Does Anyone Have Experience Of Using Lugol's Iodine Solution? For Deficiency/Methylation/Other

[PatJ]

tried 5mg lithium orotate, but gives me intense eardrum pressure plus tinnitus

That's a curious reaction. I just read that LO may be useful for treating Meniere's disease which is characterized by the symptoms you experienced (and others.) LO is supposed to reduce those symptoms, not cause them.

I don't think my previous tinnitus increase was related to LO because my tinntus has been fluctuating a lot lately. I'll try LO again soon to see what happens.

I'm reducing my iodine intake from 100-112mg/day down to 50mg/day to see if I feel any different. Heading up to 50mg I noticed a libido increase (generally seen as a sign of better health) but then it decreased. Maybe 50mg/day, or lower, will be a better dose for me.

Also, the sludge build up in the toilet bowl (that I mentioned several messages ago) only lasted for a week, and the excessive urine odor has been decreasing over the past week.

 

[Leopardtail]

I think it's more likely that unless you're makimg and absorbing T3, serotonin production fails.

I am not aware of serotonin being part of the T4-T3 conversion process. It's largely done by a liver enzyme called 5'deiodinase, which removes one of the four attached molecules of iodine on T4 (hence T4), this becoming T3 - 3 iodine molecules attached.

Where in the pathway is serotonin involved in converting T4 to T3?

Ditto oestrogen making serotonin - I don't understand. Please give me some references to look at .

The peak of production both of T4 and T3 occurs during sleep - in other works after Melatonin peaks.

Serotonin in concentrations of 1 and 10 μg/ml greatly stimulated the organification of iodine and the formation of iodothyronines in suspensions of isolated thyroid cells. Iproniazid enhanced the stimulatory action of low, but not of high, concentrations of serotonin. The effects of serotonin on the iodine metabolism of isolated cells were blocked by phentolamine, but not by either propranolol or reducing agents (ascorbate, sodium bisulfite). Serotonin also stimulated the conversion of glucose-l-14C to 14CO2, the incorporation of 14C-labeled amino acids into TCA-precipitable proteins by isolated cells. In addition, adenyl cyclase activity was stimulated by serotonin in both intact and sonicated preparations of isolated cells. The precursors of serotonin, L-tryptophan and 5-hydroxytryptophan, as well as its metabolite, 5-hydroxyindolacetic acid, did not stimulate either iodine metabolism or adenyl cyclase activity, while tryptamine did. These findings suggest that the stimulatory effect of serotonin depends upon the amine, rather than the 5-hydroxyl, group. (Endocrinology88: 620, 1971)
​

The paper above appears to indicate that the up-regulation occures via increasing Iodine availability rather than through substrate provision or allosteric regulation.

 

[Leopardtail]

iodine as an antibiotic wow.

I had been fancifully wondering if that was its impact in my blood. I have been wondering what happens to all of that bacteria that gets into our blood in PEM and what benefit urinating a lot of iodine/iodide could have, but what it did/might do in our guts somehow escaped me.

According to this abstract http://journals.sagepub.com/doi/abs/10.3181/00379727-106-26366 it is chiefly absorbed in the small intestine and stomach, but I suppose some will still make it to the colon.

Also from this abstract https://www.ncbi.nlm.nih.gov/pubmed/23006481 taking more iodine should reduce our ability to absorb it.

Thanks for both papers Richard.

I had seen material by an american doctor who advocates taking 50mg of Iodine every second day to combat infection. He too indicated that Iodine was formerly used as an antibotic - it destroys the cell walls of all three classes of infective microbes. I had been concerned about killing microflora in the colon (similar concerns about oregano oil).

I wonder whether that Alternate day usage will avoid the issue of Symporter loss?

 

[Leopardtail]

Immediately after:
TSH 15.02
FT4 0.99 (0.9 - 1.7 ng/dL)
FT3 2.45 (2 - 4.4 pg/mL)

One month later:
TSH 8.57
FT4 0.85 (0.9 - 1.7 ng/dL)
T4 5.36 (6 - 12.23 ug/dL)
T3 91.50 (80 - 200 ng/dL)
FT3 2.83 (2 - 4.4 pg/mL)
RT3 0.23 (0.10 - 0.35 ng/mL)

Taking too much Iodine (not selenium) can raise the ratio of T4 to T3. I have yet to see any proof as to why. Also Iodine supplementation can be a problem if people suffer hyptothyroidism due to Hashimotos. You will get a lot more information on this at ThyroidUK where they specialiste in these issues.

The purpose of Selenium in reducing antibodies is to get Glutathione up in order to lower toxic stress - how well that would work in an ME patient with your dysfunctional immune systems is hard to guess. The whole process of producing Glutathione requires adequate Methylation (in turn requiring activated B3) and Cysteine.

The type of Cysteine also matters Sodium Selenite is nasty stuff, SelenoCysteine is ideal for Glutathione, SelenoMethionine is ideal for conversion to T3.

Did the lab provide a freeT3:rT3 ratio and a normal range for that ratio?
(the units are not directly comparable)

 

[Gondwanaland]

Also Iodine supplementation can be a problem if people suffer hyptothyroidism due to Hashimotos. You will get a lot more information on this at ThyroidUK where they specialiste in these issues.

Thanks, I will navigate there. I have been considering to take some diluted Lugol's at 100-200% RDI 1x weekly since eating sardines about 2x monthly seems to greatly help. Taking Lugol's wuold exclude the ammonia issues, and this would be a + factor.

The type of Cysteine also matters Sodium Selenite is nasty stuff, SelenoCysteine is ideal for Glutathione, SelenoMethionine is ideal for conversion to T3.

I never tolerated Selenomethionine - it gives me instant acute brain fog. I used to take Selenium chelate (I think Se-Glycine? not sure), but lately I haven't tolerated any Selenium at all. FOr glutathione Milk Thistle extract is what works best for me.

Did the lab provide a freeT3:rT3 ratio and a normal range for that ratio?
(the units are not directly comparable)

No

 

[Thewonders92]

I think it's more likely that unless you're makimg and absorbing T3, serotonin production fails.

I am not aware of serotonin being part of the T4-T3 conversion process. It's largely done by a liver enzyme called 5'deiodinase, which removes one of the four attached molecules of iodine on T4 (hence T4), this becoming T3 - 3 iodine molecules attached.

Where in the pathway is serotonin involved in converting T4 to T3?

Ditto oestrogen making serotonin - I don't understand. Please give me some references to look at .

https://www.ncbi.nlm.nih.gov/pubmed/7776715

Nicotinic Acid lowers serum T3 and T4 levels in the blood.

Higher levels of serotonin mean lower or normalized IDO activity.

10-15% of tryptophan becomes Serotonin and then Melatonin.

The rest goes down the Kynurenine pathway to eventually produce Niacin, and some steps later NAD+.

High levels of Kynurenine are indicative of many illnesses including CFS in an incredibly high percentage of patients. Many cofactors and processes involved between Tryptophan and NAD+, the first of which is underfunctioning FAD (riboflavin dependant) enzymatic function, FAD is a cofactor to the first rate limiting step of kynurenine metabolism.

The thyroid is heavily involved in the kynurenine pathway.

To generalize and simplify, low serotonin+high kynurenine in serum will imply serious thyroid dysfunction amongst a great many disorders of human metabolism, poor gut function is the main culprit for this, very high dose probiotic rounds in mice have shown to substantially lower kynurenine and speed it's processing, along with raising serotonin and increasing energy (possibly through a greater amount of NAD+), haven't researched much.