Iritu1021
Breaking Through The Fog
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- 586
Over the last few months, there were several of us who have failed miserably on high dose T3 or NDT, made quite remarkable improvement after working ourselves up slowly to full replacement doses of T4 (which also required some initial adjustment period). At least one person I know of even had elevated rT3 and still did better on T4 than on T3 which goes completely against the grain of current alternative thyroid theories. We have already talked plenty about how TSH is essentially useless when it comes to determining response to the thyroid.
I've written quite a bit about T1AM before both on this forum and on my website but this is a new article that really reaffirms my interest in this - because it tells you that overproduction of T1AM (likely related to gut microflora) can impair thyroid synthesis without effect on hypothalamic-pituitary-thyroid axis. It also affects intracellular calcium which could explain many of the common CFS symptoms.
I really hope someone studies this hormone more in CFS population. I'm posting the complete abstract of the article below. The reason why T3 didn't work for us the way it works for regular hypothyroid patients could be that while it is more effective, it is also more likely to upregulate T1AM (that's a speculation on my part, there could be many other reasons of course, such as CNS preference for T4).
3-Iodothyronamine Decreases Expression of Genes Involved in Iodide Metabolism in Mouse Thyroids and Inhibits Iodide Uptake in PCCL3 Thyrocytes.
Schanze N1,2, Jacobi SF2,3, Rijntjes E1, Mergler S4, Del Olmo M1, Hoefig CS1,2, Khajavi N3, Lehmphul I1, Biebermann H3, Mittag J2,5, Köhrle J1.
Author information
Abstract
BACKGROUND:
3-Iodothyronamine (3-T1AM) is an endogenous decarboxylated thyroid hormone (TH) metabolite. Pharmacological doses of 3-T1AM decrease heart rate, body temperature, and metabolic rate in rodents-effects that are contrary to classic TH excess. Furthermore, a single dose of 3-T1AM was shown to suppress the hypothalamic-pituitary-thyroid (HPT) axis in rats. It was hypothesized that 3-T1AM might play a role in the fine-tuning of TH action and might have a direct regulatory effect on the thyroid gland.
METHODS:
This study tested whether repeated 3-T1AM treatment interfered with thyroid function and the HPT axis in mice. Therefore, male C57BL/6 mice were intraperitoneally injected with 5 mg/kg of 3-T1AM or vehicle daily for seven days. Additionally, the effects of 3-T1AM on the differentiated rat thyrocyte cell line PCCL3 were analyzed.
RESULTS:
Repeated administration of 3-T1AM decreased thyroidal mRNA content of the sodium iodide symporter (Nis), thyroglobulin, and pendrin in mice. No interference with the HPT axis was observed, as determined by unaltered pituitary mRNA levels of triiodothyronine-responsive genes, including thyrotropin subunit β. Furthermore, 3-T1AM treatment did not change transcript levels of hepatic triiodothyronine-responsive genes, such as deiodinase 1. In line with this, serum TH concentrations were not changed after the treatment period of seven days. In concordance with the in vivo findings, 3-T1AM decreased the thyrotropin-dependent expression of Nis and functional iodide uptake in PCCL3 cells in vitro. Additionally, uptake and metabolism of 3-T1AM by PCCL3 cells was observed, as well as 3-T1AM-dependent changes in intracellular Ca2+ concentration that might be involved in mediating the reported effects.
CONCLUSIONS:
In conclusion, 3-T1AM application decreased expression of selected TH synthesis genes by acting directly on the thyroid gland, and it might therefore affect TH synthesis without involvement of the HPT axis.
@BadBadBear, @drob31, @debored13, @pattismith, @Hip
I've written quite a bit about T1AM before both on this forum and on my website but this is a new article that really reaffirms my interest in this - because it tells you that overproduction of T1AM (likely related to gut microflora) can impair thyroid synthesis without effect on hypothalamic-pituitary-thyroid axis. It also affects intracellular calcium which could explain many of the common CFS symptoms.
I really hope someone studies this hormone more in CFS population. I'm posting the complete abstract of the article below. The reason why T3 didn't work for us the way it works for regular hypothyroid patients could be that while it is more effective, it is also more likely to upregulate T1AM (that's a speculation on my part, there could be many other reasons of course, such as CNS preference for T4).
3-Iodothyronamine Decreases Expression of Genes Involved in Iodide Metabolism in Mouse Thyroids and Inhibits Iodide Uptake in PCCL3 Thyrocytes.
Schanze N1,2, Jacobi SF2,3, Rijntjes E1, Mergler S4, Del Olmo M1, Hoefig CS1,2, Khajavi N3, Lehmphul I1, Biebermann H3, Mittag J2,5, Köhrle J1.
Author information
Abstract
BACKGROUND:
3-Iodothyronamine (3-T1AM) is an endogenous decarboxylated thyroid hormone (TH) metabolite. Pharmacological doses of 3-T1AM decrease heart rate, body temperature, and metabolic rate in rodents-effects that are contrary to classic TH excess. Furthermore, a single dose of 3-T1AM was shown to suppress the hypothalamic-pituitary-thyroid (HPT) axis in rats. It was hypothesized that 3-T1AM might play a role in the fine-tuning of TH action and might have a direct regulatory effect on the thyroid gland.
METHODS:
This study tested whether repeated 3-T1AM treatment interfered with thyroid function and the HPT axis in mice. Therefore, male C57BL/6 mice were intraperitoneally injected with 5 mg/kg of 3-T1AM or vehicle daily for seven days. Additionally, the effects of 3-T1AM on the differentiated rat thyrocyte cell line PCCL3 were analyzed.
RESULTS:
Repeated administration of 3-T1AM decreased thyroidal mRNA content of the sodium iodide symporter (Nis), thyroglobulin, and pendrin in mice. No interference with the HPT axis was observed, as determined by unaltered pituitary mRNA levels of triiodothyronine-responsive genes, including thyrotropin subunit β. Furthermore, 3-T1AM treatment did not change transcript levels of hepatic triiodothyronine-responsive genes, such as deiodinase 1. In line with this, serum TH concentrations were not changed after the treatment period of seven days. In concordance with the in vivo findings, 3-T1AM decreased the thyrotropin-dependent expression of Nis and functional iodide uptake in PCCL3 cells in vitro. Additionally, uptake and metabolism of 3-T1AM by PCCL3 cells was observed, as well as 3-T1AM-dependent changes in intracellular Ca2+ concentration that might be involved in mediating the reported effects.
CONCLUSIONS:
In conclusion, 3-T1AM application decreased expression of selected TH synthesis genes by acting directly on the thyroid gland, and it might therefore affect TH synthesis without involvement of the HPT axis.
@BadBadBear, @drob31, @debored13, @pattismith, @Hip
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