High TSH, Low T4 Could Rebuild Thyroid Tissue?

Isadora

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According to this (stunning) article summary, people who had their thyroids (partially) removed could benefit from high TSH level, as TSH rebuilds thyroid tissue... :eek:

So they take them off levothyroxine (T4) in order to achieve thyroid reconstruction and the results are pretty amazing!

So... maybe my doctors are right in insisting that I let my TSH go as far as 10 in the hope that my thyroid might regain full function on its own? Would you interpret things in that manner? Or is it wishful thinking on my part?

In this case, I don't know, maybe some of you who are suffering from Hashimoto's might consider not supplementing, after all? And the Peatian thyroid optimization might not be the ideal thing to do under such circumstances?

I'll try to find the full text, for now, here is the abstract:

Influence of the endogene TSH stimulation of thyroid volume increase in the patients after total thyroidectomy due to differentiated thyroid cancer
[Article in Polish]
Pietz L, Michałek K, Waśko R, Ruchała M, Sowiński J.
Source
Katedra i Klinika Endokrynologii, Przemiany Materii i Chorób Wewnetrznych, Uniwersytet Medyczny im Karola Marcinkowskiego, Poznan, Poland. endosk2@amp.edu.pl

Abstract
INTRODUCTION:
The treatment-of-choice for differentiated thyroid carcinoma (DTC) is a total thyroidectomy with subsequent radioiodine therapy. In order to increase an iodine uptake in thyroid tissue remnants, the L-thyroxine withdrawal is required. It is recommended to achieve TSH levels higher than 25 mU/ml. As TSH is a known key factor in thyroid cell proliferation regulation, prolonged stimulation of the cells during L-thyroxine withdrawal can be a causative factor for a re-growth. Our aim was to assess the degree of thyroid re-growth in the patients after total thyroidectomy due to DTC and its possible clinical implications.

MATERIAL AND METHODS:
23 patients operated due to papillary and follicular thyroid cancer were included into the study. Biochemical determinations and ultrasound thyroid imaging were performed (TSH, Tg) during suppressive L-thyroxine therapy as well as 4-5 weeks after the withdrawal.

RESULTS:
The mean volume of thyroid tissue remnants increased after withdrawal for substantial 30.1%. The difference was extremely significant.


CONCLUSIONS:
L-Thyroxine withdrawal in the patients after total thyroidectomy due to DTC can cause re-growth of the tissue remnants. The phenomenon may be of a clinical significance in the selected cases influencing therapeutic decisions.

http://www.ncbi.nlm.nih.gov/pubmed/18465686
 
J

j.

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One thought is, if your life is too miserable without supplementation, supplement. Otherwise, try to do without it.
 
J

j.

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So when you supplement with thyroid, your thyroid gland doesn't regrow, right?
 

Isadora

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That's what it sounds like, j.... I would happily soldier on through some more (relatively) bad times if I knew that they are a price to pay to have my thyroid back, kicking at its own pace with healthy new cells replacing those that look like they're missing in action on ultrasounds, instead of relying on external combinations of T4/T3, always at the mercy of potential imbalances due to factors I cannot fully control (see the examples on this forum, thyroid storms, etc.)

I found another study, this time linking insulin, TSH and thyroid cell creation in dogs. This got me thinking, maybe my low insulin Paleo year contributed to my thyroid's destruction and this Peatian sugar-friendly diet will contribute to some serious rebuilding of my thyroid gland, hopefully. TSH and insulin, who would have thought...

The orchestration of these hormones is pure awesomeness... I am getting some high grade aesthetic pleasure from reading PubMed these days..:)

http://eje-online.org/content/140/1/94.long

Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells
Takao Kimura, Jacques E Dumont, Alfredo Fusco1 and Jacqueline Golstein

In the rat thyroid cell lines PC Cl3, FRTL-5 and WRT, proliferation is mainly regulated by insulin or IGF, and TSH. However, the mechanism regulating cell mass doubling prior to division is still unknown. Our laboratory has shown that in dog thyroid cells insulin promotes growth in size while TSH in the presence of insulin triggers DNA replication. In the absence of insulin, TSH has no effect on cell growth. In this report we investigated insulin action on both cell mass and DNA synthesis and its modulation by TSH and insulin in PC Cl3 and FRTL-5 cells. In PC Cl3 cells, insulin activated not only DNA synthesis but also protein synthesis and accumulation. Although TSH potentiated the stimulation of DNA synthesis induced by insulin, enhancement of protein synthesis by both agents was additive. All TSH effects were reproduced by forskolin. Similar effects were also obtained in FRTL-5 cells. This suggests that insulin and TSH, via cAMP, modulate both growth in size and DNA replication in these cell lines.
 

Isadora

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j. said:
Crazy thought: supplement with both thyroid and TSH?

TSH comes from the pituitary, I've never heard of it being ever supplemented. Peat views it as the "bad guy" that needs to be kept as low as possible. TSH signals the thyroid gland to produce more T4, which the liver turns into T3, which can be used by the body. When Peat or others here say they supplement with "thyroid", they mean T4 and/or T3 -- there are many "recipes". Introducing T4 in the body, the pituitary doesn't perceive a need for extra T4, so stops producing TSH -- which is simply the hormone bugging the thyroid to act and produce more T4.

Now I find out that the picture is more intricate, and TSH is also helping rebuild the thyroid gland in case something happened to it! And it makes SO MUCH SENSE! Of course it is the good guy, coming to the body's rescue and fixing things up.

Which is not what Peat sees it as, or he never mentioned this side of the picture in any of the papers I have read.

Food for thought for all the Hashis out there...

P.S.
kiran said:
And surprise, apparently such a thing exists!

Thyrogen (Thyrotropin alfa)
http://www.thyrogen.com/home/thy_home.asp

It's only used to check for resurgence of a thyroid cancer, so it's probably expensive.

Whoa, so they do make synthetic TSH! Interesting...

But I don't think I'd bother, especially that my own T4 and T3 production is within limits -- at least whenever I test for it, and my TSH has been steadily increasing and is now at a whopping 7! You know, sometimes I think that having access to all this testing is not a good thing... :) I would have been better off not knowing about the inner workings of my thyroid, much less stressed out... And my body would have done its job in silence, like it was programmed to... I won't mess with it anymore...
 
J

j.

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Now I wonder about pregnenolone. Pregnenolone can give you some of the same benefits of thyroid, because lack of thyroid reduces pregnenolone, so my question is, does pregnenolone reduce TSH as well?
 

Isadora

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j. said:
Now I wonder about pregnenolone. Pregnenolone can give you some of the same benefits of thyroid, because lack of thyroid reduces pregnenolone, so my question is, does pregnenolone reduce TSH as well?

I didn't know lack of thyroid reduces pregnenolone. If it does, then everything else is messed up with! From progesterone to estrogen to testosterone and aldosterone, the whole steroid chain is compromised. Hence, aches, pains, fatigue, etc. Yes, it makes sense...

Peat says that progesterone promotes thyroid... But if lack of thyroid involves a metabolic domino effect via all the steroids missing in action, does it really make sense to supplement with sex steroids in order to regain thyroid action? Chicken and egg kind of thing.

Whether pregnenolone reduces TSH... Hmm... What does it mean that "it can give you some of the same benefits of thyroid" -- does it promote T4 production? Or does Peat refer to perceived effects at a metabolical level -- more energy, etc.? So, if pregnenolone or its descendant, progesterone, impact production of T4 or T3, then yes, probably TSH is reduced.

Meanwhile, check this guy out, I had never heard of it, it has a funny name: FORSKOLIN... I am officially intrigued. In the study above, they say

All TSH effects were reproduced by forskolin.

I hope I can buy the stuff somewhere, before they patent it and sell it back to us for thousands of dollars a pop :)

Just kidding, but I am inclined to do some hacking there... Not before I read some more... Back to PubMed/Google Scholar.
 

jyb

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Isadora said:
I didn't know lack of thyroid reduces pregnenolone. If it does, then everything else is messed up with! From progesterone to estrogen to testosterone and aldosterone, the whole steroid chain is compromised. Hence, aches, pains, fatigue, etc. Yes, it makes sense...

If I'm correct yes, pregnelonone typically decreases with age as a result of low thyroid but I don't know the details. In any case you need cholesterol and retinol to make pregnelonone.
 
J

j.

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Isadora said:
Peat says that progesterone promotes thyroid... But if lack of thyroid involves a metabolic domino effect via all the steroids missing in action, does it really make sense to supplement with sex steroids in order to regain thyroid action? Chicken and egg kind of thing.

My impression is that Peat thinks that if the body is in a low energy state, it's hard to get out of that state, but if you help it with the appropriate supplement, it can get into a high energy state and in some situations continue in that state without supplements. So it's important to somehow just restore a high energy state.

I don't remember the where I read that, will post if I do.
 

Isadora

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It's a fine balance to strike if you play at the thyroid level, though... If people start from euthyroid and push up their levels of T4 and T3, then they risk hyperthyroidism which, to me at least, sounds worse than hypothyroidism. I mean, yeah, those guys lose weight like crazy, have huge metabolism, and their eyes are pushed out of their sockets because of an overactive thyroid -- so much so that doctors need to intervene with radiation or even worse, and push them into good ol' hypothyroidism before something bad happens to them.

I always wondered about that -- how come it's so hard to come down from too high a metabolic state caused by a thyroid in overdrive? Around here we seem to complain of low energy. If Graves folks became paleo, low carb couch potatoes, that should work, right?.. Theoretically, they could become euthyroid through diet. I never heard of anyone doing that, maybe it does happen.

Again, theoretically, thyroid should respond to diet. And not much else. And maybe both high TSH and low steroids serve a purpose. What could that be?

Let's say, an accident happens -- a saber toothed tiger caused a human a scratch on his or her :) neck, causing the thyroid to become out of commission for a while, as it heals. Or the paleo person I am talking about ate some huge amounts of goitrogenic food, like I did a year ago ( :oops: ). Good. There is less T4 and T3, the person becomes sluggish, she feels like she needs some rest. Her tribe lets her withdraw in a cave and feed her milk, oranges and honey; they also bring her the best pieces of game when they hunt -- organ meat. Bone both is served to her every day. Fine. She is on her way to recovery. She regains strength, little by little, and hopefully knows better than to touch broccoli again. Voila! Problem solved, naturally.

Who cares that throughout her recovery process she had lower pregnenolone, progesterone, estrogen, everything and that she could barely walk. She wasn't supposed to! That was the idea -- her thyroid wanted her to stop walking and wasting energy and doing the stupid stuff that harmed her. She was supposed to feel so bad that she would not venture again into the wild to fight other tigers or even to cook and/or eat the damn broccoli, while her body was fixing her thyroid -- which then would send the correct signals, restoring her steroids to where they should be so she can live a productive life out there. It was all embedded by nature in her systems, all she needed to do is listen to her body.

Sorry for the rant, I need to wrap my head around these things and sometimes a scenario will help.
 
J

j.

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According to Peat, Graves disease is compatible with being hypothyroid, euthyroid, and hyperthyroid.
 

Isadora

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j. said:
According to Peat, Graves disease is compatible with being hypothyroid, euthyroid, and hyperthyroid.

Graves' does turn into Hashimoto's even without radioactive iodine and other dire interventions, so Peat probably sees them both as "so-called autoimmune" thyroid diseases:

The Link between Graves’ Disease and Hashimoto’s Thyroiditis: A Role for Regulatory T Cells

Hyperthyroidism in Graves’ disease is caused by thyroid-stimulating autoantibodies to the TSH receptor (TSHR), whereas hypothyroidism in Hashimoto’s thyroiditis is associated with thyroid peroxidase and thyroglobulin autoantibodies. In some Graves’ patients, thyroiditis becomes sufficiently extensive to cure the hyperthyroidism with resultant hypothyroidism. Factors determining the balance between these two diseases, the commonest organ-specific autoimmune diseases affecting humans, are unknown.

Gotta love that last sentence. :|

The relationship between Graves’ disease and Hashimoto’s thyroiditis has been debated for decades. Although initially considered to be two separate diseases, the present view is that they represent the opposite sides of the same coin, or the two ends of a spectrum.

Hence, probably Peat's view...

We report that Treg are a major factor in the intermolecular spreading of the immune response from the TSHR to TPO and Tg as well as in the shift from hyperthyroidism to full-blown Hashimoto’s thyroiditis with massive thyroid lymphocytic infiltration and hypothyroidism. These findings provide novel insight into the enigmatic balance between hyperfunction and thyroid destruction in human Graves’ disease.

I always wondered what caused the initial destruction of thyroid cells in my case. It is probable that stress caused physical damage to the thyroid, which had me go into Graves initially (maybe -- I remember some funky times, but brief enough) and then descend into Hashimoto's, while keeping mostly euthyroid. Since I started checking it, my T4 was on a downward trend, constantly. I guess this is where it's played. Will I go under the limit into symptomatic hypothyroidism or will I hang in the euthyroid zone and heal? The antibodies have been in constant decline, maybe, who knows, if I know what to eat and how to increase metabolism, I will avoid the trap of hypothyroidism and the damage will heal.

What evidence is available of a role for Treg in human thyroid autoimmunity? In humans, the number and function of Treg are still unclear, depending on the Treg markers and assays employed as well as the disease. Abundant Treg were found infiltrating the thyroid gland of Graves’ patients in one study, but the suppressor function of peripheral Treg was decreased (42). In another study, intrathyroidal Treg were reduced compared with those in peripheral blood, possibly because of increased apoptosis (43). Despite the limited number of studies (and in some cases the limited number of patients investigated), these data are consistent with our findings for the association between thyroiditis and Treg in mice and (incidentally) with the early studies of Volpe and Iitaka (44) concerning a suppressor T cell defect. Future studies on the evolution of Graves’ disease into Hashimoto’s thyroiditis with hypothyroidism will be of interest to determine whether this shift is accompanied by an alteration in Treg number or function.

So they really don't know much... Maybe Peat and Haskell are right to question the very notion of autoimmunity and lymphocytes attacking our own tissues.

Incidentally, my T-cells were in good numbers and proportions, my B-cells were slightly depressed when I had my immunophenotype done. As if they had just been depleted, after hard work done somewhere.
 

Isadora

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Another study that explains how TSH acts on miRNA to promote thyroid cell growth... And forskolin is mentioned again, as having a similar effect. Could supplementation with forskolin be beneficial, would it hurry the cellular recovery process?

http://mend.endojournals.org/content/26/3/493.long

Identification of microRNAs that mediate thyroid cell growth induced by TSH.
Akama T, Sue M, Kawashima A, Wu H, Tanigawa K, Suzuki S, Hayashi M, Yoshihara A, Ishido Y, Ishii N, Suzuki K.

Laboratory of Molecular Diagnostics, Department of Mycobacteriology, Leprosy Research Center, National Institute of Infectious Diseases, 4-2-1 Aoba-cho, Higashimurayama-shi, Tokyo, Japan.

Abstract
TSH is a major regulator of thyroid cell growth and endocrine function. It is known that cAMP and phosphatidylinositol 3-kinase (PI3K) are responsible for mediating the action of TSH. Activation of these signals results in the induction of a series of transcription factors and cell cycle regulating proteins, which induce cell proliferation. In addition to such canonical transcriptional regulation, it was recently shown that microRNA (miRNA or miR) constitutes another key mechanism for the regulation of gene expression. However, whether TSH action is mediated by miRNA in the thyroid is unknown. In this study, we have performed miRNA microarray analysis and demonstrated that TSH significantly decreases expression of 47 miRNA in thyroid cells. Among these, we have shown, using their specific agonists, that overexpression of miR-16 and miR-195 suppressed cell cycle progression and DNA synthesis that was induced by TSH. In silico analysis predicted that Mapk8, Ccne1, and Cdc6, the expression of which was up-regulated by TSH, are potential target genes for these miRNA, and overexpression of miR-16 and miR-195 suppressed expression of these target genes. The decrease of miR-16 and miR-195 expression by TSH was reproduced by forskolin and N(6),2'-O-dibutyryladenosine cAMP and reversed by the protein kinase A inhibitor H89 and the PI3K inhibitor LY294002. These results suggest that TSH activates cAMP/protein kinase A and PI3K cascades to decrease miR-16 and miR-195, which induce Mapk8, Ccne1, and Cdc6 to activate cell proliferation.

Now, if only one could be sure that the said "cell proliferation" would refer to "healthy cells" and not to cancerous growth... Which TSH is also known for -- and Ray Peat does mention that, although more like a hypothesis than a sure thing, hmm:

Ray Peat said:
TSH has direct actions on many cell types other than the thyroid, and probably contributes directly to edema (Wheatley and Edwards, 1983), fibrosis, and mastocytosis. If people are concerned about the effects of a TSH “deficiency,” then I think they have to explain the remarkable longevity of the animals lacking pituitaries in W.D. Denckla's experiments, or of the naturally pituitary deficient dwarf mice that lack TSH, prolactin, and growth hormone, but live about a year longer than normal mice (Heiman, et al., 2003). Until there is evidence that very low TSH is somehow harmful, there is no basis for setting a lower limit to the normal range.

Some types of thyroid cancer can usually be controlled by keeping TSH completely suppressed. Since TSH produces reactions in cells as different as fibroblasts and fat cells, pigment cells in the skin, mast cells and bone marrow cells (Whetsell, et al., 1999), it won't be surprising if it turns out to have a role in the development of a variety of cancers, including melanoma. (full article here

Many things, including the liver and the senses, regulate the function of the thyroid system, and the pituitary is just one of the factors affecting the synthesis and secretion of the thyroid hormones.
Full article here.

So he lists a study that mentions TSH impacting other types of cells, but simply speculates on TSH being a potential carcinogenic... So there I was, worrying unnecessarily that a high TSH is a terrible thing to have, even if my T4 and T3 were within range...

In another article, "The Thyroid", Ray Peat states:

In this culture of misunderstanding and misrepresentation, the mistaken idea of hypothyroidism's low incidence in the population led to the acceptance of dangerously high TSH (thyroid stimulating hormone) activity as "normal." Just as excessive FSH (follicle stimulating hormone) has been shown to have a role in ovarian cancer, excessive stimulation by TSH produces disorganization in the thyroid gland.

Disorganization? It builds new tissue. There's bound to be some disorganization on a construction site... And sometimes the result may not correspond to the constructor's wishes, as in cancer, if it turns out, but I am still looking for proof of that.

Ray Peat said:
In hypothyroidism, the pituitary secretes more TSH to activate the thyroid gland, but TSH itself has a variety of pro-inflammatory actions. The C-reactive protein (CRP), which is recognized as a factor contributing to atherosclerosis, is increased in association with TSH. CRP activates mast cells, which are found in the atheroma plaques, to produce a variety of pro-inflammatory substances, including histamine.
-- in "Cholesterol, longevity, intelligence, and health"

This doesn't scare me as much, either, if there is a chance that poor TSH is busy rebuilding one's thyroid gland.
 

charlie

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