In the previous sections, I said I was sensitive to iodine, and I also said that iodine was like taking T3 for me. So it’s no surprise that I am exquisitely sensitive to T3 also. Since there is no difference between T3 and Iodine for me, I am very sensitive to both of them. And taking both created like an “additive” effect in me. For example, if I took T3 AND Iodine, it was like “doubling up” on the T3 dose (or the Iodine dose). I never tested serum T4 and T3 in me before being floxed, so I don’t know what my normal values were. But post flox, I definitely was very sensitive to T3 medication, and, just like Iodine, could not handle a lot of it without developing painful, and potentially dangerous, symptoms. When I was ON thyroid hormones, which included a small dose of T3, I was very sensitive to the “T3 Wobble”. What I didn’t realize at the time, was that my dietary iodine was contributing to this sensitivity “wobble”, which may be one reason I couldn’t tolerate a higher dose of T3.
Not everyone does well with T3 blood levels being higher than T4 blood levels. I am one of those people. I simply cannot tolerate having more T3 in my blood stream than T4. If I do, I have all kinds of symptoms, ranging from unpleasant to downright debilitating, many of which are the same or similar to my floxing symptoms. This is one reason I cannot tolerate the “natural” thyroid medications, such as Armour or Naturethroid. The ratio of T3:T4 in these medications is way too high for me.
Unfortunately, there is a common misconception in some thyroid communities that “everyone” with a thyroid problem “should” have a higher T3:T4 ratio in their blood, with T3 around 75-80% of the normal ranges and T4 around 50%. This is why the “natural” medications are touted as being more effective. Unfortunately, although plenty of people do get benefit from the “natural” medications, not everyone will, and I am one of them. And one of the reasons I can’t tolerate them, is because the T3 dose, and resultant serum level, is simply too high for me, relative to the T4 dose and serum level. In my case, the highest serum ratio I could tolerate was a 50:50 serum T3:T4 ratio. And this was accomplished with a medication dosage ratio of 10% T3, 90% T4 dosing regimen* (see below), and even that dosing level of T3 was difficult for me to maintain. 7.5% T3 with 92.5% T4 actually turned out to be the most optimal medication ratio for me.
Here might be a good place to mention rT3 (Reverse T3). Reverse T3 is kind of like another form of T3, except it does not have the same biological activity that T3 does. So rT3 does not stimulate or provide your cells with energy, the way T3 does. Both T3 and rT3 are produced from T4 for the most part. A simplistic way to think about it is, if the body needs more energy, then T4 will produce more T3 and less rT3. If the body needs less energy, then T4 will produce less T3 and more rT3 . This may be why people who are chronically ill, or in starvation mode, often have what’s called “Low T3 Syndrome”, which is lower levels of serum T3 and higher levels of serum rT3. If you’re chronically ill and inactive all the time, you don’t want “the gas” (T3) on all the time, putting you in a “hypermetabolic” state. The same is true if you’re starving: your body is trying to conserve energy, not expend it. I sometimes think of rT3 as the “overflow valve”. If too much T3 is being made from T4, it will start “shunting” the reaction to making more rT3, thereby protecting the body or cells from excess T3. This is yet another homeostatic mechanism that naturally occurs in the body.
Some thyroid groups think that when serum rT3 is too high relative to T3, that’s automatically a bad thing. Google or do a search on “T3:rT3 ratio” to learn about the benefits, risks, and controversies surrounding this. I did track rT3 quite closely along with my other parameters. It was true that the higher my serum levels of T4 (and T3) went, the more and more rT3 was produced. In fact, the only time I had the “recommended T3:rT3” ratio (according to some of these groups) is when my serum levels of both T4 and T3 were very very low, around 10-20% of range. The higher my T4 and T3 levels were, the more was shunted to rT3 instead of T3.
Symptom wise, it became clear that I simply couldn’t tolerate the higher levels of serum T3 that I was often reading about on other websites. All kinds of potential reasons were given on these websites as to why this might be, and other things I needed to do to try and “force” a higher T3 level. However, one of the questions I felt had to be asked from the start was: If T4 is “shunting” more to rT3, is there a good reason for this? In other words, is this a compensatory mechanism in me, rather than a “faulty” one? As time went on, I felt confident that for myself at least, this was a compensatory mechanism. Over and over again, any time I tried to “push” the T3, I was met with making my symptoms worse, no matter what I tried. And over and over again, there seemed to be a “natural” ratio of T3:T4 for me – the 5-7.5% T3 with 95- 92.5% T4 medication dose that I mentioned before actually turned out to be the most optimal medication ratio for me. And the lower my serum TH levels were over all, the better my T3:rT3 ratio was, and the better I felt – as long as I had larger amounts of iodine on board. (If I did not have the larger amounts of iodine, then my serum levels of TH had to be higher, or else I would flare). My post flox body and cells, at least, simply couldn’t tolerate higher levels of T3. Again, I came to see this as a compensatory protective mechanism, rather than a pathologic one in my case. There are plenty of other people out there who can tolerate much higher levels of T3 than me, either medication wise or serum-level wise, and there are people who do well or resolve their problems with T3-only medication as well. But I’m not one of them – and I don’t know if this is due to the floxing issues, my own personal genetics, or both.
I haven’t discussed cortisol in this document so far, so here might be a good place to mention this as well. Low adrenal function is highly suspect under all kinds of situations, and there is a strong correlation between thyroid issues and adrenal issues. So there was the possibility that I could not handle a higher ratio of T3 due to low cortisol. I really didn’t want to take over another endocrine axis if I didn’t have to, and in particular, the adrenal one. In an effort to help rule this out, I repeated numerous tests, including both serum and urine, for free and bound cortisol, ACTH, CBG, and all three antibody markers. Just because all my lab values were “normal” doesn’t guarantee I don’t have a functional problem somewhere with cortisol, but I did the best I could to rule it out. Additionally, and maybe even more importantly, I was never an infection prone person and still wasn’t post flox, my WBC count was always in a good range, I always cleared colds well, and I had a robust “Dawn Effect” for glucose, presumably due to the cortisol peaks about 4 am. Although I never did a full trial with cortisol, I did attempt taking 5-10 mg on occasion, just to feel what would happen. Lastly, when I was on an appropriate suppressive dose of TH, I experienced a great improvement in my floxing symptoms overall, and the 6-point salivary tests I utilized the most came back looking text book perfect as well . For these reasons, I avoided doing a full physiological dose of cortisol trial, although it’s still something that’s always on my radar.
So I think it’s important to be aware that everyone has their own personal physiology, and that some of us simply can’t tolerate taking a higher dose of T3, or having a higher blood level of T3 than T4. I don’t know how much of this is due to my own personal physiology, either pre or post flox, or how much of it is due to the iodine pathology I am definitely experiencing post flox. As I’ve stated elsewhere in this document, it could very well be that I was experiencing other problems post flox, such as Myasthenia Gravis or mitochondrial damage/depletion, for example. If these were underlying problems in me, then increasing levels of T3 may have been “pushing it”, asking my muscles and mitochondria to provide more energy than they were capable of due to these other issues.
Why am I mentioning this T3 sensitivity? Well, as I’ve already made clear, it means that I couldn’t tolerate taking higher dosages of T3 medication. But another implication of this is that if for some reason my thyroid gland started spitting out more T3 – in other words, if endogenous T3 were to suddenly increase in me, I would very much feel the effects just as I would as if the T3 had come from a pill. This is important to realize in the case of thyroid hormone flares that often occur with AITD. I also suspect that such a T3 “thyrotoxicosis” was part of my March 2010 acute Cipro floxing reaction.
* For example, if 100 ug of total thyroid hormone are being taken per day, then 90 ug of that would be T4 and 10 ug would be T3, or, in the second example, 92.5 ug = T4 and 7.5 ug = T3.