HER2 Support Group Forums - View Single Post - Iodine deficiency ! - falling intakes - goitregens

R.B. · 12-08-2013, 11:46 AM

Essence = adequate selenium is very important if you are eating iodine rich foods viz kelp or using iodine supplementation.

This is a bit nerdy but hopefully the detail below will help with the gist; don't worry I do not understand all of it either (-:

This paper looks at the effects of higher iodine intakes on the thyroid and the response of the thyroid which includes the productions of selenium related antioxidants.

The graphs plotting the action of the iodine importer shows it reduces in activity, but interestingly does not 'shut down' totally. http://mend.endojournals.org/content...expansion.html

Similarly T3 and T4 fall but do not 'shut down'. http://mend.endojournals.org/content...expansion.html

This leaves me wondering how accurate the common descriptions of the Wolff-Chaikoff as a 'shut down' effect are, or if something different to what is observed in this paper happens at much higher intakes.

The idea of a healthy normal thyroid that efficiently and rapidly adapts its intake to the amount of iodine in the system has a ring of natures common sense about it - is this what this data and the Wolff-Chiakoff data suggests? - the data above raises the question was the choice of the description 'shut down' used for the sometimes rapid auto-regulation of iodine uptake / fall in hormone production by the thyroid an unfortunate one because it implied a reaction that was more dramatic than that observed viz rapid auto-regulation ? - hopefully there will be more research to answer these questions . . .

Also can extra thyroidal iodine when present in high amounts for example as iodine attached to lipids etc, and or extra-thyrodial production of related hormones for example from the ovaries in any way partially compensate for lower T3 and T4?

Much science has to discover yet methinks, and within the known sea of knowledge I am still not yet a toddler.

The paper is available in full - I hope that applies to you to

Regulation of Thyroid Oxidative State by Thioredoxin Reductase Has a Crucial Role in Thyroid Responses to Iodide Excess

Suzana G. Leoni,
Edna T. Kimura,
Pilar Santisteban and
Antonio De la Vieja

http://mend.endojournals.org/content/25/11/1924.long

"In summary, our results provide new information about the molecular events involved in thyroid autoregulation by high doses of I−. First, we determined that the rapid blockade of I− uptake in thyroid cells is not occurring in parallel to NIS mRNA and protein modulation and also that it is not caused by NIS internalization. These observations suggest an inactivation of NIS localized at the plasma membrane. Second, the incorporation of large amounts of I− increases ROS species in the thyroid cell above basal levels. As a consequence, the expression and activity of TxnRd selenoproteins increase to compensate oxidation and avoid cell toxicity. Thus, these selenoproteins participate in thyroid I− autoregulation by allowing the restoration of a normal thyroid cell oxidation state and NIS reexpression"

12-08-2013, 11:46 AM	#91
R.B. Senior Member Join Date: Mar 2006 Posts: 1,843	Re: Iodine deficiency ! - falling intakes - goitregens - competition bromine and fluo Essence = adequate selenium is very important if you are eating iodine rich foods viz kelp or using iodine supplementation. This is a bit nerdy but hopefully the detail below will help with the gist; don't worry I do not understand all of it either (-: This paper looks at the effects of higher iodine intakes on the thyroid and the response of the thyroid which includes the productions of selenium related antioxidants. The graphs plotting the action of the iodine importer shows it reduces in activity, but interestingly does not 'shut down' totally. http://mend.endojournals.org/content...expansion.html Similarly T3 and T4 fall but do not 'shut down'. http://mend.endojournals.org/content...expansion.html This leaves me wondering how accurate the common descriptions of the Wolff-Chaikoff as a 'shut down' effect are, or if something different to what is observed in this paper happens at much higher intakes. The idea of a healthy normal thyroid that efficiently and rapidly adapts its intake to the amount of iodine in the system has a ring of natures common sense about it - is this what this data and the Wolff-Chiakoff data suggests? - the data above raises the question was the choice of the description 'shut down' used for the sometimes rapid auto-regulation of iodine uptake / fall in hormone production by the thyroid an unfortunate one because it implied a reaction that was more dramatic than that observed viz rapid auto-regulation ? - hopefully there will be more research to answer these questions . . . Also can extra thyroidal iodine when present in high amounts for example as iodine attached to lipids etc, and or extra-thyrodial production of related hormones for example from the ovaries in any way partially compensate for lower T3 and T4? Much science has to discover yet methinks, and within the known sea of knowledge I am still not yet a toddler. The paper is available in full - I hope that applies to you to Regulation of Thyroid Oxidative State by Thioredoxin Reductase Has a Crucial Role in Thyroid Responses to Iodide Excess Suzana G. Leoni, Edna T. Kimura, Pilar Santisteban and Antonio De la Vieja http://mend.endojournals.org/content/25/11/1924.long "In summary, our results provide new information about the molecular events involved in thyroid autoregulation by high doses of I−. First, we determined that the rapid blockade of I− uptake in thyroid cells is not occurring in parallel to NIS mRNA and protein modulation and also that it is not caused by NIS internalization. These observations suggest an inactivation of NIS localized at the plasma membrane. Second, the incorporation of large amounts of I− increases ROS species in the thyroid cell above basal levels. As a consequence, the expression and activity of TxnRd selenoproteins increase to compensate oxidation and avoid cell toxicity. Thus, these selenoproteins participate in thyroid I− autoregulation by allowing the restoration of a normal thyroid cell oxidation state and NIS reexpression" Last edited by R.B.; 12-08-2013 at 04:56 PM..