Update: September 2015


Update:  September 2015

Update Summary:    Despite my “magnesium setback” (see the last update), I continue to improve in many areas at what I call “glacial speed”, meaning:   very, very slowly, sometimes almost imperceptibly, in a “millimeter by millimeter” fashion.   Thyroid hormone and Iodine continue to be major players in my symptoms.    Controlling the amount of both TH and Iodine is giving me some amount of control over these symptoms.   I continue to have extreme leg weakness, and for the most part, can only walk in my house as a result.   Most other symptoms are slowly improving.  I experimented with Acetylcholine-affecting substances, with some success as well as some setbacks.

Here, I throw together progress notes and other musings.    As with the previous updates, the rest of this update goes into more detail about the above (so once again, it’s long).   It may be hard to follow or understand if you haven’t read the rest of this website or don’t have a good understanding of some of the topics I addressed in this website.   So you may want to skip it for that reason.   I also repeat myself a lot here; much of what is written here has been covered in other sections.    But for those interested in the details, I think it always helps to have the information written in several different contexts and perspectives.


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

Were My Problems With TH/Iodine a Primary or Secondary Problem?  I asked this question on that webpage.    And I still don’t know the answer to that.

Since starting thyroid hormones again, I’ve mentioned several times in several places that “pushing” the thyroid hormones make my symptoms worse.    I’ve suggested that this is due to potential underlying problems that I probably now have, such as a Myasthenia Gravis type syndrome (ACh transmission problems), Mitochondrial Damage or Depletion (mitochondrial toxicity), Addison’s Disease (cortisol problems), or some other FQ-Induced damage (a billion other possibilities).   If this is the case, then my thyroid hormone limitations, in particularly with T3, could be considered adaptive and compensatory in nature, and not necessarily pathological.   In other words, because I’ve got some other major illness process going on, my energy requirements by my cells are much lower, and my body naturally is trying to keep T3 low so as not to “overload” my cells with “hyper” amounts of these hormones.   This is a protective response, and I think it’s important for people to be aware this protective response exists and how and why it works.   Trying to push T3 and “high energy” into cells that can’t respond is like flooring the gas accelerator while keeping the car in park:    you’re not only not going anywhere, but it’s dangerous.   There is a name for this response, which is called Nonthyroidal Illness Syndrome.    In this case, one could argue that my thyroid axis was working properly then, by keeping the amounts of both T4 and T3 low, and rT3 high, when I was NOT taking thyroid hormones.   In this case, my “thyroid problems” would not be primary in nature, and wouldn’t even reflect a true thyroid pathology.   Instead, my thyroid axis would be acting appropriately to a primary insult elsewhere caused by the FQ’s.    Now that I am taking thyroid hormones, and have “control of my axis” (meaning, I control the amount of thyroid hormones my body is getting), I have to “manually” adjust and keep my thyroid dose low.   I have to do what my body would do naturally.   I’ve got a low TSH while on the meds, but that’s with taking a very low overall dose of TH, much lower than most people take.   This, too, may therefore be an indication that my energy problems lie elsewhere, and not necessarily primarily thyroid-related.

However, the above observations and interpretations don’t explain the vast improvements that occurred with me the first time I started taking thyroid hormones.   And despite the fact I’m still not in very good shape overall, some rather vast improvements have occurred once again since taking thyroid hormones this second time around too.   This suggests that actual thyroid-related pathology exists, or at least “thyroid-responsive pathology” exists, and that my lower TH levels are not simply compensatory in nature.   It’s also generally accepted by the scientific and medical communities that observable serum anti-thyroid antibody titers are an indication of “something wrong” with the thyroid axis somewhere with most people who have them (in particular, with symptomatic people), and I’ve got high levels of all three that are generally tested for (TPO, Tg, TSI).  (Keep in mind there is always a small percentage of the population who have these antibodies and are asymptomatic, that “natural autoantibodies” exist, and that these antibodies may be compensatory or therapeutic in nature as well).   Even with this, I still can’t answer the question of if my thyroid problems were primary or secondary.   However, I do think there’s enough evidence to say there are, in fact, thyroid-related problems which exist.   And in my case, as a result of this, taking thyroid hormones helped improve many of my symptoms, both times I took it.

I’m of the opinion that nothing beats having a fully functioning and healthy thyroid gland.   Taking lump sum doses of thyroid hormone once or multiple times daily will never replicate the finely tuned nuances of a normally functioning thyroid axis.   When pressed, many people who say that they’re 100% “back to normal” after starting thyroid meds, will qualify their answer and say yes, there are differences, and it’s not 100% equivalent.   I’m of the opinion that once your thyroid truly konks out, you are never the same.   Meds can help a lot, and make you feel pure relief, because AITD and hypo and hyper thyroidism are such hell to live with.   But it’s never really the same as having a working thyroid axis.   So I think if there’s anything at all you can do to help preserve, protect, and support your naturally functioning thyroid axis, then that’s the first choice in all this.   I think deciding to go on thyroid medication should be a thoughtful choice, and the last resort.

In my case, I feel like I proved to myself (the hard way) that taking thyroid hormone was the better choice for me after being floxed.   Regardless of the other fluctuations that are going on due to loss of homeostasis, by taking the meds I am stabilizing to some extent that one aspect, and it does seem to help me.

I should mention that although I am on a suppressive dose of TH hormone, and this TH is helping greatly with my thyroid-related symptoms and autoimmune flares, I don’t think this alone can prevent some kinds of flares from happening.  For starters, I still have a thyroid and thymus gland, and I think these are highly antigenic tissues in me right now.  For example, they are still sensitive to my iodine and TH ingestion, and can still get a little painful if I’m out of the “sweet spot” with my meds or iodine.    In addition, suppressing the TH axis can help lower the antibody status, but not necessarily get rid of the antibodies entirely.  Part of this is due to the varying half lives of these antibodies (weeks to years), which is why some of them can remain for years.   In my opinion, I think part of this is also because the antigenic targets of these antibodies include extra-thyroidal enzymes and cells as well, which may be yet another reason they can persist for years even in people with presumed total thyroidectomies (see “Iodine: Like T3 in Me“).   This is where many people try diet changes and supplements to try and lower their antibody status.  The autoimmune component of my condition appears to be huge in me, is systemic in nature, and I think also extends well beyond “just” the anti-thyroid antibodies (which were bad enough).    I feel like I am still susceptible to some kind of reaction (ie, a cholinergic/anti-cholinergic or serotonergic reaction; or hypersensitivity reaction), just maybe not the thyroid one so much now that I’m back on TH meds.  I suspect there could easily be any number of autoimmune antibodies that are as yet unknown, or a systemic mast cell hypersensitivity which includes both my thyroid and thymus glands as targets, or cytokine storm – like reactions that could be triggered by any number of exogenous — or endogenous — substances.   Interestingly enough, I just read an article about how one of the first symptoms of a blood transfusion reaction (immune system attacks blood cells of another type) is a sense of “impending doom”.    That plunge into “impending doom” is an all too familiar one when I’m having a reaction, can happen within moments, and often times is one of the first signs I’m “heading down” into a physical reaction.   So even though I’m on an appropriately suppressive dose of TH, that doesn’t mean my autoimmune problems are over, or even that my positive TH antibody status will disappear.  What it appears to have done is helped tremendously with some of my TH-related symptoms, and unfortunately, unmasked others now such as the progressing neuromuscular weakness problems.


T4, T3, and Iodine Continue to be Major Players in My Symptoms

I continue to be amazed at how incredibly sensitive I am to serum levels of T4, T3, and Iodine.   Ingesting any of these continue to affect me greatly, as discussed throughout this website and summarized here.

Most “thyroid normal” people will be able to withstand some variation in serum levels of TH and in particular, Iodine, without “feeling” it all the time.   In other words, most “thyroid normal” people could take T4 and T3, and their thyroid axis (hypothalamus, pituitary and thyroid gland), and carrier proteins (thyroxine-binding globulin, transthyretin, and albumin) will automatically and quickly adjust to keep serum levels stable.   Additionally, the real “fine tuning” of this homeostasis then occurs at the cellular level, intracellularly and at the cell membrane, for localized control of TH and Iodine.   Each cell then gets exactly what it needs, when it needs it; no more, and no less.    Most importantly, a “thyroid normal” person will never even feel these adjustments; they are automatic, quick, and effective.    So if you get a little endogenous spurt of T4 or T3 for some reason, or head off to Iceland and eat a ton of iodine-rich seaweed and seafood, your body won’t have a catastrophic meltdown, and you won’t feel like you’re dying or on some rollercoaster from hell.   In fact, you won’t even feel it.

However, in my case, post-flox, somewhere in this chain of events, this homeostasis mechanism no longer works in me, as I described in “It Felt Like a Homeostasis Problem“.   What this means is that I feel every dose of T4/T3 I take; I feel it “metabolizing off” throughout the day; and I feel like a junkie the last 1-2 hours before my next dose as my body suffers through “hypo” symptoms until it’s time to take my meds.  (No, I can’t take them early – that would throw off the whole cycle, and I have to keep in mind the half-lives of each and how that is going to affect me).

In my case, there are additional underlying mechanisms which feel like they are progressing, making me even more sensitive to TH and Iodine.   For example, in a very general way, I am to the point where I can feel that my brain needs more TH/Iodine than my skeletal muscles, in particular, my thigh skeletal muscles.   How do I know that?   Now that I am back on TH meds again, I am in control of how much T4 and T3 my body gets.   If I lower my TH meds by just a microgram or two, it decreases my thigh muscle weakness, burning, “coldness”, etc – but it can bring on the vertigo acutely (literally feels like suddenly there’s no TH available in my brain).   If I then raise my TH by just a microgram or two, my brain cells are flooded again and I feel relief (no vertigo), but I’ll get increased burning, weakness, coldness, etc., in my thigh muscles.   If I continue to raise my TH by a bit more, I’ll develop my “hyper” CNS symptoms of increased intracranial pressure, severe dry eyes and sinuses, ear pain, dizziness/disorientation, cardiac issues, emotional symptoms, etc.    In addition, I would develop increased peripheral neuropathy symptoms in my legs and elsewhere, such as “electric shocks”, “bugs or trickling water” feeling, tingling, numbness, and the burning and weakness in my skeletal muscles will worsen as well.   If I lower my TH “too much”, below the “sweet spot”, not only will I develop full out vertigo and “hypo-head CNS symptoms”, but the severe fatigue will develop – although the burning, electric shocks, and other peripheral neuropathies in my skeletal muscles will stop.   Although I’m always juggling a multitude of symptoms, the CNS symptoms of severe vertigo and disorientation, the cardiac issues, and the neuromuscular symptoms of severe weakness (with concern of respiratory failure) are at the forefront right now.   So I am “locked in my TH dose”, which I can gauge by my symptoms alone.   I feel every dose of T4 and T3 that I take (ie, it’s “high” for the first couple of hours after taking the meds), and the last 1-2 hours before my next dose, I feel a little like a junkie going through detox, as my cells desperately start to need more meds again.   I take T4/T3 every 12 hours, with a third tiny dose of T3 in between.   But I still feel these “dosage fluctuations” acutely and intensely.   Since Iodine is Like T3 in Me, this, too continues to play a major role in my symptoms, so I am always balancing my Iodine ingestion along with the TH meds.

All this continues to tell me that T4, T3, and Iodine continue to play a major role in my symptoms, and that there is probably a major problem somewhere with my TH/Iodine homeostasis, most likely, at the cellular level.   However, once again, I still can’t say with any certainty if my TH problems are a primary problem, or are secondary due to “fallout” from a cascade effect of other mechanisms in action – although I still suspect the answer is “both” for me.


As My Underlying Neuromuscular Symptoms Continue to Progress, I Can Tolerate Less and less TH/Iodine

When I started taking TH the first time, I discovered that I needed a relatively small dose compared to most people to suppress my axis (TSH = 0 or approaching zero).   I was on about 50 ug T4 with 5 ug T3 for a total of 55 ug TH per day.   I responded well, and at that time, didn’t experience any fatigue or weakness, and being on TH helped my symptoms tremendously.   Scroll about ½ down the page here where I discuss my lower doses a bit in “I Believe I Had a Predisposition“.

When I started back on TH again, it became apparent that I had an “energy threshold” that couldn’t be breached without developing symptoms.   This essentially limited my TH to an even lower TH dose of about 50 ug total/day.    As usual, I couldn’t do the once a day dosing for T4 due to my ‘dosage fluctuations’, so I split the T4 into twice a day dosing of about 23-24 ug each.   T3 dose was even lower, at about 1 ug or a little less three times per day.   This meant shaving off a sliver of T4 after splitting the tabs, or crunching off what I needed for T3.    Yes, measurements were imprecise, but it’s amazing how good you can get at estimating your dose in this way when your symptoms depend on it.   For the most part, it worked, although with the narrow range I’m in, not to mention extenuating circumstances (ie, I got a cold which changed my requirements for a few days), I was always fluctuating a bit and sometimes “over” or “under” shot.    It is also rather amazing at how much of the vertigo and disorientation, and many of the CNS symptoms and other symptoms, that the TH has cleared up (as long as I limit Iodine).    I notice the simple things, like turning my head, rolling over in bed, and getting up and walking without feeling like I’m at sea.   I don’t miss those plunges into feelings of “impending doom” with those autoimmune/hypersensitivity flares either.

Without that little bit of T3, the fatigue (different from ‘weakness’) was crushing to the point I couldn’t function.   So even though it was a very tiny amount, I needed it very much.  If I took a little too much T3, the weakness would kick in, equally leaving me nonfunctional.   As ever, I also had to strictly control and limit the amount of iodine I was ingesting, since in many ways iodine had a ‘T3’ effect in me.   I could really feel the value of having the TH doses under my control, rather than allowing my damaged axis with the autoimmune component flaring all over the place; with the incredibly narrow range I was functioning in, at least I had a chance of controlling some of these symptoms.   I don’t want to imply my CNS symptoms cleared up completely; they didn’t.  And I still had plenty of problems.  It’s just that some of the most bothersome TH-related symptoms cleared up, which enabled me to keep going.   I didn’t bother to run labs, because no matter what the numbers would be, it wasn’t going to make a difference in my dosing.    I was solidly ‘locked’ into my dose by my symptoms.   Going any lower – or higher – by just a few micrograms could bring on TH-related symptoms again.   So I knew I was at the ‘right’ dose for me.   The overall lower dose of TH makes sense given my increasing neuromuscular symptoms; there was simply no way to ‘push’ the ‘gas’ or energy on muscles that couldn’t respond.

Eventually, I ended up with a new physician due to changing health insurance, and she wanted to test my TSH.  The first time the blood draw was at about 4 hours post T4/T3 dose, and my TSH was at 0.68.  She then wanted to run it again a few days later (I think she couldn’t believe it because I was on such a low dose of TH overall).  The second time was an AM blood draw about 12 hours post both T4/T3 and my TSH was about 2.5.   This is a nice example of the fluctuation that can occur in TSH for any number of reasons that I discuss in “TSH and T4:  Useful or Useless?”  In this example, I suspect the difference in TSH is due to the half life of T3 playing a role.

I suspect that over time, if the neuromuscular symptoms worsen, that I would require even less TH as a result, and be forced to lower the dose accordingly.    Iodine “dosage” also continues to be a huge problem (and solution) for me, which means I have to ingest just the “right” amount to limit symptoms.   Although Iodine in many ways seems to function like T3 in me, I am finding that I need both T3 and Iodine.   In other words, I can’t seem to substitute one for the other.  This is particularly evident in that I can’t cut out the little bit of T3 and utilize iodine in its place  (essentially, be on T4-only replacement therapy and let ingested iodine from my diet supply for all the functions T3 normally would).   Part of this may be because it takes larger doses of Iodine, at least according to available research studies, to feel this effect.   And the only way I can take larger doses of Iodine would be at the expense of T4 (I would have to lower my T4 intake), and I’m not about to do that now (read the rest of this website to try and understand this concept).   So this means I have to limit my iodine, and take just the “right” amount, as with both T4 and T3, or else I become more symptomatic.


Acetylcholine-Related Updates:    Hup A (AChEi), Potatoes, Chocolate, Caffeine (AChEi), and Nicotine (ACh agonist)


Huperzine A:  A Brief Trial

For the neuromuscular issues, I decided to try something called Huperzine A, an AChE inhibitor.  Hup A is a supplement that is easily ordered over the internet, so it was a quick and easy way for me to try something without expending a lot of energy, physically or emotionally, of trying to get in to see a specialist.   A traditional Pharma equivalent could be Mestinon (Pyridostigmine), although in theory I think that this drug should be more specific for skeletal muscle (nicotinic receptors) than muscarinic.

I took 1/8 of a 200 mcg tablet Hup A.  Within minutes, my eyes and/or the muscles surrounding them, became extremely painful, almost intolerably so.  Thankfully, this severe pain only lasted a few minutes, and then, as the pain slowly dissipated to a tolerable level, I could literally feel the moisture flood my eyes as the tear film returned.   The tearing was not excessive – it was like almost in an instant, my eyes just went back to ‘normal’ again.  What an amazing, incredible thing the normal tear film is; how comfortable it makes our eyes.  It’s something you just never think about until you’ve lost it.  After over five years of these dry, gritty eyes, it’s an amazing experience to have the normal tear film restored, even if it is for only a short while.

I could feel some other mild, non-specific effects in my head and elsewhere, as the stuff slowly hit the receptors, but none of it was unpleasant or extreme and it was mild enough that I couldn’t really define it.

Then about 15-20 minutes later, the message of this newfound substance hit my cardiac receptors/SA/AV nodes/whatever, and in an instant a very forceful tachycardia occurred.  Not just a simple “speeding up of my heart rate”, but what felt like that rapid ‘machine-gun’ firing of well over 250 bpm, with a few flips thrown in.  Thankfully, this only lasted 5-10 seconds, because this kind of tachycardia is just plain dangerous.  I had grown used to these ‘tachycardic runs’ during ‘hyper flares’, but this particular run was different in that the force of the contraction was very strong as well.  It felt like my heart could jump out of my chest, and had the rate and force of that continued, I would have been in serious trouble.   So, that was pretty scary, and ensured my brief trial of Huperzine A was over.   “Reflex tachycardia” can possibly occur from taking an AChEi, but I would presume that’s more of simply an increased heart rate in general.   What I experienced was a complete “switch” or “flip” into a dangerous supra or ventricular tachycardia.  I’m not sure what the metabolic chain of events was to cause this type of tachycardia.   Is there a chance that with continued use and slow titration up I would have developed more tolerance for this supplement?  Yes.  But was I going to take that chance?  No, not after this particular adverse effect.  My cardiac cells were already extremely sensitive to minute fluctuations in TH, Iodine, catecholamines, etc., and I didn’t want to throw Hup A into the mix.  In general, as receptors upregulate and downregulate, and entire systems shift with each change, I can work through some of those effects.  But this extreme tachycardia was not one of them.   I only experienced this episode once about 15-20 minutes in after taking the dose; after that, my heart rate and rhythm went back to normal.  But consider I only took 1/8 of a tablet.  I shudder to think what could have happened had I taken a full tablet.

There is always something to be learned from whatever experiences we have, both the positive and negative ones.  In this case, the almost immediate tearing that occurred helped support the idea that more ACh transmission would really help my eyes, and is involved in providing the normal tear film.  From this brief experiment, it appeared that both my lacrimal glands, as well as the physical nerves supplying them, were still functional and not necessarily damaged.  It appears the additional ACh is what made the difference, again, supporting the suggestion that I’ve developed an ACh transmission problem from being floxed as well as a TH/Iodine problem .

TH hormone itself appeared to contribute greatly to my dry, gritty eyes.  Over and over again, repeatedly and predictably, the higher my serum TH levels were, the drier and grittier my eyes were.   This was even evident with my “dosage  fluctuations” – eye dryness and grittiness were worst for the first hour or two after taking T4 or T3, when serum levels were presumably highest.  This dryness and grittiness would improve as TH was metabolized off over time, and provided I was on an appropriate replacement dose of TH.   The lower my serum TH, the more moisture my eyes had.  This was most evident when my tear film returned back to normal during my ‘iodine trial’ when my serum TH levels were very low, my TH axis was shut off, and ingestion of iodine was high.  Both TH and ACh appear to play a large role in my level of eye dryness, and at least in my own case, I suspect iodine alone does as well.   I find myself wondering if ‘free’ iodine (unattached to Tyrosyl residues) plays a role in ACh transmission.   Selenium, necessary for deiodination, made my eyes and/or eye muscles excruciatingly painful when I supplemented it alone, as if the muscles around my eyes were being squeezed or “wrung out”, but no tear production occurred.   Free iodine – or perhaps iodothyronines other than T4/T3 – may be needed for proper tear production, possibly by way of interacting with ACh/AChE.   Available research seems to have focused on antibodies cross reacting to common epitopes between TH and ACh systems; however, the mechanism of interaction could be anything, not simply an autoimmune one.   I’ve often wondered if my TH-related problems are with deiodination, given that I can no longer take iodine while serum TH levels are normalized.

Regarding the cardiac response, I think this is a good example of the “on/off” responses I talk about in “It Felt Like a Homeostasis Problem”.    When the Hup A hit my cardiac cells – or other cells initiating cardiac cell mechanisms – it hit suddenly and hard.  And then just as suddenly, it stopped.   There was no “homeostasis” of metabolism occurring; regulation of the processes Hup A initiated were either ‘on’ or ‘off’ with delayed responses.   This reaction is not unique to Hup A for me; it’s occurring with one or more fundamental reactions that are common to oral and transdermal medications and supplements, foods and eating, and reactions initiated by exercise or movement.   I listed some of these potential mechanisms in “TH/Iodine Problems Were Not the Only Issues”, and “Additional Mechanisms to Consider” as well as throughout this website.    It often feels like ion channels or other transporters are either wide open or slammed shut, signal transduction becomes an amplified ‘runaway freight train’ with no brakes or never starting at all, regulatory enzymes are either ‘on’ or ‘off’ in terms of function, Ca or Mg is “rushing in” or “rushing out” of compartments or cells, antibodies/mast cells/cytokines are ‘on’ or ‘off’, or the “all or nothing” threshold potentials have changed.   This makes taking any medication or supplement, or changing my diet, fraught with danger for me, and accounts for the extreme ‘tightrope’ I am always walking on.  This is also one reason that I don’t believe Mestinon would work any better than Hup A for me.   Although I’ve tried many alternative treatments and supplements, this is also the major reason I never tried any of the intravenous treatments; the cardiac and extreme encephalopathy symptoms react so quickly with both oral and transdermal substances, that I can’t imagine what would happen if an adverse effect slammed into my brain via the IV route.   And as I’ve discussed in several places in this website, this is why any ‘thyrotoxic flares’ – or any other types of flares – felt so devastating to me.   At this point in time, as the underlying damage to my homeostasis or regulatory processes in me continues to progress, I am walking an ever finer and finer ‘tightrope’ as my sensitivities continue to increase.

As far as the rest of my day after taking Hup A, I did not experience any more cardiac issues after that, and the eye moisture remained good for a couple of hours, and then slowly wore off throughout the day.   I did notice I was walking around the house a little better, with a little less fatigue, so it’s too bad I couldn’t try it out more to see if that effect was real.   After a few days, I started adding in a bit of choline supplement daily.   I tolerated this well with no adverse effects, but it didn’t improve my situation any.   I also have some CDP-Choline and phosphatidylcholine on hand from previous trials when I was OFF TH.  I’ll probably try those again as well, now that I’m ON TH again.


Nicotine as AChR Agonist

A nicotine agonist is a drug that mimics the action of acetylcholine (ACh) at nicotine acetylcholine receptors (nAChRs).   I bought some nicotine gum, thinking I might try it.  However, I’m pretty sure it will be a heart thumping experience as well, and I haven’t had the guts to try it yet.   I remember reading one flox recovery story where the person said ““Believe it or not, smoking cigarettes helped immensely.”   I wouldn’t recommend taking up smoking, but from a molecular mechanism aspect, perhaps this person was being helped not only psychologically, but physiologically due to nicotinic stimulation.


Potatoes (Nightshades), Chocolate, and Caffeine as AChE inhibitors

After the Hup A experience, I decided to try potatoes, which are in the Nightshades family. Nightshades contain substances (solanaceous glycoalkaloids (SGA’s); note the steroidal backbone) that are AChE inhibitors as well.   Other common substances, such as caffeine and chocolate, can also act as AChE inhibitors.

I would imagine that anyone in the throes of a cholinergic crisis, such as what may be occurring in some FQ victims especially during the acute phase of FQT, might be highly sensitive to Nightshades and other AChEi’s, making symptoms worse.    On the other hand, for people experiencing extreme weakness and fatigue without the cholinergic symptoms, such as myself right now, Nightshades and other AChEi’s might help.  So I started eating home made French Fries made from one medium Red Potato cooked in coconut oil at night, with a lot of ketchup (another “nightshade” type food).  Potatoes have a lot of nutrients in them, not just AChEi’s, so I figured any AChEi effects would probably be tempered somewhat by all the other substances in potatoes.   Also of note is that potatoes are considered a higher lectin food (1), and I had concerns about Mast Cell Activation or other hypersensitivity reactions.    But I decided to forge ahead none the less.

The first day, I noticed an immediate difference, with some increased extreme tiredness, “hyper head CNS” stuff and headache, right after my first potato, but after this wore off, I noticed I felt better. So I ate one potato every night, and noticed, that overall, I was feeling better after eating the potato.  I also noticed how the effect would slowly wear off during the next day, to where I was feeling worse right before my next “dose” of potato.  So I added a second potato to breakfast.  I started feeling even better, and even went through a “sweet spot” where the neuromuscular weakness in my legs improved to the point I felt almost back to normal for about one day – no weakness, and no burning.   Overall, I was feeling much better too:  mood was great, sleeping much better, eyes felt much better with better tear production all around.   Fries were a good choice for me as well, because adding the oil slowed down the metabolism of the starch and kept the effect in my system longer.   I felt stuffed all the time with all this starch, my glucose was higher that it should be, and to top it off, I don’t even like potatoes very much except as fries, and I was sick to death of eating potatoes.   But I didn’t care about any of that – they were working, so I kept it up.  Unfortunately, this “sweet spot” didn’t last long, as around Day 6 of the potatoes I started developing some familiar symptoms of heart pounding, and then tachycardia, then palps, and difficulty sleeping at night as a result of this.  Within another day or two, I was starting to develop symptoms similar to my “Kombu” experience (see “Anatomy of an Iodine-Induced Flare“).  I guess I was so focused on the ACh/SGA aspect of potatoes, I didn’t think of iodine.   It took me a few days to think of it, but I finally checked the Iodine content of potatoes.  Turns out that Red Potatoes, medium sized, have about 40 ug Iodine in them (this will depend on the soil conditions of where the potatoes were grown as well).  Obviously this isn’t very much overall, but for someone like me, sensitive to just a few micrograms either way, getting an additional 80 ug/day, this was a tremendous amount.   So I cut my TH dose by a microgram or so just for that evening so I could sleep, and got the best night’s sleep I had in a long time.

However, from here on out, my TH dose is a given, and I’m not going to cut back on that for a whole host of reasons (described throughout this website).   So I had to cut back on the potatoes to cut back on the iodine.   I didn’t eat any for one day – what a mistake.  I “crashed” big time – could barely get up and move, mood plummeted, eye pain, blurriness, and dryness came back, and the severe burning, along with severe muscle weakness, in my legs occurred.  Presumably this was because I suddenly lost both iodine (which can provide energy for me in the “right” dose) and AChEi at the same time.  I lost whatever “homeostasis” momentum I was on, and I was miserable for the next several weeks trying to figure out some happy mediums between these foods and my symptoms.

I finally got on a schedule where I could eat one medium potato every other day due to the iodine limitations.   Obviously, there are a lot of nutrients in potatoes, not just iodine.  But I knew my symptoms of too much or too little iodine well enough that I could still feel the “iodine contribution” versus whatever else is in there (potassium, magnesium, Vitamin C, other minerals and of course the SGA’s and a lot of starch).   Every other day was a “high iodine” day for me, which I calculated out to be about 150 ug iodine.  I would follow this with a “low iodine” day, which I calculated out to be about 60-80 ug.  On the “high iodine” days, all my symptoms as described in this website increased, with “recovery” occurring on the “low” iodine days.  The “high iodine” days left me with increased tendon pain, nerve pain, and muscle pain and weakness, and often, some insomnia.   Magnesium would relax those symptoms, and despite my sensitivities to magnesium, I didn’t want to give it up completely.  So I started taking hot baths with a little Epsom salt on the night of the “high iodine” days, and this seemed to help with those symptoms as long as I didn’t over do it.  Meaning, if I added too much Epsom salts to the bath, or tried to do this every day, the severe weakness due to the magnesium worsened the following day.  Finding a balance between T4, T3, Iodine, the “AChEi” SGA’s in potatoes, and magnesium eventually helped to stabilize me further, and I finally entered another “quiet period” where I felt half human again.

It’s hard to describe, but I also felt as if some kind of “build up” was occurring with the potatoes.   Meaning, that even eating one medium potato every other day became “too much” after a while, and I had to cut back to a small potato every other day for a couple of times.   I suspect I was feeling the buildup of SGA’s, which is described in the excerpt below.  Of course, potatoes are going to vary in their amount of SGA’s as well, depending on any number of factors.   There’s no way to prove or confirm whether or not I’m feeling an “SGA accumulation” occurring, but it does feel like it to me, and I’ve been “adjusting my dosage” accordingly.

I also tried Russet and Yukon potatoes, with notable adverse reactions, and felt that some kind of hypersensitivity reaction was occurring with them, separate from the other reactions I was having.   My best guess right now would be lectin content, but it could have been anything.  I tried different brands of red potatoes, both organic and non-organic, and for the most part, they were tolerable regardless.   Sweet potatoes were also OK for me.

I also started eating a few Tollhouse chocolate chips, which not only acted as an AChEi, but had magnesium and of course the theobromine (another alkaloid).   It also started introducing me to a tiny bit of dairy again.  The chips seemed to help the most on my “low iodine/no potatoes” day.   As with everything else, I have to be careful as to how many chips I can eat:  usually about 1/4 – 1/3 cup at a time, once or twice a day, not too late in the evening, and sometimes not on “high iodine” days at all, or else I end up feeling “hyper”, “jittery”, pounding heart, tachycardia, and insomnia.   But it can be a real “pick up” on my “no iodine/potatoes” day if I time it just right.

I have not tried caffeine, but for an account of someone who did utilize caffeinated coffee successfully in recovering from being floxed with a subsequent diagnosis of Graves disease, read “Darby’s” account here.

For anyone sick of reading about the details of my diet and my play by play experiments and experiences with TH, Iodine, and potatoes, here is a very interesting paper worth the read to learn more about SGA’s in potatoes, and why they may be helping with my particular symptoms.   I hope no one reading this gets the idea that potatoes are “bad” or “toxic” in all cases.   They are not.  They, like all other foods and dietary nutrients, are neither “good” nor “bad”.   They are simply another food stuff that people have been eating for thousands of years, and genetic and epigenetic modifications have no doubt developed to accommodate this (which is why I included the last paragraph).    Note the relationship of Nightshades –> Alkaloids –> –> –> keep going to FQ’s.

From “Natural Inhibitors of Cholinesterases: Implications for Adverse Drug Reactions“:

Solanaceous glycoalkaloids received scrutiny as a result of documented outbreaks of toxicity in humans and livestock after potato consumption. The long history of potato toxicity includes some fatalities. The clinical symptoms of potato toxicity in humans are fairly consistent throughout documented cases: acute gastrointestinal disturbances (abdominal pain, vomiting, and diarrhoea) progressing in severe cases to profound neurological symptoms (apathy, drowsiness, mental confusion, stupor, visual disturbances, dizziness, hallucinations, and trembling).  Many of these symptoms mimic the clinical syndrome of massive cholinergic stimulation. Symptoms last approximately 2–24 hr after ingestion of potatoes.  The most recent major outbreak involved 78 British schoolchildren in which the most severely affected child recovered only after one week of hospitalization. Butyrylcholinesterase concentrations in 10 to 17 children analyzed were abnormally low six days after exposure. In all but one case, levels had returned to normal after four to five weeks.  This analysis suggests a substantial reservoir of SGAs after consumption of potatoes.

Individuals consuming a standard serving of potatoes can ingest as much as 20 to 60 mg SGA. This amount overlaps the potentially toxic range of SGA in small children and heavier consumption of foods containing SGAs would also reach the toxic range in adults. Although severe direct toxicity caused by SGAs is rare, the possibility that SGAs under typical dietary conditions may alter BuChE-mediated metabolism has not been addressed experimentally. Given the wide range of commonly used drugs that appear to depend on BuChE for proper termination of action, the effects of SGA inhibition warrant careful study.

Solanaceous glycoalkaloids inhibit both BuChE and AChE in in vitro and in vivo studies (see below). Since symptoms of potato and SGA toxicity resemble the syndrome of massive cholinergic stimulation, inhibition of AChE at cholinergic synapses probably accounts for most of the direct toxic effects of SGAs described above.

In humans, SGAs are sequestered in the body for long periods and may have long-term effects on BuChE and AChE activity . . . The data above suggest that SGAs may be stored in the body for extended periods. Thus, chronic SGA consumption may result in a considerable SGA pool.

The effects of SGAs on BuChE may be a rationale for the persistence of certain atypical BuChE alleles for thousands of years. The sera of individuals who are dibucaine “resistant” (i.e., they are homozygous for the “atypical” BuChE allele) show markedly lower degrees of cholinesterase inhibition after in vitro application of approximately 3 μM solanine and solanidine. Recombinant atypical BuChE is also resistant to SGA inhibition (Figure 3). Variant BuChE alleles may confer a selective evolutionary advantage against exposure to natural glycoalkaloids. An association between cultivation of the Solanum eggplant (S. melongema) and a high frequency of variant BuChE alleles in certain Middle Eastern ethnic groups has been proposed as one possible evolutionary advantage for BuChE genetic variation (Figure 5). In addition, many ancestral species of the modern commercial potato have extremely high SGA levels (some greater than 1000 mg ·kg−1), and among them, three wild species are known to have been consumed throughout history.  The potato appears to have been first cultivated in the Andes and was transported to Europe beginning in the 16th century.  Atypical BuChE alleles occur with high frequency in the Americas, Europe, and some Middle East regions, with very low frequency in Africa and Asia (Figure 5).  This fact is consistent with the hypothesis that SGAs may be a driving force for the persistence of the mutant BuChE allele.

Please note that “normal people” — such as I was before I was floxed, can eat a reasonable number of potatoes without a problem.  I was never a big potato eater, except for fries on occasion.  I just never cared for baked or mashed potatoes that much.  But when I did eat them, I never felt any different one way or the other from doing so.   Pre-flox, I could eat whatever I wanted, and I never felt any of the inner turmoil from eating any foods that I do now.    Using potatoes as a form of AChE inhibition can only occur now because of the extreme sensitivities I’ve developed from being floxed.


Magnesium-Related Update

As I stated above, I started taking Epsom salt baths every other day.   I also started drinking water from the tap for better or worse again, because the water here is very hard, and I assumed I would get some magnesium (as well as calcium) that way.   I cannot take any magnesium supplements any more, and I have to be very careful with the Epsom baths.   I cannot use too much Epsom salt, or stay in the bath “too long”, or the following day I have extremely weak muscles.   The diaphragmatic weakness is the scariest and the most dangerous due to breathing issues, along with difficulty swallowing, if this occurs.   I estimate that due to diet alone, I’m probably getting about 125-150 mg Mg/day; this amount is obviously higher on the “Epsom salt bath” days.


Update Summary Again

So, once again in summary:   I continue to improve, albeit at “glacial speed”.   I’m now using TH, Iodine, tiny amount of estrogen/testosterone, Potatoes as an AChEi, and Mg from Epsom salt baths to “control” my symptoms with some success.   I’m on minimal supplements, with a goal towards getting all my nutrients from food.  Current supplements daily:   sea salt in capsules, Ca/Vite D combo 1/2 tab (250 mg Ca/ 200 IU Vite D), Vitamin C 250 mg, and ½ tablet multivitamin/minerals (without iodine).   Every other day:  1000 ug B12 (methylcobalamin), Epsom salt bath, probiotic (15 billion).   I continue to cautiously experiment with various supplements and foods to determine my sensitivities.   I started drinking tap water daily, and added whole wheat organic bread (yes, gluten), and one or two organic chocolate chip cookies a day into my diet; for the most part, I’m tolerating this well.   I am still housebound, and obviously spend my entire life trying to maintain some kind of homeostasis.   I consider my quality of life to be somewhere between non-existent and very poor.  However, I’m still alive and moving in the right direction, so that’s something.