CS- Why did you drop the 7-hmr lignans?

Just curious because I wasn't taking them either (as you said they were unnecessary on dutasteride), but I just found a bottle stashed away and was considering taking them again. I notice that not only did they drop from your top 6, but you don't list them under your ancillary supplements either.

JHarsh80 - Here's an older thread on this.

https://immortalhair.forumotion.com/natural-hair-regrowth-forum-f1/hmr-lignans-why-was-it-dropped-t784.htm

Perfect... thanks. I asked my Dr. about why she has taken my mom (Hashimoto's) off of her multi's with iodine. She printed up this document that I just scanned to a .pdf. If you could take a look at it I would appreciate your feedback. The part about Iodine and Autoimmune Thyroid is on page 11/14. Right off the bat this Dr. Datis Kharrazian (www.datiskharrazian.com) states that inadequate iodine is not the leading cause of hypothyroidism; it is hashimoto's. There was no reference page for the works cited throughout, but I will ask her for it. Thanks CS.... Here it is http://www.mediafire.com/?ktjmxnrnygz

JHarsh80 - Okay, here is my counter. I highlighted in a section in this text that drives the main point, although this entire paste could be read to get the full picture. In a nutshell, iodized salt is linked to Hashimoto's yet when real quantities of iodine/iodide in the form of Lugol's solution were used prior to iodization of salt, there were no reported cases of Hashimoto's. Additionally, as stated in other threads, Guy E. Abraham's colleague, Dr. Brownstein has found his patients with Hashimoto's are not only low in iodine, they get better when they take real amounts, per Lugol's like preparations. Brownstein explains that while some medical text cautions against iodine and Hashimoto's his results in real patients is the opposite finding.

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 10th 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.

Thanks a million CS, this is just what I need! Hopefully I can convince the Dr to at least look into Abraham and Browstein's work further. I know doctors typically can't stand to be told they could be wrong by patients. No one seems to want to listen to you without specific letters after your name these days