Iodine: Like T3 in Me

When I first started supplementing with iodine, I was already on a consistent dose of T4 and T3, with stable serum values for at least 6-8 weeks, confirmed with three separate lab measurements 2-3 weeks apart.  My thyroid gland was “shut off”, and I got all my hormone needs from the medication.  Everything looked good lab wise, and overall, my floxing symptoms had improved greatly.  But I was not back to 100%, and there were a number of problems I still had that were unacceptable to me.   One of them was that I still felt pretty “blah” and really didn’t have much energy.  I was on a low dose of T3 at this point in time, so I probably could have tried raising it, but I had experienced problems with that before.   So I decided to try supplementing with iodine.  Here is what I wrote in my notes about that experience:

I started 250 ug of Lugol’s iodine daily.  The first day I took it, within minutes I developed heart palps, and my peripheral neuropathy in my feet and legs and head and face really increased.  I felt “warm flushes” going through my cold feet and legs as this happened, and a number of strange wandering neuropathies.  The really odd thing was that I thought I felt better emotionally about an hour or two later – my mood improved considerably, my head seemed a little clearer.  But then I wondered if it was just “the placebo effect”. 

The second day I took another 250 ug Lugol’s.  Within an hour, I felt really good.  An hour after that, I started feeling “great”.  My legs and feet and body were warm, my head was clear, and suddenly, I felt like riding my bike.  I hadn’t ridden my bike in months, and had not done any exercise in months.  To say I was “out of shape” would be an understatement.  But I got on my bike and rode about 15 miles – at a pretty good clip too, considering.  This was definitely not a placebo effect.

The third day I took another 250 ug Lugol’s.  I was starting to feel really good.  A couple of hours after taking the iodine, I hopped on my bike and did another 12 miles – again, at a pretty good clip. 

I rode about 50 miles that week.  My peripheral neuropathy was changing, my feet and legs were warm for the first time since all this thyroid stuff had started, cardiac arrhythmias stopped, tendon and joint pain cleared, my head was clearing, my depression was lifting, my eyes actually had some moisture in them, and I actually FELT like doing stuff.  I was sold on iodine.

Yes, a 50-something, completely out of shape woman who had been essentially disabled for most of two years plus, hopped on her bike and did 50 miles in a week after starting iodine.  So of course I wanted to explore this more.  Please note that I had already been on a stable dose of TH for several months before starting the iodine, which had helped me a lot thus far in terms of reaching or getting closer to a steady state maintenance level.   But the effects of taking iodine were immediate, dramatic, and nothing less than a remarkable experience.   Even though I was already on T3 and T4, they still didn’t give me the energy that iodine seemed to, and I still had some unacceptable residual symptoms while on TH only.  I wasn’t sure what the hell iodine was doing in me.  But I was sure of one thing:  it obviously was doing something in me, and that something had nothing to do with “the thyroid gland” or “thyroid hormones”.  Eventually, this was confirmed even further with lab values as I started decreasing thyroid hormones and increasing the iodine.

What struck me the most was how similar my response to iodine was to taking T3.   My (post flox) body and cells appeared to utilize iodine as a form of energy, similar to how my body would utilize T3.   For me, taking iodine was like taking T3 symptomatically, clinically, and metabolically.  It was virtually the same, except onset of action was a lot quicker (could be within minutes) versus the 45-60 minutes it took T3 to take effect (because of the fillers in the tablets).  Half life of both was about 5 hours in me, and once the first “wave” of iodine or T3 ran out or left my cells, the “withdrawal” symptoms I experienced were the same.   When people who are taking only T4 medication start to add in T3 medication, they often have to decrease their T4 medication to adjust and prevent symptoms of hyperthyroidism.  And just like T3, it turned out that if I increased the iodine, I had to decrease the T4 medication I was taking for the same reasons.  In me, iodine = T3, except it was like “mainlining” it, rushing straight into my cells.  I was very familiar with how my body reacted to T3, as I had experienced T3-only, various ratios of synthetic T3 with T4, and T3 in Armour and Naturethroid by this time.  I knew what T3 felt like in my body, both the positives and negatives.  There were a few differences between iodine and T3, which I’ll touch on later, but for all practical purposes, in my body, T3 = Iodine (Lugol’s).

My ultimate conclusion about all of this was that iodine had to be entering my “non-thyroidal” cells and/or mitochondria directly, and that these cells and mitochondria were either 1) utilizing iodine directly for creating energy, or 2) producing endogenous localized intracellular T3 with that iodine for energy use.  “Non-thyroidal” or “Extra-thyroidal” cells means all the other cells of my body, excluding the thyroid gland cells.

When I went looking for support of this interpretation in published scientific research papers, I didn’t find much.  It became apparent that an entire generation of thyroid researchers had basically long ago decided the iodine component of thyroid hormones was not a particularly important or outstanding active participant in all the numerous functions of thyroid hormone.   As far as I could tell, this decision had basically been based on one paper written in the 1960’s which tried to delineate if it was the iodine or the tyrosine which was necessary for thyroid hormone actions.

However, I did find some support for this argument in a few scientific publications.  Unfortunately, the few abstracts I found implicating the potential for iodine to act similarly to T3 were also quite old, from the 70’s.  More recent anecdotal experiences (such as mine), were mostly coming from the “alternative community”, where people were trying large doses of iodine with varying rates of success for all kinds of problems.  But for the most part, it appeared the traditional scientific and research communities were still ignoring the potential significance of the role iodine might be playing within our bodies.  For the most part, any studies done on iodine, and its uptake, function, and metabolism is limited to its relationship with thyroid hormones and the thyroid gland and axis in general.

In general I don’t provide references within the specific sections of this document.  Instead, a list of references will be provided under the “References” menu tab.  But I will make an exception here because I understand my interpretation and conclusion of this phenomenon is going against the grain of almost all of the published research.  However, there are a few recent researchers revisiting this topic, with one of them questioning again the possibility of extra-thyroidal thyroid hormone synthesis.  This commentary by this author gives a nice summary of the topic, and provides many of the historical references in support of this hypothesis.

Ludgate, M.,  Extrathyroidal Thyroid Hormone Synthesis?, Journal of Endocrinology (2011) 210, 3–4  (Website link)

Extrathyroidal TH synthesis Ludgate 2011  (PDF downloadable link)

 

There also appears to be renewed interest in the inter-relationship between thyroid hormones and mitochondria, both genomic and non-genomic, and this includes iodine.  This next reference is an interesting and  important paper from my perspective for a number of reasons:  1) it’s recent,  2) discusses extra-thyroidal organification of iodine, including within mitochondria,  3) suggests the “Wolff-Chaikoff effect” occurs in extrathyroidal cells as well, including mitochondria,  4) provides another strong link between thyroid and mitochondria,  5) re-iterates previous study suggestions that iodine is protective against [breast] cancer (cancerous cells do not organify iodine the way normal tissue does), and  6) a number of other thought provoking ideas can be generated from this article alone.   The full paper is worth the read:

http://www.ncbi.nlm.nih.gov/pubmed/16120321   Uphadhyay, G.  Differential action of iodine on mitochondria from human tumoral- and extra-tumoral tissue in inducing the release of apoptogenic proteins.   Mitochondrion. 2002 Dec;2(3):199-210.

 

The following is another very interesting (older) paper which reached the following conclusions:  1. De-iodination of the thyroid hormone constitutes a necessary step in the realization of its effect upon the structure and function of mitochondria.  2. The active components in the molecule of the thyroid hormone, as regards its biochemical effect, are the iodine atoms. 3. The possible places of interaction between the membrane and the iodine ions (I +) are the negative charges fixed in the membrane. 4. Neutralization of the charges of the mitochondrial membrane is the major event leading to changes in its resistance, conductivity, permeability and coupling mechanisms of the oxidative phosphorylation.

Effects of Iodine upon the Structure and Function of Mitochondria

 

And this very interesting paper is worth the read for a number of reasons, only one of which is that they basically reached some similar conclusions as I did in my experiences with iodine:  “In all indices of thyroxine action examined in thyroidectomized rats, namely, growth, metabolic rate, heart rate, and pituitary, adrenal and reproductive function, the restorative or maintenance activities of large quantities of iodide were identical with those of minute quantities of thyroxine.  Effective doses of iodide presumably resulted in the formation of thyroxine in quantities equivalent to the daily injection of 0.25-0.5 ng”.

Biological Evidence for Extrathyroidal Thyroxine Formation

 

Additional related references of interest:

Peroxidase-catalysed iodotyrosine formation in dispersed cells of mouse extrathyroidal tissues.
Endocrine control of extrathyroidal peroxidases and iodide metabolism.
Role of thyroid gland on the peroxidase and iodinating enzymes of submaxillary gland.
Iodide transport & organification in extrathyroidal tissues.

 

There’s a lot more I could say about this phenomenon, but for now, there are several important points of this section to take note of:

1.   My experiences with iodine were that it was acting much like T3 would in my “non thyroidal” cells and body overall.  In me, taking iodine was equivalent to taking T3.

2.  Whenever I would take iodine while I was NOT on TH medication, I had to be aware that it would affect two populations of cells:  the thyroidal cells (which would be trying to make thyroid hormones out of that iodine), and the “extra or non-thyroidal” cells (many, and possibly all, of the other cells of my body, which were using iodine for energy and/or other processes).  Iodine was going to affect these two populations of cells differently, which had repercussions for me and how I felt symptom wise.

3.  I have Hashi’s, which is considered an “iodine organification problem” within the thyroid gland, and therefore a thyroid gland disease.  It became apparent to me, that whatever my problems with iodine were, they included more cells than just the ones in the thyroid gland.  Iodine appeared to be affecting many, if not all, of the cells of my body.  As such, Hashi’s was much more of a “systemic” disease condition within me, affecting many, if not all, of the cells of my body.  It’s well known and accepted by all factions of the medical and research community that those with Hashi’s have more symptom complaints overall, and report a lower quality of life overall.  I question if this is due to an iodine metabolism and homeostasis problem in all cells of the body, not just the thyroid gland.  As such, autoantibodies, depending on the part they may be playing in all this, may be attacking multiple cell types, not just thyroidal cells.  An example of potential antigenic targets might be peroxidases such as LPO (lactoperoxidase) and MPO (myeloperoxidase) as well as TPO (thyroid peroxidase).

4.  In general, if a normal, healthy person with a normal healthy thyroid axis takes T3 hormone medication, this will suppress the thyroid axis from making more TH.  On the other hand, if this same person ingests a normal dietary amount of iodine, in general, this will stimulate the thyroid gland to make more TH.  This is a major difference between taking T3 (the “finished product” of TH) versus taking Iodine (a major ingredient used to make the finished product TH).   Interestingly enough, it seemed like even the tiny amounts of ingested iodine from my diet would temporarily suppress my thyroid gland from making more TH — at least, until the iodine metabolized off.  This was yet another way that iodine appeared to function more like T3 in me.

5. In this section, I am suggesting that iodine itself is playing a much greater role in energy metabolism than is currently recognized. In no way am I trying to imply that the tyrosine component of thyroid hormones, or any other iodinated proteins, have less significance or are not important. To the contrary, an entire system, ie, the thyroid axis, has evolved utilizing both tyrosine and iodine together in the form of iodothyronines for innumerable functions in the body. Tyrosine itself has unique properties as well, and is absolutely crucial for many cellular reactions, including reactions that involve iodine. If most or all of the cells of our bodies are able to utilize iodine directly for energy or other purposes, my feeling right now is that this is adjunctive in nature to thyroid hormones. This might include possibilities such as an additional form of localized intracellular control, or to be used in times of temporary catastrophic failure of some part of the HPT axis. The key word here being “temporary”, because human beings and most other higher life forms were not designed to “live off iodine alone” without thyroid hormones or a working HPT axis. In my case, I could not take iodine without driving down serum thyroid hormone, and there were consequences to that, both positive and negative for me. There are many people out there experimenting with varying amounts of iodine supplementation. I would not recommend doing so unless you are carefully monitoring your HPT axis at the same time to find out how it’s affecting your thyroid hormone and antibody status.

 

 

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