yeah you are
I mean there's so many ants in my eyes! And there are so many TVs, microwaves, radios... I think, I can't, I'm not 100% sure what we have here in stock.. I don't know because I can't see anything! Our prices, I hope, aren't too low!
I think the real secret magic that some of these fine folks aren't telling the Panda is that they are taking the Iodine supplements... but also SKIPPING the Lithium supplements.
“You have your way. I have my way. As for the right way, the correct way, and the only way, it does not exist.”
And that's why I'm here eating HFLC Primal/Paleo.
Now, can we get back to discussing iodine? Does ANYONE have any real evidence to counter what has already been presented here?
The bitters take a bit to get used to. Do you need to drink lots of water when you take them (seems to defeat the point) or just later?
Here, let's see if we can get this thread back on topic:
Thyroid. 2001 May;11(5):501-10.
Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis AG.
Department of Medicine, University of Patras Medical School, Greece.
Iodine is an essential element for thyroid hormone synthesis. The thyroid gland has the capacity and holds the machinery to handle the iodine efficiently when the availability of iodine becomes scarce, as well as when iodine is available in excessive quantities. The latter situation is handled by the thyroid by acutely inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff effect, by a mechanism not well understood 52 years after the original description. It is proposed that iodopeptide(s) are formed that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff effect lasts for few a days and then, through the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T4) and triiodothyronine (T3) returns. This is achieved by decreasing the intrathyroidal inorganic iodine concentration by down regulation of the sodium iodine symporter (NIS) and therefore permits the TPO-H202 system to resume normal activity. However, in a few apparently normal individuals, in newborns and fetuses, in some patients with chronic systemic diseases, euthyroid patients with autoimmune thyroiditis, and Graves' disease patients previously treated with radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the inhibitory effect of large doses of iodides is not achieved and clinical or subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been observed in patients with a history of postpartum thyroiditis, in euthyroid patients after a previous episode of subacute thyroiditis, and in patients treated with recombinant interferon-alpha who developed transient thyroid dysfunction during interferon-a treatment. The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but transient T4 replacement therapy may be required in some patients. The patients who develop transient iodine-induced hypothyroidism must be followed long term thereafter because many will develop permanent primary hypothyroidism.