid folks believe cause these thyrotoxic flares, and this is the reason diet can play such a big role for a person with AITD.    Iodine, both in tiny and small amounts, as well as larger amounts, can cause these flares in some people as well.    I feel pretty convinced for myself that, among other things, the March 2010 Cipro caused a massive thyrotoxic flaring in me, and that a T3/T4 thyrotoxicosis was actually a part of my initial acute flox reaction.    On the other hand, I also suspect that there may have been a sudden and dramatic drop in TH overall due to the Cipro or, a sudden and dramatic drop in my cell’s abilities to utilize T4 or create T3 from T4.    In other words, there may have been a sudden and acute “wipe out” either literally or functionally, of my thyroid hormones, or thyroid hormone production, by the FQ.    How could it be both?

I don’t really know what happened, but I can speculate.    I can guess on theories, but that’s all they would be right now, just guesses.    There is no way to know what’s really happening without research.    But I actually suspect that this T3/T4 thyrotoxicosis may have partially been a compensatory response to an initial sudden and dramatic drop in TH overall due to the Cipro — FQ’s acting as functionally blocking structural analogs of T3/T4/Tg or their receptors, FQ’s promiscuously binding reversibly or irreversibly to enzymes necessary for TH/Iodine production, metabolism, or utilization, or FQ’s chelating selenium in selenoenzymes with the same result.    These are just a few examples out of probably hundreds of how a sudden and acute drastic literal or functional drop in TH could occur.    Or perhaps this thyrotoxicosis was a compensatory response to a sudden drop and “wipe-out” of something else entirely – similar to the above examples, except related to acetylcholine, glutamate, or direct targeting of mitochondria for example.   This could conceivably initiate a thyrotoxic compensatory response to make up for a deficit elsewhere.

In my particular case, I tend to think of the actual thyrotoxicosis as being an autoimmune response.    I had taken 5 pills of Cipro in January 2009, which I believe sensitized my already subclinical AITD to the FQ.    When I took Cipro again in March 2010, the autoimmune reaction was swift and dramatic:  the sensitized autoimmune cells attacked ferociously and with swiftness.    I suspect my thyroid gland “blew up” – essentially “exploded” in a thyrotoxic flare, spewing out T3, T4, Tg, Iodine, calcitonin, and everything else that’s typically found within thyroid glandular tissue into my bloodstream.    After this initial explosion, my already struggling thyroid gland simply stopped producing thyroid hormone at all, or production of it was drastically decreased (again, see “Thyroid Damage Due to Collagen/Connective Tissue Damage” for one hypothesis of how this could happen).  T3 production would continue intracellularly at the expense of T4, which would be decreasing over time, with the nadir of T4 occurring at about the 3-6 week post range.    As available T4 and T3 stores run out, there may have also been a compensatory shift to start utilizing iodine itself in a last ditch effort to keep up T3 production, which is absolutely necessary for life to continue.  In this scenario, an unproductive cycle of flaring occurs:  when the “SOS” went out about the sudden loss of TH due to the FQ, my WBC/immune cells continued to attack and got T3, T4, and Iodine the only way they knew how:    by continuing to “dive-bomb” my thyroid gland follicular cells, releasing the contents into my blood stream.   Given my peripheral cellular sensitivity to TH, which was also developing at the time as a result of the FQ (probably for the same reasons or mechanisms), this was a rather brutal, but effective response.    Brutal because even the slightest increases in TH affected me greatly, and now I was experiencing these massive “dumps” of it into my bloodstream.    Effective, because if there was a sudden and drastic total or near complete “wipe out” of my serum and/or cellular TH availability, this was a last-ditch effort to try and rectify the problem.    An overall effect of this would be normalized serum values of T4 and T4, by the way, and probably TSH too, as all these wild fluctuations were occurring.

Whenever I think of my acute reaction, I always seem to think of a huge Fourth of July firework exploding high in the sky, and then slowly trailing down, with multiple smaller explosions on the way down, before dying completely.   The explosions are the T3 and T4 elevations that occur with thyrotoxicosis, and the trails are the decreasing levels of T3 and T4 over time.    My acute floxing symptoms “peaked” about 3-6 weeks post Cipro, most likely, in my opinion, representing the half life of T4 as part of a thyrotoxic reaction as part of my flox reaction.    Delayed symptom response of much longer could occur, of course, depending on the initial health of the thyroid axis, the status of T4, and the recovery ability of the thyroid gland and axis.    Once the fireworks (major initial thyrotoxic flare) were over, this left me in a chronic state of lower serum levels of T4 overall (as my thyroid gland could not produce T4 well or fast enough due to the Hashi’s), and higher levels of T3 due to compensatory flaring.    A compensatory “shift” to utilizing iodine as T3 in my non-thyroidal cells may have occurred as well.    And if you’ve read through the previous sections, you already know that I am highly sensitive to T3 serum levels being higher than T4 serum levels.   It actually left me feeling both “hypothyroid” (due to low T4) and “hyperthyroid” (due to higher T3) – which is what contributed to the severity of my symptoms.   These speculations are based on the knowledge I gained over almost four years of learning how T4, T3, and Iodine, and the ratios of each, affected my floxing symptoms.

How do I know these were T3/T4 flares and not something else (cortisol, ACh, adenosine, other)?    I don’t, at least not with 100% certainty or any “proof”.    These “flares” could be due to any number of other hormones or neurotransmitters.    But I could make some reasonable guesses and rule outs, based on the existing available information about AITD, my diagnosis of Hashi’s/AITD, and my own experience:

  1. “Flaring” of thyroid hormones is a commonly accepted mechanism of AITD pathology in general.   Most, if not all, of the published literature talks about destruction of the follicles with release of contents in the case of Hashi’s, spontaneous excessive boluses of hormone in the case of Autonomously Function Nodules or Grave’s, or excessive hormone production due to antibodies in Grave’s overall.   This is true in both the traditional mainstream scientific and medical communities, as well as the alternative communities.
  1. Taking T3 in excess of T4 brought on many of the same symptoms and feelings as these flares did for me.   The onset of a single dose of T3 was not as immediate or dramatic as a single flare was for me, but one can presume the difference is that the flare was like an “IV injection of T3” versus the slower onset of an oral ingestion of T3 due to fillers and tablet dissolution.   These experiences and experimentation with T3, along with the accepted premise in #1 above, made me feel as though the “flares” that I was experiencing were most likely due to the T3 affects.   These T3 affects may have been due to the action of T3 directly, most likely non-genomic in origin due to their rapidity.   Or, just as importantly and plausibly, these T3 affects may have been due to secondary hormones, neurotransmitters, or other common underlying mechanisms that are directed or initiated by T3 (cholinergic, adrenergic, signal transductions).
  1. I could take bugleweed, which according to published research binds up T3/T4, and it would very effectively stop the flaring symptoms within 10-20 minutes in me.
  1. Ibuprofen would help, often within 20-40 minutes, to relieve symptoms, indicating some kind of inflammation or inflammatory attack, which presumably was the autoimmune component of my AITD.    This could have been affecting other antibodies or inflammatory processes as well I suppose (NMDA, ACh), but knowing I had the anti-thyroid autoimmune cells supported this mechanism.   Interestingly enough, I never had any elevated common inflammatory markers, such as CRP or ESR, despite my moderately high AITD antibody titer levels, even during the acute stages of my March 2010 reaction.  So the autoimmune component of inflammation, must be somewhat different than the more “common” form of inflammation represented by CRP and ESR.


As I said, there’s simply no way to really know how FQ’s affect the thyroid axis and related parameters such as antibodies, without controlled studies.    I often wished I had a sensor implanted in one of my veins or arteries, measuring a number of different variables, that I could get values off of when I was flaring and when I was not.    But I didn’t have that.    The best I could do was work with the symptoms that I knew T3, T4, and Iodine caused in me, and work backwards and forwards in interpretations from there.


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