I have written before about this important topic, which doesn’t seem to be reflected in most thyroid treatments plans - namely the role that the autonomic nervous system plays in regulating the work of the thyroid gland.
This explains, for example, why the thyroid continues to produce t3 and t4 when TSH approaches zero with individuals showing hyperthyroid symptoms. This is because the nervous system, which richly innervates the thyroid, continues to stimulate it outside of TSH.
I was on 125 g lactose free thyroid tablets without letting me know the new doctor just changed it to 100 since then my body is going down with constantly fevers , flu earache .Also ankles are swelling up face and body puffy.
If you would like some support for your thyroid issues then do start a new post.
Are you able to post the pdf? I can't get access to your article
i initially thought it wouldn't let me see it without signing up (which i didn't do) ,,, but then i realised it was there~ just a lot further down the page .
That was very a interesting read ( mind you, i might have to get the dictionary out and read it again so i understand a lot of it )
i don't get how you concluded it shows T4/T3 are still produced when TSH 'approaches zero' though ?
i (so far~ lol )understood it to say that if you knock out the bit that regulates the body clock .. then TSH and fT3 were not affected but fT4 was lower ( i don't really agree with their comment that TSH / fT3 were 'not affected' .. they have clearly lost the up / down daily rhythm and appear to be much 'flatter' )
However as i say , didn't understand a lot of it . so i'm not disagreeing with your comment on what it shows . just trying to understand why you say T4/T3 still produced with zilch TSH
well if you don’t understand Tatts then there is no chance for me 😂.
But please carry on with the dumbed down version
No ... (it's past marmalade-o-clock now . i only ever try to understand complex science pre-marmalade)
well my body clock was badly affected but my thyroid made nothing of anything in the end!
in people displaying hyperthyroidism there are two primary indicators from blood tests - very low TSH (approaching zero) and very high t3 and t4. If TSH alone were responsible for the stimulation of the thyroid to produce and release t3/t4, then it would follow that if TSH was low, so would T3/t4, but it is the reverse. The explanation, not just in hyperthyroid patients, but in all people (and animals) is that the nervous system is a parallel and very important stimulator of the thyroid gland.
except that in Graves Disease (autoimmune hyperthyroidism) it is the TRab antibodies (Thyroid Stimulating Hormone Receptor antibodies) which stimulate the thyroid to continue producing T4/T3.
'Stimulating' TRab mimic the action of TSH ~ They attach to the TSH Receptors on the thyroid and act just like TSH ~causing over production of T4/T3.. despite the absence of any 'real' TSH.
When these are present , you get high T4/T3 with 0 TSH
( there are also Blocking TRab , which prevent 'real' TSH getting to the TSH receptors . if these are present , you get low T4/T3 and very high TSH)
But like you, i have always thought that the nervous system must be v. important for proper thyroid function.
so if antibodies are the stimulant in the case of Graves’ disease, what is the explanation for excessive t3/t4 production in the absence of antibodies in hyperthyroidism?
i would have to look into that , or else i risk spouting rubbish ...lol .... be back later .. got to go and take a kitten to the vet .
x Hope you are well ThyoidLady.. i enjoy our conversations .
So in graves there is excess SYNTHESIS of T4/T3 (from the 'stimulating' TRab antibodies which act like TSH )
in thyroiditis (eg hashimoto's and other forms of thyroiditis).. there is no excess synthesis of T4/T3 , but there is excessive RELEASE of stored / ready made T4/T3, (without increased synthesis) due to damage to the thyroid gland. " Symptoms of hyperthyroidism are common early in the disease because of hormone release from the disrupted follicles..... After several weeks, the thyroid is depleted of T4 and T3 stores, and transient hypothyroidism develops " msdmanuals.com/en-gb/profes... professional/endocrine-and-metabolic-disorders/thyroid-disorders/subacute-thyroiditis
msdmanuals.com/en-gb/profes... ...there's some interesting stuff in here about differences between subacute (de quervains) thyroiditis / silent lymphocytic thyroiditis (post partum) / hashimoto's thyroiditis/ .. all of which can have transient hyperthyroid phases.
I'm not quite so clear what causes excessT4/T3 production in autonomous functioning 'hot' nodules , ,or any of the less common forms of hyperthyroid but this might help , i haven't read it yet:
i'd love to read the rest of this one , but it's behind a paywall and i'm not buying the book 
sciencedirect.com/topics/me....
Mohtashem Samsam, in Epidemiology of Thyroid Disorders, 2020
Etiology of hyperthyroidism
Hyperthyroidism may occur from increased TH synthesis and secretion, due to thyroid stimulators in the blood, or from autonomous thyroid hyperfunction. It can also develop from excessive release of TH from the thyroid, without increased synthesis. This release is usually due to destructive changes from various forms of thyroiditis. Various clinical syndromes also cause hyperthyroidism. The following three common causes of thyrotoxicosis are related to hyperfunction of the thyroid gland:
• Diffuse hyperplasia of the thyroid—associated with Graves’ disease (approximately 85% of cases)
•Hyperfunctional multinodular goiter
•Hyperfunctional thyroid adenoma
The etiology of hyperthyroidism is due to overproduction of T4, T3, or both. Diagnosis of overactive thyroid and treatment of underlying causes can relieve symptoms and prevent complications. Causes of hyperthyroidism include the autoimmune disorder known as Graves’ disease; as well as excess iodine, thyroiditis, toxic adenomas, and other tumors, toxic multinodular goiter, and large amounts of tetraiodothyronine received through dietary supplements of medications (Fig. 6.1). Overstimulation of the thyroid gland by the TSH receptor and mutations of this receptor are common causes of hyperthyroidism. Other causes include damage to thyroid follicles that cause them to passively release thyroid hormones. Additional causes of hyperthyroidism include as follows:
•Thyroiditis (inflammatory thyroid disease)—includes Hashimoto’s thyroiditis, subacute granulomatous thyroiditis, and silent lymphocytic thyroiditis; there are destructive thyroid gland changes and release of stored hormone not because of increased synthesis; hypothyroidism may then follow.
•Excessive iodine ingestion—there is a low thyroid radioactive iodine uptake (RAIU); this usually occurs with a nontoxic nodular goiter of patients (mostly in elderly) who are given iodine-containing drugs or who have radiologic studies that use iodine-rich contrast agents; the excess iodine may provide substrate for non-TSH regulated, autonomous areas of the thyroid to produce hormone; hyperthyroidism usually lasts as long as the excess iodine is in the circulation.
•Thyrotoxicosis factitia—due to conscious or accidental overingestion of TH.
•High human chorionic gonadotropin (hCG) levels—due to molar pregnancy, choriocarcinoma, or hyperemesis gravidarum; levels of hCG are highest in the first trimester of pregnancy, causing decreased serum TSH and slightly increased serum fT4; increased thyroid stimulation may be due to higher levels of partially desialated hCG, which seems to be stronger in its thyroid stimulation than more sialated hCG; overall, this cause is transient; normal function resumes once the condition resolves or is treated.
•Plummer’s disease—also called toxic solitary or multinodular goiter; may be due to TSH receptor gene mutations that produce continuous thyroid stimulation; toxic nodular goiter results in no autoimmune manifestations or circulating antibodies seen in patients with Graves’ disease; toxic solitary and multinodular goiters usually do not remit.
•Drug-induced hyperthyroidism—can be from amiodarone and interferon alfa; these can cause thyroiditis with hyperthyroidism and other disorders; lithium, in rare cases, can cause hyperthyroidism but is more commonly a cause of hypothyroidism; patients receiving these drugs require close monitoring.
•Struma ovarii—occurs when ovarian teratomas have enough thyroid tissue to cause true hyperthyroidism; in the pelvis, RAIU occurs; uptake by the thyroid is usually suppressed.
•Nonautoimmune autosomal dominant hyperthyroidism—in infancy, this results from TSH receptor gene mutations, producing continuous thyroid stimulation.
•Metastatic thyroid cancer—rarely, overproduction of thyroid hormone occurs from functioning metastatic follicular carcinoma—especially in pulmonary metastases.
•Inappropriate TSH secretion—rare; in hyperthyroidism, TSH is basically undetectable, except when there is a TSH-secreting anterior pituitary adenoma or pituitary resistance to TH; the TSH levels are high; the TSH produced by both disorders is biologically of higher activity than normal TSH; increased alpha-subunits of TSH in the blood occur when there is a TSH-secreting pituitary adenoma.
Graves’ disease will be discussed in detail in Chapter 7, Thyroiditis and Graves’ disease. Various causes of hyperthyroidism are illustrated in Fig. 6.1.
Figure 6.1. Various causes of hyperthyroidism.
This is really interesting - thank you. It confirms what I empirically knew about my thyroid condition being partially caused/driven by long term NS dysregulation and stress. I agree not enough treatment programs focus on things to strengthen vagus nerve and dampen down SNS dominance. Since diagnosis daily breath work, meditation and somatic practices have been a big part of my recovery plan and I know play a huge role in getting and staying well.
absolutely right - there are clinical reports of patients recovering from thyroid issues, I have deffinitely seen a case of recovery from hyperthyroidism, following lifestyle interventions aimed at the reduction of stress. This is not trivial in the slightest.
I learnt about my " Graves ' through the Elaine Moore Graves Disease Foundation ;
True- 10 years too late for me as I had RAI thyroid ablation for Graves back in 2005 a few months after having being physically threatened and verbally abused by a man I employed as my assistant manager.
I became very unwell around 8 years post RAI thyroid ablation with I believe the consequences of RAI ingestion and finding no answers nor resolve through the NHS system started researching - thinking maybe that Graves has come back, only to read it never went away.
I know now I have been hypothyroid since a child, very slow to develop, compared to my brother born 4 years earlier before WW2. I was born in 1947 .
i was dealing with dyslexia, was left handed and grossly over weight wearing a boy's school blazer and shoes and at the 11 plus my hair fell out in clumps and painted the patches with brown iodine and felt further ashamed as of course I failed the exams as I couldn't read.
My father was medically discharged towards the end of WW2 what with I have no idea - but he went in a heavyweight boxer and came out as skinny as a rake according to my mum - and with a personality change - and remember being scared of my father growing up but he seemed to mellow when in his 50's.
Most of my father's side of the family look hypothyroid compared to my mothers side.
Despite various visits to the doctors my hypothyroidism was never picked up and my symptoms at diagnosis no worse than what I was living with but now I had insomnia and further exhaustion and a physical symptom of a shaky middle finger.
So I now presume I have been with Graves since birth, but with blocking antibodies as my TSH never rose enough to get a diagnosis of hypothyroidism - until I was attacked and that threw me off sufficiently for my bloods to be fully tested and the antibodies run and immediately commenced ' the treatment ' of the anti thyroid drug.
i was well on the AT drug and around a year in experienced a phase of increased metabolism, felt amazing, dropped some weight, had good energy and thought this is what it was like to be well and just wish I had been allowed to stay on the AT medication.
We are looking at an auto immune disease that tends to be triggered by stress and anxiety, for which there is no cure, though Graves can burn itself out given enough time.
I self medicate now with full spectrum thyroid hormone replacement and have my life back as best as I can.
To be well I need my TSH fully suppressed which the NHS would not allow as I was presumed over medicated and dose reduced until the TSH scraped in the range at the cost of my health deteriorating even further.
The most recent research is suggesting the longer one stays on the AT drug the better the outcome for the patient -
pubmed.ncbi.nlm.nih.gov/338...
Quite why we persist in destroying the target of an attack from one's own immune system in health care settings is beyond me :
Just adding a link to your previous post in this subject as the conversation with diogenes is also a very interesting read :
healthunlocked.com/thyroidu... thyroid-stimulated-by-sympathetic-nervous-system-without-tsh
Thyroid hormone deficiency during zebrafish development impairs central nervous system myelination
Thyroid review appointment systemNew paper that consolidates the notion of FT3 protection as the chief aim of the body's thyroid system
Mathematical modeling of the pituitary-thyroid feedback loop: role of a TSH-T3-shunt and sensitivity analysisA Role of Thyroid Hormones in Acute Myocardial Infarction: An Update
