Iodine and your thyroid

This page is meant to be a com­pi­la­tion of iodine infor­ma­tion rela­ted to your thy­roid. If you have more infor­ma­tion you want to see me add, just use the Con­tact Me form below. Give refe­ren­ces to where you found your information.

1) There has been great inte­rest in the rela­tionship bet­ween iodine and your thy­roid health.  http://lpi.oregonstate.edu/infocenter/minerals/iodine/

2) Iodine is an indis­pen­sa­ble com­po­nent of the thy­roid hor­mo­nes, com­pri­sing 65% of T4’s weight, and 58% of T3’s http://www.thyroidmanager.org/Chapter2/chapter2.pdf

3) Videos by Browns­tein on iodine:  http://vitamincfoundation.org/videos/#BROWNSTEIN

4) Iodine publi­ca­tions by Abraham: http://www.optimox.com/pics/Iodine/opt_Research_I.shtml

5) Also iodine is one of the major pla­yers in hea­ling a thyroid.

* http://www.vrp.com/art/1781.asp?c=1151353583312&k=/vrpsearch.asp&m=/includes/vrp.css&p=no&s=0
* http://www.vrp.com/art/561.asp?c=1154980649328&k=/articlesalpha.asp&m=/includes/vrp.css&p=no&s=0
* http://www.vrp.com/art/1860.asp?c=1154980649328&k=/vrpsearch.asp&m=/includes/vrp.css&p=no&s=0
* http://www.laurapower.com/iodinedeficiency.htm

6) Iodine info:

http://www.optimox.com/pics/Iodine/opt_Research_I.shtml
http://www.optimox.com/pics/Iodine/IOD-09/IOD_09.htm
http://www.optimox.com/pics/Iodine/IOD-02/IOD_02.htm
http://www.quackcenter.com/ideficiency.html
http://www.lewrockwell.com/miller/miller20.html
http://www.iodine4health.com
http://www.optimox.com/pics/Iodine/loadTest.htm
http://www.askdoctordavid.com/articles/iodine3_news_82005.html

7) * T3 = C15H12I3NO4 = molar mass of 650.9776;
* T4 = C15H11I4NO4 = molar mass of 776.87
* Iodine has a molar mass of 126.90;
* Iodine con­tent of T3 = (3 * 126.9)/650.9776
* T3 is 59.725 % iodine
* Iodine con­tent of T4 = (4 * 126.9)/776.87
* T4 is 65.339 % iodine.

8 ) Armour has 38 mcg T4 & 9 mcg T3.
.65339 * 38 mcg = 24.828 mcg iodine
.59725 * 9 mcg = 5.37525mcg iodine

9) Each grain of Armour has 30.20325 mcg iodine.  Each grain of Armour has 1/5 the RDA of iodine (150 mcg).

10 ) FACTS ABOUT IODINE AND AUTOIMMUNE THYROIDITIS by Guy E. Abraham, M.D.

In 1912, patho­lo­gist H. Hashi­moto published in the Ger­man lan­guage and in a Ger­man medi­cal jour­nal (1), his his­to­lo­gi­cal fin­dings in four thy­roid glands remo­ved at sur­gery: nume­rous lymphoid follic­les; exten­sive con­nec­tive tis­sue for­ma­tion; dif­fuse round cell infil­tra­tion; and sig­ni­fi­cant chan­ges of the aci­nar epithe­lium. He called this patho­logy of the thy­roid “struma lympho­ma­tosa”, but it became popu­lar under the name “Hashi­moto Thy­roi­di­tis”. At the time of Hashimoto’s publi­ca­tion, autoim­mune thy­roi­di­tis was not obser­ved in the U.S. popu­la­tion until the iodi­za­tion of salt. Hashimoto’s thy­roi­di­tis is now clas­si­fied as goi­trous autoim­mune thy­roi­di­tis AIT because the gland is enlar­ged, in dis­tinc­tion to atrophic autoim­mune thy­roi­di­tis where atrophy and fibro­sis are pre­do­mi­nant. Both con­di­tions are chro­nic, pro­gres­sing over time to hypothy­roi­dism in a sig­ni­fi­cant per­cen­tage of Patients (2).

In seve­ral com­mu­ni­ties world­wide, an inc­rea­sed inci­dence of AIT was repor­ted follo­wing imple­men­ta­tion of  iodi­za­tion of sodium chlo­ride (3). In areas of the Uni­ted Sta­tes where this rela­tionship has been stu­died, mainly in the Great Lakes Region, a simi­lar trend was repor­ted. In 1966 and 1968 Wea­ver et al (4,5) from Ann Arbor Michi­gan repor­ted: “The salient his­to­patho­lo­gi­cal fea­ture of the thy­roid glands, remo­ved at ope­ra­tion in a five-year period before iodine prophy­la­xis (1915 to 1920), was the pau­city of lymphocy­tes in their parenchyma, and, more impor­tantly, the absence of thy­roi­di­tis of any form” “It should be empha­si­zed that the thy­roid glands prior to the use of iodi­zed salt were devoid of lymphocy­tes, and nodu­lar colloid goi­ters with dense lymphocy­tic infil­tra­tes were found after the intro­duc­tion of iodi­zed salt in 1924″.

Furszy­fer et al (6), from the Mayo Cli­nic, stu­died the ave­rage annual inci­dence of Hashimoto’s thy­roi­di­tis among women of Olms­ted County, Min­ne­sota during 3 con­se­cu­tive periods cove­ring 33 years of obser­va­tion, from 1935 to 1967. They found the inci­dence to be higher in women 40 years and older ver­sus women 39 years and less. Howe­ver, in both groups, there was a pro­gres­sive inc­rease in the inci­dence of Hashimoto’s thy­roi­di­tis over time. During the 3 periods eva­lua­ted, that is 1935 – 1944; 1945 – 1954; 1955 – 1967; the ave­rage annual inci­dence of Hashimoto’s per 100,000 popu­la­tion were 2.1; 17.9; and 54.1 for women 39 years and less. For women 40 years and older, the ave­rage annual inci­dence over the same 3 periods were: 16.4; 27.4; and 94.1.

It is impor­tant to point out that the Mayo Cli­nic study star­ted 10 – 15 years after imple­men­ta­tion of iodi­za­tion of salt in the area. Therefore,even during the first decade of obser­va­tion, the pre­va­lence of autoim­mune thy­roi­di­tis was already sig­ni­fi­cant. Again, it must be empha­si­zed that prior to the imple­men­ta­tion of iodi­zed salt as obser­ved by Wea­ver, et al,(4.5) this patho­logy of the thy­roid gland was not repor­ted in the US, even though the Lugol solu­tion and potas­sium iodide were used exten­si­vely in medi­cal prac­tice at that time in daily amount two orders of mag­ni­tude grea­ter than the ave­rage intake of iodide from table salt.

It is of inte­rest to note that prior to iodi­za­tion of salt, AIT was almost non-existent in the USA, although Lugol solu­tion and potas­sium iodide were used exten­si­vely in medi­cal prac­tice in amounts 2 orders of mag­ni­tude grea­ter than the ave­rage daily amount inges­ted from iodi­zed salt (2). This sug­gests that ina­de­quate iodide intake aggra­va­ted by goi­tro­gens, not excess iodide, was the cause of this con­di­tion. To be dis­cus­sed later, AIT can­not be indu­ced by inor­ga­nic iodide in labo­ra­tory ani­mals unless com­bi­ned with goi­tro­gens, the­re­fore indu­cing iodine deficiency.

The pathophy­sio­logy of AIT is poorly unders­tood. Expe­ri­men­tally indu­ced autoim­mune thy­roi­di­tis in labo­ra­tory ani­mals by acu­tely admi­nis­te­red iodide requi­red the use of antithy­roid drugs, essen­tially goi­tro­gens, to pro­duce these effects (7 – 10). These goi­tro­gens indu­ced thy­roid hyper­pla­sia and iodide defi­ciency. Antioxy­dants either redu­ced or pre­ven­ted the acute iodide-induced thy­roi­di­tis in chicks (11) and mice (12). Bagchi et al (11) and Many et al (12) pro­po­sed that the thy­roid injury indu­ced by the com­bi­ned use of iodide and goi­tro­gens occurs through the gene­ra­tion of reac­tive oxy­gen species.

We have pre­viously pro­po­sed a mecha­nism for the oxi­da­tive damage cau­sed by low levels of iodide com­bi­ned with antithy­roid drugs (2): Ina­de­quate iodide supply to the thy­roid gland, aggra­va­ted by goi­tro­gens, acti­va­tes the thy­roid peroxy­dase (TPO) sys­tem through ele­va­ted TSH, low levels of iodi­na­ted lipids, and high cyto­so­lic free cal­cium, resul­ting in excess pro­duc­tion of H2O2. The excess H2O2 pro­duc­tion is evi­den­ced by the fact that antio­xi­dants used in Bagchi’s expe­ri­ments did not inter­fere with the oxi­da­tion and orga­ni­fi­ca­tion of iodide and the­re­fore neu­tra­li­zed only the excess oxy­dant (11). This H2O2 pro­duc­tion is above nor­mal due to a defi­cient feed­back sys­tem cau­sed by high cyto­so­lic cal­cium due to mag­ne­sium defi­ciency and low levels of iodi­na­ted lipids which requi­res for their synthe­sis iodide levels 2 orders of mag­ni­tude grea­ter than the RDA for iodine (2). Once the low iodide supply is deple­ted, TPO in the pre­sence of H2O2 Molar and orga­nic subs­trate reverts to its peroxy­dase func­tion which is the pri­mary func­tion of halo­pe­roxy­da­ses, cau­sing oxi­da­tive damage to mole­cu­les nea­rest to the site of action: TPO and the subs­trate thy­ro­glo­bu­lin (Tg). Oxy­di­zed TPO and Tg eli­cit an autoim­mune reac­tion with pro­duc­tion of anti­bo­dies against these alte­red pro­teins with sub­se­quent damage to the api­cal mem­brane of the thy­roid cells, resul­ting in the lymphocy­tic infil­tra­tion and in the cli­ni­cal mani­fes­ta­tions of Hashimoto’s thy­roi­di­tis. Even­tually, the oxi­da­tive damage to the TPO results in defi­cient H2O2 production.

Hypothy­roi­dism occurs in AIT when oxi­da­tion and orga­ni­fi­ca­tion of iodide in the thy­roid gland become defi­cient enough to affect synthe­sis of thy­roid hormones.

In vitro stu­dies with puri­fied frac­tions of calf thy­roid glands by De Groot et al (13) gave com­pe­lling evi­dence that iodide at 10 – 5 Molar con­fers pro­tec­tion to TPO against oxi­da­tive damage. To achieve periphe­ral levels of 10 – 5 Molar iodide, a human adult needs a daily amount of 50 to 100 mg. DeGroot’s fin­dings can be sum­ma­ri­zed as follows:

1. TPO is inac­ti­va­ted by H2O2.

2. KI at 10 – 5 Molar pro­tects TPO from oxi­da­tive damage.

3. Potas­sium Bro­mide and Potas­sium Fluo­ride do not share this pro­tec­tive
effect of KI.

4. The pro­tec­tive effect of KI is not due to the cova­lent bin­ding of iodine
to TPO but due to the pre­sence of KI itself in the incu­ba­tion media.

Based on the above facts, it is obvious that iodine defi­ciency, not excess, is the cause of AIT.

Refe­ren­ces

1) Hashi­moto, H., Zur Kennt­niss der lympho­ma­to­sen Veran­de­rung der Schild­druse (Struma lympho­ma­tosa). Arch. Klin. Chir., 97:219 – 248, 1912.

2) Abraham, G.E., The safe and effec­tive imple­men­ta­tion of orthoio­do­sup­ple­men­ta­tion in medi­cal prac­tice. The Ori­gi­nal Inter­nist, 11:17 – 36, 2004.

3) Gai­tan, E., Nel­son, N.C., Poole, G.V., Ende­mic Goi­ter and Ende­mic Thy­roid Disor­ders. World J. Surg., 15:205 – 215, 1991. (Autoim­mune Thyroiditis)

4) Wea­ver, D.K., Batsa­kis, J.G., Nishi­yama, R.H., Rela­tionship of Iodine to “Lymphocy­tic Goi­ters”. Arch. Surg., 98:183 – 186, 1968. (Autoim­mune Thyroiditis)

5) Wea­ver, D.K., Nishi­yama, R.H., Bur­ton, W.D., et al, Sur­gi­cal Thy­roid Disease. Arch. Surg., 92:796 – 801, 1966. (Autoim­mune Thyroiditis)

6) Furszy­fer, J., Kur­land, L.T., Wool­ner, L.B., et al, Hashimoto’s Thy­roi­di­tis in Olms­ted County, Min­ne­sota, 1935 through 1967. Mayo Clin. Proc., 45:586 – 596, 1970. (Autoim­mune Thyroiditis)

7) Weet­man, A.P., Chro­nic Autoim­mune Thy­roi­di­tis. In Wer­ner & Ingbar’s The Thy­roid — Bra­ver­man LE and Uti­ger RD Edi­tors, Lip­pin­cott Williams & Wil­kins, 721 – 732, 2000. (Autoim­mune Thyroiditis)

8 ) Follis, R.H., Further obser­va­tions on thy­roi­di­tis and colloid accu­mu­la­tion in hyper­plas­tic thy­roid glands of hams­ters recei­ving excess iodine. Lab Invest., 13:1590 – 1599, 1964. (Goiter)

9) Belshaw, B.E., Bec­ker, D.V., Nec­ro­sis of Folli­cu­lar Cells and Discharge of Thy­roi­dal Iodine Indu­ced by Admi­nis­te­ring Iodide to Iodine-Deficient Dogs. J. Clin. Endocr. Metab., 13:466 – 474, 1973. (Goiter)

10) Mah­moud, I., Colin, I., Many, M.C., et al, Direct toxic effect of iodine in excess on iodine-deficient thy­roid gland: epithe­lial nec­ro­sis and inflam­ma­tion asso­cia­ted with lipo­fus­cin accu­mu­la­tion. Exp. Mol. Pathol., 44:259 – 271, 1986.

11) Bagchi, N., Brown, T.R., Sun­dick, R.S., Thy­roid Cell Injury Is an Ini­tial Event in the Induc­tion of Autoim­mune Thy­roi­di­tis by Iodine in Obese Strain Chic­kens. Endoc­ri­no­logy, 136:5054 – 5060, 1995. (Autoim­mune Thyroiditis)

12) Many, M.C., Papa­do­pou­laous, J., Mar­tic, C., et al, Iodine indu­ced cell damage in mouse hyper­plas­tic thy­roid is asso­cia­ted to lipid pero­xi­da­tion. In: Gor­don A, Gross J, Hen­ne­nian G (eds) Pro­gress in Thy­roid Research. Pro­cee­dings of the 10^th Inter­na­tio­nal Thy­roid Con­fe­rence. Bal­kema, Rot­ter­dam, 635 – 638, 1991.

13) DeGroot Les­lie J., et al, Stu­dies on an Iodi­na­ting Enzyme from Calf Thy­roid. Endoc­ri­no­logy Vol. 76  p.632 – 645,1965.

14) Oker­lund, M.D., The Cli­ni­cal Uti­lity of Fluo­res­cent Scan­ning of the Thy­roid. In Medi­cal Appli­ca­tions of Fluo­res­cent Exci­ta­tion Analy­sis, Edi­tors Kauf­man and Price, CRC Press, Boca Raton Flo­rida, pg 149 – 160, 1979.

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