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Hashimoto's And Iodine Supplementation, Lugol's.

Jigsaw

Senior Member
Messages
420
Location
UK
Just found some super-critical info that explains why some people get Hashimoto's auto-immune thyroiditis, thyroid nodules, etc, on Lugol's.


My summary:

- Iodine stimulates thyroid hormone production.

- Thyroid hormones made from thyroglobulin + tyrosine, which then has iodine bound to it via TPO (thyroid peroxidase enzyme). TPO by-product is hydrogen peroxide.

- Hydrogen peroxide neutralised by glutathione, via glutathione peroxidase enzyme.

- Insufficient glutathione peroxidase = accumulation of highly damaging hydrogen peroxide. High levels of accumulated Hydrogen peroxide damages and or destroys thyroid gland cells and can result in thyroid nodules.


- In an effort to protect itself, body produces TPO /Tg antibodies to reduce amount of thyroid hormones being made, and/or, hydrogen peroxide alters TPO /possiby Tg so much that body no longer recognises TPO /Tg as a friendly host-protein and TPO enzyme /Tg is attacked because it appears to be a foreign substance. I think that TPO antibodies are probably destructive to the thyroid gland as well as to (obviously) TPO itself, ditto thyroglobulin.


The lack of T4 and T3 would show on blood tests as elevated TSH with inappropriately low T4/T3/ FT4/FT3.

The article here: https://docs.google.com/document/d/1gbUGdOWDUzCnWdt8Zqc4jFEi4HM6MMcc8F4Lk__NhIM/mobilebasic

(I think it's by Bill Thompson, but the article itself isn't signed, and if I try to go to the previous article, which is by Bll Thompson, I just get an invite to sign up to Google Drive.)



"Furthermore, within his own more recent research, Dr Guy Abraham has already completely explained the biochemical reasons for thyroid nodule formation whenever higher dose iodine is supplemented. Within the thyroid cell itself, thyroglobulin is normally converted to T3 (triiodothyronine) and T4 (thyroxine) via moderation by the thyroid peroxidase catalytic enzyme. This conversion process quite naturally produces hydrogen peroxide as a normal byproduct of reaction. But if glutathione peroxidase – a critical enzyme and anti-oxidant for the thyroid – is not present in the thyroid cell in appropriate amounts, then a dangerous build-up of hydrogen peroxide will occur within the thyroid cell itself. Excess hydrogen peroxide build-up further acts to change the nature of the thyroid peroxidase protein so that the immune system is unable to recognize it anymore as friendly host protein. As a consequence, the antibodies will attack and remove this “foreign” thyroid peroxidase enzyme so essential for T3 and T4 production in the body. The excess hydrogen peroxide builds up to unhealthy levels, which also tends to disrupt and destroy thyroid cells, with resulting thyroid nodule formation., within his own more recent research, Dr Guy Abraham has already completely explained the biochemical reasons for thyroid nodule formation whenever higher dose iodine is supplemented. Within the thyroid cell itself, thyroglobulin is normally converted to T3 (triiodothyronine) and T4 (thyroxine) via moderation by the thyroid peroxidase catalytic enzyme. This conversion process quite naturally produces hydrogen peroxide as a normal byproduct of reaction. But if glutathione peroxidase – a critical enzyme and anti-oxidant for the thyroid – is not present in the thyroid cell in appropriate amounts, then a dangerous build-up of hydrogen peroxide will occur within the thyroid cell itself. Excess hydrogen peroxide build-up further acts to change the nature of the thyroid peroxidase protein so that the immune system is unable to recognize it anymore as friendlhy host protein. As a consequence, the antibodies will attack and remove this “foreign” thyroid peroxidase enzyme so essential for T3 and T4 production in the body. The excess hydrogen peroxide builds up to unhealthy levels, which also tends to disrupt and destroy thyroid cells, with resulting thyroid nodule formation."





I hope this helps people who are concrned about Hashi's and Lugol's. I haven't done any fact-finding on this mechanism yet, because it seems to make sense that this is what's happening when people develop Hashi's from using iodosupplementation.

Other sites I've looked at, and forum posts all over the net, say that everyone's response to iodine is different, that some people who develop Hashi's unknowingly already had a degree of it prior to using Lugol's, or had another auto-immune disorder (allergies, R.A, Lupus, etc) which made them prone to developing it, some say they've been taking 50mg for 8 years with nothing but postive benefits and ne'er a hint of Hashi's, still others say that an elevated TSH always happens once you take iodine and that it's a transient "adjustment" effect which normalises after a period of time. Studies by Drs Abraham, Flechas, and Brownstein would seem to bear out that last statement.

Most everyone says that sufficient selenomethionine prevents Hashi's, but then I've seen forum posts elsewhere that say posters have still developed Hashi's despite religiously taking the companion nutrients daily (2x 500mg niacinamide [not flushing niacin], 200-400mcg selenium as selenomethionine, 400-600mg magnesium [not oxide], 2x 100mg B2, 2x1500mg Vit C as ascorbic acid, plus optional ALA, NAC, Milk Thistle) and the salt loading protocol.

From what I already know about thyroid function and physiology, I think this is the most likely explanation as to why an elevated TSH happens in the presence of iodosupplementation.

I think it's highly feasible that the raised TSH is in response to lowered T4 and T3 manufacture, which is brought about by an accumulation of hydrogen peroxide caused by poor glutathione peroxidase activity/levels damaging the thyroid peroxidase enzyme and/ or Tg.


The hydrogen peroxide and/or the TPO /Tg antibodies further damage the thyroid tissue, resulting in even less ability to make thyroid hormones, which would then go on to create a vicious circle of
- elevated TSH telling the thyroid to make more hormones
-»more Tg called upon to make thyroid hormones
- »more TPO called on to make thyroid hormones
- »more hydrogen peroxide produced by TPO action
- »more damage to TPO by hydrogen peroxide IF INADEQUATE GLUTATHIONE PEROXIDASE
-»poss damage to Tg
- »more TPO antibodies
-»poss Tg antibodies
- »more damage to thyroid gland tissue/cells from antibody activity
- »insufficient thyroid hormones for health
- »even more elevated TSH.

The author of the article says that the companion nutrients are enough to ensure that there is sufficient glutathione peroxidase enzyme floating about to activate glutathione. I think I'm going to be happier taking not only those, but also sulfur-high foods (a bit problematic, possibly, as I suspect I don't metabolise sulfur optimally) and the three amino acids that comprise glutathione - cysteine, glycine, and glutamine.

I also already take a Source Natural's product called Chem Defense, whuch is 1.7mg FMN, 120mcg molybdenum amino acid chelate, and 50mg reduced glutathione.

I'm not about to stop taking my Lugol's, because I've already lost the last ten years to breast cancer and if I'd known about iodine deficiency actively causing it, I might have avoided all that. I certainly don't want a repeat performance. On top of that, I want to resolve - or at least try to resolve - my hypothyroid and hypoadrenals, and all the attendant signs and symptoms that come with them.

Who knows? Maybe it will be the solution to my CFS/ME and FMS, too.

I live in hope!
 
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David Jackson

Senior Member
Messages
195
Thanks for that post, Jigsaw. Very relevant to me right at this point in time. I am just now turning back to focus on the thyroid issues, after dealing with something else.

The last blood test I had, around 6 months ago, showed elevated TSH, with a lower (but still just within the reference range) T3 and T4... and guess what I've done in the past... yep, taken large amounts of Lugos... so what you describe might be happening with me... I think I need to get another blood test to see what the thyroid hormones are doing now, though.

So... if you were me, what would you do?
 

Jigsaw

Senior Member
Messages
420
Location
UK
Thanks for that post, Jigsaw. Very relevant to me right at this point in time. I am just now turning back to focus on the thyroid issues, after dealing with something else.

The last blood test I had, around 6 months ago, showed elevated TSH, with a lower (but still just within the reference range) T3 and T4... and guess what I've done in the past... yep, taken large amounts of Lugos... so what you describe might be happening with me... I think I need to get another blood test to see what the thyroid hormones are doing now, though.

So... if you were me, what would you do?
You're welcome :)

Depends on a)how you're feeling, what signs and symptoms you have, b)what your thyroid panel was like before Lugol's, c)how much Lugol's in mg you were taking before, and d)how long you took it when you last did so.

And yes, not unreasonable to get another blood test done now, as it's 6mo since the last one. Would also be useful to have your thyroid antibodies (thyroid peroxidase and thyroglobulin) checked, as well as FT4, FT3, T4, T3, TSH. RT3 if you can persuade them to run it.

When you say "a lower T4..." do you mean lower in relation to TSH, or lower in relation to previous readings?
 
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PatJ

Forum Support Assistant
Messages
5,288
Location
Canada
Stephanie Buist also has some information about treating Hashimoto's in her Iodine Supplementation Guide v2:

Why does iodine work for Hashimotos?

There are many healthcare professionals that are warning of the terrible consequences for those with Hashimotos who take high doses of iodine. But they are VERY wrong. The lack of iodine is actually part of the reason as to why Hashimotos has occurred. Iodine is needed to support the body in balancing this autoimmune condition. There are several things that you need to look at and consider when listening to these doctors warnings.

a. How much iodine do they discuss?
In most cases they discuss microgram (mcg) or low milligram (mg) dosing in the examples they site that had outcomes resulting in disaster. Yes, this is exactly what may happen. In some individuals when given microgram amounts you do “stoke the fire” and cause an increase in antibody attack on the thyroid gland. That’s not what we teach.

b. Where do they stop their discussion?
In watching many videos and reading the articles of the doctors sounding the alarm, they take iodine through the biological process in the gland where iodine enters the cell and is oxidated from iodide to iodine and then they exclaim – “See the oxidation creates inflammation and that increases antibodies.” Right again! But there is one problem. The body’s process doesn’t stop there. When iodine is supplied in levels OVER what is needed to create thyroid hormones there is a magical substance that is created called iodolipids. These iodolipids are the regulatory factor on the oxidation process. Iodolipids, when created, will put the brakes on the oxidative process before it runs out of control and “burns” the cells creating an inflammatory response. The body sees inflammation / abnormal cells and creates an antibody attack against them as a natural response. The key is to stop this from occurring.

c. Where they go wrong.
Dr Brownstein has written about this in his book Iodine Why you Need it Why You Can’t Live Without It. He has determined that when iodine is supplied in amounts 100x the RDA of 150 mcg (or 15 mgs) that the body will begin to create these iodolipids. So you can see that giving microgram amounts causes a big issue for those with Hashimotos. In this case the mantra of “low and slow” can actually create a bigger issue. This causes many to give up on iodine because their condition seems to worsen. So the next time you see a doctor or listen to one that discusses the dangers of high doses of iodine for Hashimotos ask them…. “What about the iodolipids?”
 

Jigsaw

Senior Member
Messages
420
Location
UK
Stephanie Buist also has some information about treating Hashimoto's in her Iodine Supplementation Guide v2:
I agree :)

Yet there are very definitely some posters on CureZone who have still developed Hashi's on 50-100mg/d, with all co-factors, no previous antibody production, etc.

Obviously iodolipids are critically important, and mcg doses may not be enough to support their production, hence more inflamm potentially triggering auto-immune antibodies.

I think that's on top of the posible mechanism that the article I posted explores.
 

Jigsaw

Senior Member
Messages
420
Location
UK
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PatJ

Forum Support Assistant
Messages
5,288
Location
Canada
Edit - Oh dear. Authors have just cited Wolff-Chaikof effect as fact, several pages in. Now I don't know how seriously I can take the rest of their info.

A read some of the interesting info in the document before brainfog rapidly closed in. As far as citing the "well known" (as they put it) WC effect it depends how much the misinformation biases their arguments and research. The more I learn about poorly done studies, human bias, difficulty in doing research properly, lack of reproducibility etc. the less trust I have in research documents and studies.
 

Jigsaw

Senior Member
Messages
420
Location
UK
A read some of the interesting info in the document before brainfog rapidly closed in. As far as citing the "well known" (as they put it) WC effect it depends how much the misinformation biases their arguments and research. The more I learn about poorly done studies, human bias, difficulty in doing research properly, lack of reproducibility etc. the less trust I have in research documents and studies.
Absolutely.

It's a pain in the butt, because it means I have to now fact check each reference for accuracy, because they obviously haven't. They've taken everything published as unopposed fact.

They only published this paper in 2014. It's basically looking at the evolutionary reasons as to why iodine is so important, and how it affects different tissues.

There's one claim, aside from the WC effect being presented as truth, that I find particularly bizarre; they state that there is a mechanism whereby "excess" iodine is automatically inhibited via NIS blockage to prevent lesions, then they say lesions happen anyway, except in the lactating breast:-

"On the other hand, high quantities of iodine intake are toxic and cause degenerative, necrotic and neoplastic lesions in thyroid, stomach and salivary glands (Venturi & Venturi, 2009; Janta et al., 2006; Küpper et al., 2011; Stroev & Churilov, 2012), but not in the lactating breast where the toxic hyperaccumulation of iodine is not possible. On the contrary, Japanese women, who have the highest dietary iodine intake (largely from seaweed) of 1-3 mg/day, have the lowest breast cancer mortality in the word."

1. That iodine intake figure is not anywhere near the 12-13mg/d cited by the Japanese authorities as the average daily consumption of seaweed in dried weight, which is used consistently by Abraham, Flechas and Brownstein to support their studying of 12.5mg/d iodine administration and its effects.

2. Why would the lactating breast "disallow" "the toxic hyperaccumulation of iodine", making such a claimed event "not possible", which by implication means it IS possible for non-lactating mammary glands to store "toxic hyperaccumulation of iodine"? Where's the non-lactating breast to compare it with so we can see how differently the lactating breast is behaving in regard to iodine levels? What do they mean? Do they mean they found lower levels of iodine in lactating breast tissue than in non-lactating breast tissue? Or higher levels that produced no toxicity? Whare are the references? There are none directly attached to this strange statement.

Also, Mother Nature typical prioritises new life over old, because new life has a better chance of successful reproduction than already older life. So the priority would have to be providing the infant with iodine rather than letting the mother hold on to it. Foetuses tend to pull iodine out of the mother, so that they have enough for proper development and the rigours of birth (one reason for PND is hypothyroidism post-natally). If they simply compared iodine levels between lactating and non-lactating breasts, a lactating gland could easily show lower iodine levels than a non-lactating one, as the infant would be feeding frequently and effectively drawing out more iodine each time. They don't mention any of this.

3. They cite four studies supporting this supposed toxically high iodine damage, and one of them is themselves.

4. If I'd written a paper like that at uni, I would rightly have been slammed for providing neither reference nor argument to support such bald statements.


Having said all that, I still find it an interesting paper re iodine, extrathyroidal use, thyroid function, T4, T3, PUFAs, selenium, and regeneration.

Iodine is necessary for the metamorphosis of vegetarian tadpole into big carnivorous frog. Apparently, tadpoles given iodine achieve this much faster than those that aren't given iodine.


- Then there's another very odd reference they make to hypothyroid signs and symptoms, whereby they suggest that the similar "reptilian quality" of some hypo t signs (dry, hairless, scaly skin, hypothermia, slowed digestion, slower mental function, etc) might be a throwback to when we were still living in water, and is somehow beneficial / protective as a result!

(Last time I posted this, it landed on the board with 75% text showing strike-through lines. I've had to re-type it. If it does it again, readers will just have to look through the lines, because I'm wiped out now. Sorry!)












 
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