SPINA THYR a research tool to evaluate thyroid function, deiodinases activity, TH resistance

[alicec]

maybe that's why iodine forms allows for more controlled influx.

Yes I can see that the need for conversion to iodide could affect the action of different iodine forms.

Experiments conducted in rats

Interesting that further along in the abstract they say

This human experiment failed to confirm the differential effect of I2 on maintenance of serum T4 concentrations relative to the effect of I- that was observed in prior experiments in rats.

I recall spending quite some time delving into the evidence for the claimed separate role for iodine as opposed to iodide, and reading a few tantalising studies such as the one you cited.

In the end I concluded that the evidence is very thin and far from compelling. There could be something to it and maybe there is some kind of facillitated diffusion of I2 into cells, independently of NIS, but there has been no real follow-up on a few very old studies. We still know nothing about what these observations really mean nor what mechanism is behind them.

If there is some independent role for I2, again it seems that in the overall scheme of things, it is a minor secondary role.

 

[Lolinda]

Is iodine all about the thyroid?

https://www.ncbi.nlm.nih.gov/pubmed/4078642
sweat iodine concentrations were about 37 µg per liter, regardless of serum and urinary iodine levels modulated by the dietary iodine level

https://en.wikipedia.org/wiki/Perspiration
water lost in sweat daily is highly variable, ranging from 100 to 8,000 mL/day

➞ There is substantial extrathyroidal usage of iodine for sweating:
If we assume a sweat excretion of a mere 1L per day, it already amounts to more than 1/5th of the iodine RDA of 150µg. And this is not recycled but gone. And this can vastly increase: During one hour of soccer, 38% of players lost more iodine through sweat than excreted in urine the entire day.

I like a lot @alicec 's argument of iodine recycling, because it simplifies things: when thinking about extrathyroidal iodine needs, it may be a good idea to focus on iodine usages that leave the body (stool, urine, sweat, sebum?...). Btw, I see these as usages and not simply loss: Just google "urinary tract infection iodine" and you will see people reporting results for their UTI from iodine. Desinfecting sweat makes sense again, but in severe iodine deficiency people cannot sweat, so it may be more than that. I do not know if or how much iodine passes in stool, but again that could be a well-spent and not fully recoverable investment into health as part of mouth➞stomach➞gut desinfection:

anti-microbial

Why is all this of interest?
Everywhere people cite the guideline that urinary excretion of 100-199 µg iodine per 24h is the healthy norm. But I bet few people ever looked into the sources to see that for adults, this is merely the range for avoiding goiter, hypothyroidism and "impaired mental function"! The range comes from the attached WHO document. Just look into the PDF!
.... I happen to have also other health goals than avoiding goiter ...

(PS: I really enjoy this thread!! - A discussion of facts, supported by references, which motivates me to respond with the same )

 

[Iritu1021]

@Lolinda, I saw this and thought you might find this interesting: acetylcholine can mimic the action of TSH when it comes to iodine release.

http://fluoroquinolonethyroid.com/wp-content/uploads/2014/11/References-3.pdf

ACETYLCHOLINE when added to incubated thyroid slices in vitro results in an increased rate of glucose catabolism and an increase in the proportion of glucose catabolized by the hexose monophosphate shunt pathway. Added thyroid stimulating hormone (TSH) has a similar effect1 . This suggests that acetylcholine (ACh) may be able to mimic the action of TSH or that TSH acts by releasing ACh or an ACh-like substance to the target cells.

 

[Iritu1021]

Found more on the subject of iodine vs iodide:

http://biolargo.com/industry-news/iodine-the-next-vitamin-d-part-ii/

Despite reports of the enhanced expression of NIS in human breast cancer tissue, I2 may be the preferred form of iodine supplementation for the prevention and treatment of breast cancer since non-lactating breast tissue is known to be peroxidase-poor and thus is less capable of iodide organification. The use of I2 bypasses the need for NIS involvement and peroxidase activity. Not surprisingly, the mammary gland more effectively captures and concentrates I2 than the thyroid, and more I2 is concentrated in breast than thyroid tissue.

Therefore, wouldn't it be theoretically possible to have a similar bypass mechanism in a thyroid with an insufficient or poorly functioning peroxidase? That would explain my differential response based on the form of iodine supplementation.

 

[alicec]

Therefore, wouldn't it be theoretically possible to have a similar bypass mechanism in a thyroid with an insufficient or poorly functioning peroxidase? That would explain my differential response based on the form of iodine supplementation.

But does such a bypass mechanism exist?

I can't find any evidence for the claims of the author that you quote. As far as I am aware, there is no evidence for uptake and concentration of iodine by the non-lactating breast.

There are some very old studies showing that both iodide and iodine treatment of women with fibrocystic breast disease led to significant and similar levels of improvement in the disease. The two forms weren't compared directly but in separate studies. Molecular iodine was preferred because of fewer side effects.

This series by Ghent seems to form the basis of all the claims about the role of iodine in the breast, but it doesn't really tell us very much - just that iodine/iodide treatment helps fibrocystic breasts.

It might have nothing to do with the direct action of iodine on the breast, in fact, this study shows that oral administration of molecular iodine does not result in the appearance of molecular iodine in the blood. Rather, some is converted to iodide while the bulk reacts with lipids and proteins before or during absorption and circulates in this form.

I have never seen any detailed follow-up studies of the fate of this iodinated protein and lipid and what biological role it might play, but it puts paid to the notion that breast cells somehow take up and respond to molecular iodine. It could well be that these iodinated species have some biological effect and this could be the basis of the different apparent action of molecular iodine and iodide but no-one seems to be studying it anymore.

Another study showed that molecular iodine in the gut reacted with deiodinated T4 metabolites to reform T4, leading to increased T4 in the blood.

These studies were in rats and the situation may be different in humans. What they do show, however, it that the fate of oral doses of molecular iodine is complex and doesn't fit with the simplistic assumptions made by the proponents of the special role for iodine.

I don't discount that there could be a role, it's just that there is no good evidence to even hint what it is.

 

[pattismith]

But does such a bypass mechanism exist?

I can't find any evidence for the claims of the author that you quote. As far as I am aware, there is no evidence for uptake and concentration of iodine by the non-lactating breast.

There are some very old studies showing that both iodide and iodine treatment of women with fibrocystic breast disease led to significant and similar levels of improvement in the disease.

I am not convinced that the positive effect of iodine on fibrocystic breast is a direct effect.

Benign breast issues have shown to be more frequent in hypothyroidism, so my feeling would be that iodine improves benign breast issues by enhancing thyroid hormons (TH).

Improvement then may be related to enhancement of the SHBG by TH, which leads to lowering of circulating estrogens.

Edit: I have myself mastosis and tenderness, and it resolved as soon as I started T3

 

[alicec]

I am not convinced that the positive effect of iodine on fibrocystic breast is a direct effect.

Yes, there's no evidence for it and no known mechanism.

 

[frozenborderline]

interesting discussion on iodine all. I tried kelp once and had a flushing feeling and felt better for probably like an hour or so. But then read ray peat talking about how true iodine deficiency is rare since iodine was added to salt, and how iodine excess can cause hypothyroidism, etc. The thing is, I have been eating sea salt, not morton's, for awhile... I don't eat much salt, don't eat much seafood, and don't live by the sea. So I'm wondering if it would be possible for me to have some kind of iodine deficiency. I do feel good when I eat shellfish but that's possibly attributable to all the other micronutrients.

My cynomel and cynoplus came in the mail as well as a pill cutter. I'm sort of nervous to try this stuff, any tips? I don't want to push the dosage too high, so if it doesn't work for me I think I'll just give it up. Is it fairly safe at the small doses? I'm talking like 3 mcg.

 

[pattismith]

interesting discussion on iodine all. I tried kelp once and had a flushing feeling and felt better for probably like an hour or so. But then read ray peat talking about how true iodine deficiency is rare since iodine was added to salt, and how iodine excess can cause hypothyroidism, etc. The thing is, I have been eating sea salt, not morton's, for awhile... I don't eat much salt, don't eat much seafood, and don't live by the sea. So I'm wondering if it would be possible for me to have some kind of iodine deficiency. I do feel good when I eat shellfish but that's possibly attributable to all the other micronutrients.

My cynomel and cynoplus came in the mail as well as a pill cutter. I'm sort of nervous to try this stuff, any tips? I don't want to push the dosage too high, so if it doesn't work for me I think I'll just give it up. Is it fairly safe at the small doses? I'm talking like 3 mcg.

According to what I heard, sea salt is not providing enough iodine. I take iodine supplement but I stay at the daily recommended dose.
T3 3mcg is not a big dose. Do not take more than once a day or every other day if you wish to avoid any hyper.

 

[frozenborderline]

According to what I heard, sea salt is not providing enough iodine. I take iodine supplement but I stay at the daily recommended dose.
T3 3mcg is not a big dose. Do not take more than once a day or every other day if you wish to avoid any hyper.

once a day? i thought t3, unlike t4, had fairly short half life and should be taken 3x/day

 

[brenda]

Ray Peat is wrong about that.

https://www.amazon.com/The-Iodine-C...=1363781462&sr=8-1&keywords=the+iodine+crisis

By the time the salt is in the kitchen, it has lost a lot of its potency and loses even more as the package is opened. And the dosage is far too small to make anty difference unless all you want to do is avoid a goitre. I just read the book in the link this week and it is an eye opener.

 

[pattismith]

once a day? i thought t3, unlike t4, had fairly short half life and should be taken 3x/day

Yes I do the 3x/day protocol by now, but I found interesting to start with a small dosage once a day. It showed me the quick non genomic effect of T3

 

[frozenborderline]

Yes I do the 3x/day protocol by now, but I found interesting to start with a small dosage once a day. It showed me the quick non genomic effect of T3

have you found it to be very helpful? have you had to up dose or try selenium or lithium to help with thyroid resistance?

I'm considering trying to get a lithium carbonate script since i've heard that's less toxic than lithium orotate

 

[pattismith]

have you found it to be very helpful? have you had to up dose or try selenium or lithium to help with thyroid resistance?

I'm considering trying to get a lithium carbonate script since i've heard that's less toxic than lithium orotate

well no, I stopped any supplement that can interfer with deiodinases for now, excepted selenium and iodine.

(I also take iron now, because I have evidences of deficiency, and a bit of cortisone from time to time.)

I don't know if I have some tissues thyroid resistance or not, but I have Low T3 Syndrome and pituitary hypersensitivity.

my high rT3 is blocking some of the non genomic actions of T3, so I decided a T3 trial to stimulate my D1 and lower my T4/TSH axis.

I still struggle with my brain and my muscles, but I will keep increasing the dose step by step unless my heart rate rises. If my HR and my blood pressure doesn't move, it means that peripheric thyroid resistance is a possibility.

 

[frozenborderline]

well no, I stopped any supplement that can interfer with deiodinases for now, excepted selenium and iodine.

(I also take iron now, because I have evidences of deficiency, and a bit of cortisone from time to time.)

I don't know if I have some tissues thyroid resistance or not, but I have Low T3 Syndrome and pituitary hypersensitivity.

my high rT3 is blocking some of the non genomic actions of T3, so I decided a T3 trial to stimulate my D1 and lower my T4/TSH axis.

I still struggle with my brain and my muscles, but I will keep increasing the dose step by step unless my heart rate rises. If my HR and my blood pressure doesn't move, it means that peripheric thyroid resistance is a possibility.

in short, no?? then? Have you considered triac? Part of me is scared of trying T3/T4 because of the risks but another part is scared of trying it because I don't want to be let down when it doesn't work... I don't have ideas beyond that.

I wouldn't want to push the dose very high and cause functional hypothyroidism.

 

[pattismith]

in short, no?? then? Have you considered triac? Part of me is scared of trying T3/T4 because of the risks but another part is scared of trying it because I don't want to be let down when it doesn't work... I don't have ideas beyond that.

I wouldn't want to push the dose very high and cause functional hypothyroidism.

My readings convinced me that central hypothyroidism and thyroid resistance can be associated with normal thyroid panels.
Some markers can help you to identify a lack of thyroid hormons action (HDL, beta-caroten, cardiac echography, SHBG, in my case I have low HDL and high beta-caroten), but a T3 trial is the easier way to test if you have a functional thyroid hormon deficiency.

You have to closely monitor your Heart Rate at rest, and blood pressure if you can.

My HR is still between 62 and 81 at rest, and my T3 intake is now at 31 mcg/day.

In my case, I didn't find really positive effect for now, I still have good and bad days, but if thyroid resistance is at play, you can't expect positive effect until you reach the right dose for you.

The wilson protocol may be useful to monitor the TH effects (see Wilson Syndrome on internet), I have not tryed it.

 

[frozenborderline]

My readings convinced me that central hypothyroidism and thyroid resistance can be associated with normal thyroid panels.
Some markers can help you to identify a lack of thyroid hormons action (HDL, beta-caroten, cardiac echography, SHBG, in my case I have low HDL and high beta-caroten), but a T3 trial is the easier way to test if you have a functional thyroid hormon deficiency.

You have to closely monitor your Heart Rate at rest, and blood pressure if you can.

My HR is still between 62 and 81 at rest, and my T3 intake is now at 31 mcg/day.

In my case, I didn't find really positive effect for now, I still have good and bad days, but if thyroid resistance is at play, you can't expect positive effect until you reach the right dose for you.

The wilson protocol may be useful to monitor the TH effects (see Wilson Syndrome on internet), I have not tryed it.

The bolded part is certainly what I have gleaned from reading peat and other people that have "alternative views" on thyroid. I've had fairly normal thyroid panels but never reverse T3. Do you think it's okay to do without a blood pressure monitor? Taking my blood pressure makes me nervous and I don't have the money for a good machine? I was told to take pulse rate and temperature.

 

[frozenborderline]

has anyone here tried triac yet?

 

[pattismith]

I was told to take pulse rate and temperature.

this is exactely what I would do.

here you will find how to monitor your temperature according to the Dr Wilson:

http://www.wilsonssyndrome.com/identify/how-are-body-temperatures-measured/

 

[frozenborderline]

Insulin resistance could be due to increased T1AM level:
https://www.ncbi.nlm.nih.gov/pubmed/28754352

Yes, Ray Peat is very adamant about avoiding all omega fatty acids. I believe he attributed it to improper oxidation but I trust his more on his intuition than his science.

Yes, excess T4 makes my body nervous and excess T3 makes my mind nervous. It seems that replacement T3 goes all to the brain.

That could be due to different deiodinase settings between your CNS and the rest of the body. In CNS T3 is primarily synthesized by D2 while in other organs primarily through D1.

Low dose lithium orotate might help to convert T4 to T3 better, especially within CNS.
https://www.ncbi.nlm.nih.gov/pubmed/12176672

It sounds like kelp gave you Wolff-Chaikoff effect that you never fully recovered from. Must have been a pretty high dose of iodine. Iodine is a very controversial issue in Hashimoto's, it's something that I'm struggling with right now since I suspect I do have true iodine deficiency. But apparently iodine increases oxidative damage although I doubt your couple doses would do that since this was a study on chronic use.
https://www.ncbi.nlm.nih.gov/pubmed/16796889
Did you take it together with selenium? Selenium is supposed to have a protective effect against iodine toxicity in autoimmune thyroiditis.[/QUOTE]

I read your whole thyroid experiment thing, and I'm still curious if you think it's somewhat safe to use small (physiological) doses of T3 and T4, as an experiment. As in, even if it doesn't work, I will not push the dose higher, because I don't want to deplete thyroid hormones. It sounds like people run into an issue when they don't get an effect, so they push the dose higher, and then have rebound