Iodine deficiency ! - falling intakes - goitregens - competition bromine and fluorine

[R.B.]

I do not have access to the full papers but from a wider perspective this is intriguing.

Firstly those with cystic fibrosis may commonly be iodine deficient, presumably due to uptake issues. http://www.ncbi.nlm.nih.gov/pubmed/23107148(Low selenium may be an issue too it has been suggested - selenium is important to the metabolism of iodine)

and in 1956 an salivary iodine based test was proposed for cystic fibrosis of the pancreas.

All of which raises all sorts of questions and possibilities, and particularly so given iodine's association with the mucal membranes /systems / sweating etc

A SCREENING TEST FOR CYSTIC FIBROSIS OF THE PANCREAS USING ANALYSIS OF SALIVA

Wayne Hart,
Mansour J. Naime

+ Author Affiliations

Children's Mercy Hospital, Kansas City, Missouri
The Department of Pediatrics, University of Kansas School of Medicine

Abstract

A screening test for cystic fibrosis of the pancreas utilizing analysis of saliva for iodine after oral administration of Lipiodol® is presented. Tables provide the results obtained from testing 11 children who have cystic fibrosis of the pancreas and 30 children who have no evidence of this disease. It is indicated that the test can be easily and rapidly performed.

[R.B.]

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"

[R.B.]

Here is another paper looking at the Wolff-Chaikoff effect, here again after ingestion / injection of a large amount of iodine there is a large fall in uptake, and temporary drop in T3 and T4, (T3 then recovers, and T4 increases) a metabolic adjustment but hardly a thyroid 'shutdown' as often described, in the in the normal sense of the word 'shutdown'.


http://endo.endojournals.org/content...expansion.html

http://endo.endojournals.org/content/140/8/3404.long

[R.B.]

Hashimoto's

An interesting pair of posts on Paul Jaminet's site by a Hashimoto's patient which is well referenced and highlights the importance of selenium, possible benefits at least in some of iodine supplementation, and the fundamental importance of a balanced intake of both selenium and iodine to thyroid function.

http://perfecthealthdiet.com/2011/05...iditis-part-i/

http://perfecthealthdiet.com/2011/05...iditis-part-2/

[R.B.]

Hasimoto's

Multifactoral - As ever it is important to keep in mind that most medical conditions are likely to be mutli-factoral, and have multiple associations with increased risks of other medical conditons Eg Hashimotos patients may be at increased risk of Pagets bone disease, http://europepmc.org/articles/PMC188...00365-0047.pdf which common bone conditions is linked with low vitamin D, begging the question is there maybe a link between low vitamin D and Hashimoto's . . .


The association between severity of vitamin D deficiency and Hashimoto's thyroiditis.
Bozkurt NC, Karbek B, Ucan B, Sahin M, Cakal E, Ozbek M, Delibasi T.
Author information
Abstract
OBJECTIVE:

The relation between vitamin D and autoimmune disorders has long been investigated regarding the important roles of this hormone in immune regulation. We evaluated 25-hydroxyvitamin D (25OHD) status in subjects with Hashimoto's thyroiditis (HT) and healthy controls.
METHODS:

Group-1 included 180 euthyroid patients (123 females/57 males) with HT who were on a stable dose of L-thyroxine (LT). A total of 180 sex-, age-, and body mass index (BMI)-matched euthyroid subjects with newly diagnosed HT were considered as Group-2, and 180 healthy volunteers were enrolled as controls (Group-3). All 540 subjects underwent thyroid ultrasound and were evaluated for serum 25OHD, anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-TG) levels.
RESULTS:

Group-1 had the lowest 25OHD levels (11.4 ± 5.2 ng/mL) compared to newly diagnosed HT subjects (Group-2) (13.1 ± 5.9 ng/mL, P = .002) and to control subjects (15.4 ± 6.8 ng/mL, P<.001). Serum 25OHD levels directly correlated with thyroid volume (r = 0.145, P<.001) and inversely correlated with anti-TPO (r = -0.361, P<.001) and anti-TG levels (r = -0.335, P<.001). We determined that 48.3% of Group-1, 35% of Group-2, and 20.5% of controls had severe 25OHD deficiency (<10 ng/mL). Female chronic HT patients had the lowest serum 25OHD levels (10.3 ± 4.58 ng/mL), and male control subjects had the highest (19.3 ± 5.9 ng/mL, P<.001).
CONCLUSIONS:

We demonstrated that serum 25OHD levels of HT patients were significantly lower than controls, and 25OHD deficiency severity correlated with duration of HT, thyroid volume, and antibody levels. These findings may suggest a potential role of 25OHD in development of HT and/or its progression to hypothyroidism.