Re: 3rd follow up with Dr. Spurlock

[Guest guest]

That's a good reminder about taking with food, and good to hear that you've not

had problems. At least it's not like waiting 6 weeks to find out if your porcine

T4 increase was too much.

I was wondering what amount to decrease my P-thyroid, and the .50 grain he

suggested to you seems appropriate, since 1.0 grain of Armour has 9mcg of T3, so

the Cytomel at 5mcg would replace about half that. He wasn't as specific with me

and I was going to call him about it. I guess I should anyway.

I didn't tolerate the time release cortisol, so I don't think he'd do time

release T3 for me. But can you tell me what the " MC " in the description on my

bottle shown below means? The capsules were compounded at Abrams Royal Pharmacy.

When they did the time release cortisol, it said " TR " in the description. I hope

what I have is like yours and not time release. I should call them.

" T3-MC capsule "

I guess this will be a new type of transition challenge, as T4 serum levels will

drop off over time when my P-thyroid is replaced by T3. I don't like the idea of

going through any more swings. However, I guess the T3 can be added faster if I

crash too much, and then can be stopped quickly, if I get too buzzed. I think he

wanted me to do this transition faster, but I just don't know. I think I will

have to go more slowly. If the long term means finally getting my T3 levels up

to where they need to be, and feeling better, it will be worth it.

Do keep us posted on how it goes over the next few weeks. I am interested in

whether you notice any sense of a slide developing when the T4 levels go down,

and whether T3 increases take care of it.

Thanks for the helpful info.

>

>

> I, too, had jitters about starting the Cytomel, but have had no problem

> increasing to 25 mcg rather quickly. I do take it with food, so that

> slows down the absorption. I also divide it into three doses.

>

> I will stay at this dose for 6-8 weeks, so that we can have accurate

> Free T4 and TSH levels. As a thyca patient, I am also concerned about

> possibly coming out if suppression in the process. We last saw a

> measurable TSH when I was on 225 mcg of $ynthroid.

>

[Guest guest]

He did not suggest a particular amount to reduce my thyroid when adding the Cytomel. I did the math myself. 30 mg of thyroid contains 4.5 mcg of T3. So that is the logical amount to reduce by when adding 5 mcg of Cytomel. I do not think the Cytomel is as strong as the T3 in Armour. He told me not to take it at night, but that is not possible for me, as I need some T3 after 7pm to keep me breathing all night. I actually just took my last dose at about 10:00pm. I take it in three doses.

I do not know what the "MC" designation means. Do you know what filler you got?

> >> > > > I, too, had jitters about starting the Cytomel, but have had no problem> > increasing to 25 mcg rather quickly. I do take it with food, so that> > slows down the absorption. I also divide it into three doses.> > > > I will stay at this dose for 6-8 weeks, so that we can have accurate> > Free T4 and TSH levels. As a thyca patient, I am also concerned about> > possibly coming out if suppression in the process. We last saw a> > measurable TSH when I was on 225 mcg of $ynthroid.> >>

[Guest guest]

I'm pretty sure the MC means time release. Mine is also filled at Abrams Royal and it is time release and reads the same way. They told me they use sodium bicarb as their standard filler. I LOVE how tiny the little capsules are. However, I have three different compounded meds from them and they all look the same, which could lead to confusion when using a daily med minder.I am doing well on all T3 with no T4 for over 6 weeks now. But I'm paying close attention to the next few weeks as my T4 levels could be dropping. I haven't had blood work yet.Grace

He did not suggest a particular amount to reduce my thyroid when adding the Cytomel. I did the math myself. 30 mg of thyroid contains 4.5 mcg of T3. So that is the logical amount to reduce by when adding 5 mcg of Cytomel. I do not think the Cytomel is as strong as the T3 in Armour. He told me not to take it at night, but that is not possible for me, as I need some T3 after 7pm to keep me breathing all night. I actually just took my last dose at about 10:00pm. I take it in three doses. I do not know what the "MC" designation means. Do you know what filler you got?> >> > > > I, too, had jitters about starting the Cytomel, but have had no problem> > increasing to 25 mcg rather quickly. I do take it with food, so that> > slows down the absorption. I also divide it into three doses.> > > > I will stay at this dose for 6-8 weeks, so that we can have accurate> > Free T4 and TSH levels. As a thyca patient, I am also concerned about> > possibly coming out if suppression in the process. We last saw a> > measurable TSH when I was on 225 mcg of $ynthroid.> >>

[Guest guest]

No, I will clarify with Abrams Royal this week.

>

>

> He did not suggest a particular amount to reduce my thyroid when adding

> the Cytomel. I did the math myself. 30 mg of thyroid contains 4.5 mcg of

> T3. So that is the logical amount to reduce by when adding 5 mcg of

> Cytomel. I do not think the Cytomel is as strong as the T3 in Armour. He

> told me not to take it at night, but that is not possible for me, as I

> need some T3 after 7pm to keep me breathing all night. I actually just

> took my last dose at about 10:00pm. I take it in three doses.

>

> I do not know what the " MC " designation means. Do you know what filler

> you got?

>

[Guest guest]

I have to wonder if the difference you notice between the T3 in Cytomel and Armour isn't more due to the fact that you are not getting the T2 and T1 that are also found in Armour.  I could not find human studies, but I did find a mouse study that showed that T2 got into the tissue very quickly as compared to T3. 

Here's a very interesting, recent research article on T2 and lipid handling:http://www.ncbi.nlm.nih.gov/pubmed/20625286The article notes that there are clinical trials underway for synthetic T2.

Here's another (rat study) that discusses the activity of T2 at the mitochondrial level:http://www.ncbi.nlm.nih.gov/pubmed/19464748 B.

 

He did not suggest a particular amount to reduce my thyroid when adding the Cytomel. I did the math myself. 30 mg of thyroid contains 4.5 mcg of  T3. So that is the logical amount to reduce by when adding 5 mcg of Cytomel. I do not think the Cytomel is as strong as the T3 in Armour. He told me not to take it at night, but that is not possible for me, as I need some T3 after 7pm to keep me breathing all night. I actually just took my last dose at about 10:00pm. I take it in three doses.

I do not know what the " MC " designation means. Do you know what filler you got?

> >> > > > I, too, had jitters about starting the Cytomel, but have had no problem> > increasing to 25 mcg rather quickly. I do take it with food, so that> > slows down the absorption. I also divide it into three doses.

> > > > I will stay at this dose for 6-8 weeks, so that we can have accurate> > Free T4 and TSH levels. As a thyca patient, I am also concerned about> > possibly coming out if suppression in the process. We last saw a

> > measurable TSH when I was on 225 mcg of $ynthroid.> >>

[Guest guest]

There are only trace amounts of the three T2s in Armour. T2 is mainly produced through peripheral conversion, so you might get as much T2 from eating meat, especially raw or rare meat, as you do from Armour.

I would be interested in laying my hands on some real T2. It used to be available on some of the bodybuilder sites. They now sell a supplement that they call "T2" but it bears no relation to the real thing.

Since I take all of my meds with food, including dairy, I would postulate that the synthetic thyroid hormone is more readily bound than that in Armour. The hormone in Armour is already bound to a protein. Contrary to what most folks think, I consider it desirable to have a lot of bound thyroid hormone in my system. That is the only way I can get some iodine in my system without activating my quarter of a thyroid gland and any possible thyroid cancer.

> > > >> > > >> > > > I, too, had jitters about starting the Cytomel, but have had no problem> > > > increasing to 25 mcg rather quickly. I do take it with food, so that> > > > slows down the absorption. I also divide it into three doses.> > > >> > > > I will stay at this dose for 6-8 weeks, so that we can have accurate> > > > Free T4 and TSH levels. As a thyca patient, I am also concerned about> > > > possibly coming out if suppression in the process. We last saw a> > > > measurable TSH when I was on 225 mcg of $ynthroid.

[Guest guest]

I think this may be what you’re looking for: http://www26.netrition.com/san_t2_xtreme.html Other sources sell it, but I saved this link because it had the best price when I was looking at the product. From: Texas_Thyroid_Groups [mailto:Texas_Thyroid_Groups ] On Behalf Of texasthyroidSent: Tuesday, 30 November, 2010 11:09To: Texas_Thyroid_Groups Subject: Re: 3rd follow up with Dr. Spurlock There are only trace amounts of the three T2s in Armour. T2 is mainly produced through peripheral conversion, so you might get as much T2 from eating meat, especially raw or rare meat, as you do from Armour.I would be interested in laying my hands on some real T2. It used to be available on some of the bodybuilder sites. They now sell a supplement that they call " T2 " but it bears no relation to the real thing.Since I take all of my meds with food, including dairy, I would postulate that the synthetic thyroid hormone is more readily bound than that in Armour. The hormone in Armour is already bound to a protein. Contrary to what most folks think, I consider it desirable to have a lot of bound thyroid hormone in my system. That is the only way I can get some iodine in my system without activating my quarter of a thyroid gland and any possible thyroid cancer.> > > >> > > >> > > > I, too, had jitters about starting the Cytomel, but have had no problem> > > > increasing to 25 mcg rather quickly. I do take it with food, so that> > > > slows down the absorption. I also divide it into three doses.> > > >> > > > I will stay at this dose for 6-8 weeks, so that we can have accurate> > > > Free T4 and TSH levels. As a thyca patient, I am also concerned about> > > > possibly coming out if suppression in the process. We last saw a> > > > measurable TSH when I was on 225 mcg of $ynthroid.

[Guest guest]

Sorry, I was too quick to click send. There’s also another product, but it has half the 3,5 T-2 compared to SanT2Extreme: http://www26.netrition.com/iforce_tt_33.html It’s also available on Amazon.com as a Subscribe and Save item at a slightly higher cost, but if you use S & S, there are no shipping charges. 3,5 is alleged to be the active fat-burning hormone, so I don’t entirely understand why 3,3’ is included in both products. There is a ton of articles in PubMed about 3,5 T2 and 3,3’ T2, but I took the below abstracts from elsewhere, which is why there are no links. Separately, there’s this one, which is entitled “Specific binding sites for 3,3'-diiodo-L-thyronine (3,3'-T2) in rat liver mitochondria”: http://www.ncbi.nlm.nih.gov/pubmed/8082770 The competition study results were interesting. 3,3'-Diiodothyronine (3,3'-T2) 1: Metabolism. 1978 Jun;27(6):677-83.Click here to read Links Failure of 3,3'-diiodothyronine administration to alter TSH and prolactin responses to TRH stimulation. In order to determine whether elevations in serum 3,3'-diiodothyronine (3,3'T2) concentrations influence the hypothalamic-pituitary--thyroid axis, thyrotropin (TSH) and prolactin responses to thyrotropin-releasing hormone (TRH) were assessed in five patients both prior to and during 3,3'T2 administration. Mean (+/- SE) peak TSH responses to TRH were 168 +/- 64 microU/ml during 3,3'T2 administration and 168 +/- 65 muU/ml during 3,3'T2 administration.Mean basal and peak prolactin concentrations after TRH were 6 +/- 3 ng/ml and 54 +/- 26 ng/ml, whereas during 3,3'T2 administration the basal and peak prolactin levels were 6 +/- 2 ng/ml and 55 +/- 28 ng/ml, respectively. Hypothyroid rats administered triiodothyronine (10 migrogram b.i.d.) for 5 days had a mean TSH response to TRH stimulation of 0.051 +/- 0.003 mU/ml, whereas rats to whom saline or 3,3'T2 (50 microgram b.i.d.) had been given for the same time interval had mean TRH-induced TSH responses of 1.127 +/- 0.179 mU/ml and 1.324 +/- 0.286 mU/ml, respectively. None of the TSH or prolactin responses to TRH, in either human or rat studies, were apparently altered by 3,3'T2. These observations suggest that elevation of serum 3,3'T2 levels are not associated with alterations in the hypothalamic--pituitary--thyroid axis in the experimental systems employed.PMID: 418309 [PubMed - indexed for MEDLINE]Uptake of triiodothyronine and triiodothyroacetic acid in neonatal rat cardiomyocytes: effects of metabolites and analogs. Department of Internal Medicine, Erasmus University Medical School, Rotterdam, The Netherlands. Cellular and nuclear uptake of [125I]tri-iodothyronine (T3) and [125I]triiodothyroacetic acid (Triac) were compared in cardiomyocytes of 2-3 day old rats, and the effect of thyroid hormone analogs on cellular T(3) uptake was measured. Cells (5-10 x 10(5) per well) were cultured in DMEM-M199 with 5% horse serum and 5% FCS. Incubations were performed for from 15 min to 24 h at 37 degrees C in the same medium, 0.5% BSA and [125I]T3 (100 pM), or [125I]Triac (240 pM). Expressed as % dose, T(3) uptake was five times Triac uptake, but expressed as fmol/pM free hormone, Triac uptake was at least 30% (P<0.001) greater than T3 uptake, whereas the relative nuclear binding of the two tracers was comparable. The 15 min uptake of [125I]T3 was competitively inhibited by 10 microM unlabeled T3 (45-52%; P<0.001) or 3,3'- diiodothyronine (T2) (52%; P<0.001), and to a smaller extent by thyroxine (T(4)) (27%; 0.05We conclude that i) Triac is taken up by cardiomyocytes; ii) 3,3'-T2 and, to a lesser extent, DITPA and T4 interfere with plasma membrane transport of T3, whereas 3,5-T2, Triac, or Tetrac do not; iii) the transport mechanism for Triac is probably different from that for T3.PMID: 12010632 [PubMed - indexed for MEDLINE] 3,3'-Diiodothyronine concentrations in the sera of patients with nonthyroidal illnesses and brain tumors and of healthy subjects during acute stress.Department of Radiology, Universitatsklinikum lin, Free University of Berlin, Germany.In this article we describe the development of a highly sensitive, accurate, and reproducible RIA for the measurement of 3,3'-diiodothyronine (3,3'-T2) in human serum and brain tissue. The detection limits were 1.8 fmol/g and 1.5 pmol/L in human brain tissue and serum, respectively. Serum concentrations of 3,3'-T2 were measured in 4 groups of patients with nonthyroidal illnesses (NTI), i.e. brain injuries (n = 15), sepsis (n = 24), liver disease (n = 22), and brain tumors (n = 23). The mean serum concentration of 3,3'-T2 in 62 healthy controls was 46.6 +/- 20.0 pmol/L. 3,3'-T2 levels declined significantly with increasing age. They were significantly lower in patients with brain injury (34.2 +/- 19.4 pmol/L; P = 0.006), were at the upper limit of normal in patients with sepsis (57.0 +/- 36.9 pmol/L; P = 0.06), and were elevated in patients with liver disease (72.6 +/- 56.7 pmol/L; P = 0.04) and brain tumors (89.0 +/- 40.9 pmol/L; P = 0.01). The serum levels of T3 were significantly lower than those in controls in all 4 patient groups. Serum concentrations of 3,3'-T2 were significantly enhanced in 9 patients with hyperthyroidism (85.4 +/- 43.0 pmol/L; P = 0.01) and were reduced in 12 patients with hypothyroidism (14.9 +/- 9.2 pmol/L; P = 0.001). In both normal brain tissue, obtained either intraoperatively or excised postmortem, and brain tumors, the concentrations of 3,3'-T2 ranged between 50-300 fmol/g. In healthy controls, 2 different forms of acute stress (sleep deprivation and delivering a lecture) significantly increased serum levels of T4 and T3, but did not affect those of 3,3'-T2 or 3,5-T2. In conclusion, our results show that, contrary to expectation, a low T3 syndrome in NTI is not always associated with low serum concentrations of 3,3'-T2. The production of 3,3'-T2 in NTI seems to be regulated in a disease-specific manner, resulting in unchanged, reduced, or elevated hormone concentrations. PMID: 9745405 [PubMed - indexed for MEDLINE] Effect of 3,5-diiodo-L-thyronine on thyroid stimulating hormone and growth hormone serum levels in hypothyroid rats. Dipartimento di Chimica, Facolta di Scienze, Universita degli Studi di Salerno, Italy. We have investigated the biological effects of physiological doses of 3,5-diiodo-L-thyronine (3,5-T2) and 3,3'-diiodo-L-thyronine (3,3'-T2) (at doses from 2.5 to 10 microg/100 g BW) on serum TSH and GH levels in rats made hypothyroid by propylthiouracil and iopanoic acid administration. In such animals deiodinase activities were inhibited and thyroid hormones serum levels strongly reduced. The effects of T2s were compared with those elicited by 3,5,3'-triiodo-L-thyronine (T3) (2.5 microg/100 g BW).The serum TSH level was much greater in hypothyroid rats than in euthyroid ones. T3 administration suppressed TSH by 88% compared to control (i.e, the level in hypothyroid rats); it thus reached a value not significantly different from that seen in the euthyroid rats. 3,5-T2 produced a similar effect, suppressing the TSH level by about 75% compared to control; it thus reached values not significantly different from those of the euthyroid and T3-treated rats. By contrast, 3,3'-T2 had no effect on TSH, whatever the dose. The serum GH level was much lower in hypothyroid rats than in euthyroid ones. T3 administration increased the GH level by about 5-fold, restoring it to the value seen in euthyroid rats. 3,5-T2-treated hypothyroid rats, at all the doses used (from 2.5 to 10 microg/100 g BW), showed increased serum GH levels: at a dose of 10 microg/100 g BW the level reached a value about 5-fold higher than that in hypothyroid rats. This value was not significantly different from those of euthyroid and T3-treated rats. 3,3'-T2 did not affect GH levels whatever the dose. Thus, 3,5-T2 (but not 3,3'-T2) seems to mimic the effects of T3 on serum TSH and GH levels in rats.PMID: 9651103 [PubMed - indexed for MEDLINE]Interaction of diiodothyronines with isolated cytochrome c oxidase. Dipartimento di Fisiologia Generale ed Ambientale, Universita degli Studi di Napoli Federico II, Italy. Diiodothyronines (3,3'-T2 and 3,5-T2) stimulate the activity of isolated cytochrome c oxidase (COX) from bovine heart mitochondria. Maximal stimulation of activity (about 50%) is obtained with 3,3'-T2 at pH 6.4 and with 3,5-T2 at pH 7.4. In contrast, 3,5,3'-triiodothyronine (T3) exhibited no or little stimulation of COX activity. Binding of the hormones to COX leads to conformational changes as shown by modified visible spectra of the oxidized enzyme. It is suggested that 'short-term' effects of thyroid hormones on mitochondrial respiration are at least partly due to the allosteric interaction of diiodothyronines with the COX complex. PMID: 8013649 [PubMed - indexed for MEDLINE] Effect of 3,3'-di-iodothyronine and 3,5-di-iodothyronine on rat liver mitochondria. Dipartimento di Fisiologia Generale ed Ambientale, Universita di Napoli, Italy. In the present study we report that 3,3',5-tri-iodothyronine (T3) as well as two iodothyronines (3,5-di-iodothyronine (3,5-T2) and 3,3'-di-iodothyronine (3,3'-T2)) significantly influence rat liver mitochondrial activity. Liver oxidative capacity (measured as cytochrome oxidase activity/g wet tissue) in hypothyroid compared with normal rats was significantly reduced (21%, P > 0.01) and the administration of T3 and both iodothyronines restored normal values. At the mitochondrial level, treatment with T3 stimulated respiratory activity (state 4 and state 3) and did not influence cytochrome oxidase activity. On the other hand, both the mitochondrial respiratory rate and specific cytochrome oxidase activity significantly increased in hypothyroid animals after treatment with 3,3'-T2 or 3,5-T2 (about 50 and 40% respectively). The actions of both iodothyronines were rapid and evident by 1 h after the injection. The hepatic mitochondrial protein content which decreased in hypothyroid rats (9.6 mg/g liver compared with 14.1 in normal controls, P < 0.05) was restored by T3 injection, while neither T2 was able to restore it. Our results suggest that T3 and both iodothyronines have different mechanisms of action. T3 acts on both mitochondrial mass and activity; the action on mitochondrial activity was not exerted at the cytochrome oxidase complex level. The action of the iodothyronines, on the other hand, is exerted directly on the cytochrome oxidase complex without any noticeable action on the mitochondrial mass. PMID: 8381457 [PubMed - indexed for MEDLINE] Effect of 3,3'-diiodothyronine and 3,5-diiodothyronine on rat liver oxidative capacity. Department of General and Environmental Physiology, University of Naples, Italy. We report that 3,5,3'-triiodothyronine (T3) as well as two other iodothyronines (3,3'-diiodothyronine and 3,5-diiodothyronine (T2s)) stimulate rat liver oxidative capacity (measured as cytochrome oxidase activity (COX)). In hypothyroid rats COX activity and mitochondrial protein content are significantly lower than in normal control animals. The administration of both T3 and T2s to hypothyroid rats significantly enhances hepatic COX activity with T3 having the greatest effect (+60%); moreover, T3 restores the mitochondrial protein content whereas the T2s are ineffective. Administration of T2s results in a faster stimulation (already significant 1 h after the injection) of hepatic COX activity than T3 injection. Our results suggest that T3 acts on the protein synthesis mechanism involved in the regulation of the mitochondrial mass while T2s would act directly at the mitochondrial level. PMID: 1324858 [PubMed - indexed for MEDLINE] Serum concentrations of 3, 3'-diiodothyronine, 3', 5'-diiodothyronine, and 3, 5-diiodothyronine in altered thyroid states. To investigate the thyroid hormone metabolism in altered states of thyroid function, serum concentrations of 3, 3'-diiodothyronine (3, 3'-T2), 3', 5'-T2 and 3, 5-T2 as well as T4, T3 and rT3 were determined by specific radioimmunoassays in 17 hyperthyroid and 10 hypothyroid patients, before and during the treatment. Serum T4, T3, rT3, 3, 3'-T2 and 3', 5'-T2 concentrations were all higher in the hyperthyroid patients than in age-matched controls and decreased to the normal ranges within 3 to 4 months following treatment with antithyroid drugs. In the hypothyroid patients, these iodothyronine concentrations were lower than in age-matched controls and returned to the normal ranges after 2 to 3 months treatment with T4. In contrast, serum 3, 5-T2 concentrations in hyperthyroid patients (mean +/- SE : 4.0 +/- 0.5 ng/dl) were not significantly different from those in controls (3.9 +/ 0.4 ng/dl), although they tended to decrease in 3 of 6 patients after the antithyroid drug therapy. Serum 3, 5-T2 levels in the hypothyroid patients (3.8 +/- 0.6 ng/dl) were also within the normal range and showed no significant change following the T4 replacement therapy. However, serum 3, 5-T2 as well as 3, 3'T2 concentrations rose significantly with a marked rise in serum T3 following T3 administration, 75 micrograms/day for 7 days, in Graves' patients in euthyroid state.(ABSTRACT TRUNCATED AT 250 WORDS) PMID: 6641638 [PubMed - indexed for MEDLINE] Immediate opposite effect of salicylate on thyroxine and 3,5,3'-triiodothyronine versus 3,3',5'-triiodothyronine level in plasma in rats. * Langer P, * Foldes O, * Brozmanova H, * Straussova K, * Gschwendtova K. In a total of 46 male rats polyethylene tubings were introduced into femoral artery and vein under pentobarbiturate anesthesia. Then heparin (300 U kg-1) was injected at 60-90 min after pentobarbiturate and two control blood samples were subsequently taken. After that sodium salicylate (200 mg kg-1) was injected i.v. and blood samples were taken at 30-420 min later. An immediate decrease of the thyroxine (T4) level in plasma to about 20% of original level and that of 3,5,3'-triiodothyronine (T3) to about 60% of that was found, while the level of 3,3',5'-triiodothyronine (rT3) was increased 20%. It was concluded that the administration of salicylate results in an immediate displacement of T4 and T3 from plasma protein binding and possibly inhibits the conversion of T4 to T3 and of rT3 to 3,3'-diiodothyronine which results in an increase of rT3 level in plasma. This might by partially prevented by an inhibiting effect of salicylate on the binding of rT3 to plasma proteins. From: Rhonda Lea Kirk Fries Sent: Tuesday, 30 November, 2010 11:47To: 'Texas_Thyroid_Groups 'Subject: RE: Re: 3rd follow up with Dr. Spurlock I think this may be what you’re looking for: http://www26.netrition.com/san_t2_xtreme.html Other sources sell it, but I saved this link because it had the best price when I was looking at the product. From: Texas_Thyroid_Groups [mailto:Texas_Thyroid_Groups ] On Behalf Of texasthyroidSent: Tuesday, 30 November, 2010 11:09To: Texas_Thyroid_Groups Subject: Re: 3rd follow up with Dr. Spurlock There are only trace amounts of the three T2s in Armour. T2 is mainly produced through peripheral conversion, so you might get as much T2 from eating meat, especially raw or rare meat, as you do from Armour.I would be interested in laying my hands on some real T2. It used to be available on some of the bodybuilder sites. They now sell a supplement that they call " T2 " but it bears no relation to the real thing.Since I take all of my meds with food, including dairy, I would postulate that the synthetic thyroid hormone is more readily bound than that in Armour. The hormone in Armour is already bound to a protein. Contrary to what most folks think, I consider it desirable to have a lot of bound thyroid hormone in my system. That is the only way I can get some iodine in my system without activating my quarter of a thyroid gland and any possible thyroid cancer.> > > >> > > >> > > > I, too, had jitters about starting the Cytomel, but have had no problem> > > > increasing to 25 mcg rather quickly. I do take it with food, so that> > > > slows down the absorption. I also divide it into three doses.> > > >> > > > I will stay at this dose for 6-8 weeks, so that we can have accurate> > > > Free T4 and TSH levels. As a thyca patient, I am also concerned about> > > > possibly coming out if suppression in the process. We last saw a> > > > measurable TSH when I was on 225 mcg of $ynthroid.

[Guest guest]

This is really interesting. Is the same true for T3, for example, could you get

some T3 from eating raw liver since that is where is it mostly produced (IIRC)?

Also an endo told me not to worry about not getting calcitonin (I am on

Synthroid but was wanting to go on Armour) because different cells in the

thyroid make calcitonin, not the same cells that make T4 and T3, so those cells

probably weren't involved in the autoimmune attack. Sounds logical to me... do

you think that is correct?

>

>

> There are only trace amounts of the three T2s in Armour. T2 is mainly

> produced through peripheral conversion, so you might get as much T2 from

> eating meat, especially raw or rare meat, as you do from Armour.

[Guest guest]

T2 is actually a thyroid hormone and may lower your TSH.

> > > > > >> > > > > >> > > > > > I, too, had jitters about starting the Cytomel, but have had no> > problem> > > > > > increasing to 25 mcg rather quickly. I do take it with food, so that> > > > > > slows down the absorption. I also divide it into three doses.> > > > > >> > > > > > I will stay at this dose for 6-8 weeks, so that we can have accurate> > > > > > Free T4 and TSH levels. As a thyca patient, I am also concerned> > about> > > > > > possibly coming out if suppression in the process. We last saw a> > > > > > measurable TSH when I was on 225 mcg of $ynthroid.> >>