"Honeymoon phase" in Hypothyroidism?

[Joyya]

After a diagnosis of type 1 diabetes (an autoimmune condition), there is often a “honeymoon phase” where a small percentage of the pancreatic beta cells continue to produce insulin for a period lasting from a few weeks, several months, to as much as 1-2 years. This honeymoon period continues until the remaining pancreatic cells are destroyed, or become dysfunctional. I believe a similar type of honeymoon period may also exist in some people with autoimmune hypothyroidism (Hashimoto's) and may explain the day-to-day variation in symptoms, even with an appropriate dose of thyroid hormone replacement medication.

Does anyone know of any academic papers about such a period?

Thanks.

[tattybogle]

Mmmm ......interesting theory , but if that's the case then i've been on honeymoon since 1998

[Joyya in reply to tattybogle]

For sure I think there are other reasons for fluctuations. I am simply wondering if a honeymoon phase could be one of them.

[Aurealis]

I think that you’re just describing the process of destruction of the thyroid gland by thyroid anti-bodies. Once antibodies are present the thyroid is gradually being destroyed and thyroid hormone production will be reduced unless TSH rises to such an increased level that thyroid hormone levels are maintained. But the destruction continues, so more and more TSH is needed. This is when hypothyroidism is diagnosed.

Once exogenous thyroid hormone is added, TSH production decreases, as it is no longer necessary to raise thyroid hormone levels in the blood, as this is provided by the exogenous thyroid hormone/ Levo.

While TSH is present it is possible for some thyroid hormone to be produced, but I suspect the term honeymoon period in this context would be incorrect - the thyroid gland is underactive, not destroyed.

I suspect that papers on the development of autoimmune hypothyroidism (UAT) would provide you with what you’re looking for.

[Joyya in reply to Aurealis]

Thank you for your reply. It makes total sense that the very suppressed TSH due to T4 /T3 medication would result in no endogenous T4 production.

I am guessing the exogenous T3 would significantly suppress T4 to T3 conversion of the exogenous T4.

This leads me to a few questions:

1. What is the 75 mcg Synthroid I am taking even doing, in this context? Is all the therapeutic benefit just coming from the 12 mcg Cytomel?

2. Would dietary changes such as avoiding gluten to lower TG antibodies basically change nothing in terms of symptoms?

3. What would be the reason to avoid gluten, if not to preserve thyroid function?

Thanks for your time and insights

[greygoose in reply to Joyya]

I am guessing the exogenous T3 would significantly suppress T4 to T3 conversion of the exogenous T4.

Some people believe that taking T3 increases the conversion of exogenous T4 to T3. But I've never seen any 'proof' that convinces me of that. And, I've never heard that it would suppress the conversion, either. Although suppressing the TSH could have that effect.

I don't think anyone really know what the exogenous T4 is doing, but some people just seem to need good levels of it even when they're taking T3. We're all different. I don't need any T4 at all, I'm better off without it.

3. What would be the reason to avoid gluten, if not to preserve thyroid function?

Avoiding gluten does not preserve thyroid function. The reason people avoid gluten is because they are gluten sensitive and it causes symptoms. Remove the gluten and the symptoms go away. Going gluten-free does not, by any means, help all hypos.

[Joyya in reply to greygoose]

Thanks.

From a physiological point of view, I'm not sure what the exogenous T4 I'm taking is doing.

[greygoose in reply to Joyya]

It's possible that some of it is being converted to T3. And it's possible that T4 does some things we don't know much about. There's so very little known about thyroid. We just know that some people need it and some don't. If it makes you feel well, then does it really matter why?

[Joyya in reply to greygoose]

Thanks. The meds seem to be working very well and for that I am very thankful. I am nerdy and am trying to understand the physiology. Thanks for your help. I appreciate it.

[greygoose in reply to Joyya]

You're welcome.

[Lalatoot in reply to Joyya]

For me removing gluten improved gut function which in turn improved absorption.

[greygoose in reply to Aurealis]

you’re just describing the process of destruction of the thyroid gland by thyroid anti-bodies

It's not the TPO/Tg antibodies that destroy the thyroid. The are just the system's cleaning ladies, supervising the cleaning up of the blood after an attack.

[Joyya in reply to greygoose]

Thanks. So what actually destroys it?

And if TPO/TG simply clean up after the destruction, why reduce foods like gluten to lower TG-ab?

[greygoose in reply to Joyya]

The thyroid is destroyed by the lymphocytes produced by the immune system.

Why try and reduce antibodies? Good question. Possibly because of a misunderstanding of how it all works. Even if you managed to get rid of them completely - probably impossible - you would still have Hashi's, it doesn't go away.

I've yet to see positive proof that measures like going gluten-free do actually reduce antibodies. They fluctuate all the time. So, just because you test them today and they're lower than three months ago, does not mean they won't rise again at some point if they have a job to do. Also, the more the thyroid is destroyed, the lower the antibodies will be. So, what's to say it's the no-gluten diet that has reduced them and not just the progression of the disease?

[Joyya]

Thanks.

What causes the lymphocytes to attack the thyroid?

Is there any evidence that lymphocytes mistake transglutaminase in the thyroid from recognition of gliadin in gluten that is is structurally very similar?

[greygoose in reply to Joyya]

There are probably multiple causes, but I don't think anyone really knows. I have heard the theory about the translutaminase but that's probably just one of the possible triggers.

[Joyya in reply to greygoose]

Thanks.

[Joyya in reply to greygoose]

For those who (like me) also thought Hashimoto's was caused by TPO-Ab or TG-Ab attacking the thyroid. Greygoose is quite right! endocrineweb.com/conditions...

[Valerie0106 in reply to Joyya]

I think Isabella Wentz and perhaps Amy Myers posit this

[tattybogle]

if i trawl my memory box of 'things i know i've read when trying to understand a research paper somewhere' ....i come up with these thoughts:

The thyroids release of T4 (and T3) and the conversion in the body of T4>>T3 is not an 'all or nothing , on / off' situation .

The thyroid will have a base levels of release , ( like a trickle feed. or perhaps a dripping tap) which the TSH can boost up / or not. eg. the TSH turns the dripping tap ' on' or 'off' , but even when it's 'off', it's still a dripping tap.

Surely this must be the case .... otherwise everyone who was on T3 only with a supressed TSH would end up with fT4 levels of 0.000 ... but they don't ..they still have 'some'.

i think its sort of the same principle with T4>>T3 conversion ... TSH can boost this ,or slow it down ,, (indirectly anyway ..via deiodinase action?) but i don't think it will stop completely.

[tattybogle in reply to tattybogle]

also .. as to 'what T4 is doing' .. i think ? ( jimh111 might be able to explain) that T4 has been found to have some 'non genomic' actions... i'm a bit hazy on what that means exactly.

edited .....to add reference for nonogenomic actions of T4: entokey.com/thyroid-physiol...

".... There are also nongenomic actions of iodothyronine (T4) that are not mediated by intranuclear TR. Plasma membrane-initiated actions begin at a thyroid hormone receptor on integrin alphavbeta 3 that activates ERK1/2, which leads to changes in membrane ion transport, such as the Na(+)/H(+) exchanger, and are also involved in other important cellular events such as cell proliferation.12,13 ..."

[tattybogle in reply to tattybogle]

and .. i think there are some parts of body (brain ?) that 'prefer' to convert T3 themselves from circulating T4 , rather than use circulating T3.

can't remember how it worked exactly .. might have been because they contain a different balance of deiodinase's than other parts ...

Sorry for total lack of any links or detail ... my brain is in 'sunday morning' mode

[jimh111 in reply to tattybogle]

When we talk about thyroid hormone we usually think of the action of T3 on thyroid hormone receptors on part of the DNA. This is called 'genomic action' and is responsible for the metabolic and developmental effects of thyroid hormone. This is the main function of thyroid hormones and is almost exclusively done by T3 (T4 has about one or two percent effectivness at this level if I remember correctly). So, T4 is a prohomone and T3 the active hormone.

T4 also acts as a hormone near the cell membrane, including binding to the Integrin αvβ3 Receptor which can have adverse cardiac effects and promote cancer Integrin αvβ3 Receptor . People with a low normal fT4 live longer than those with a high normal fT4. I have previously supported levothyroxine monotherapy for the many people who do well on it. in view of the harmful effects of too much T4 I now take the view that combination therapy should be the standard approach as it enables a lower fT4. I feel levothyroxine monotherapy should not be routinely used.

Tissues such as the brain and skeletal muscles get some of their T3 by type-2 deiodinase (D2) that converts T4 to T3 locally. The brain gets most of its T3 this way. This is important because D2 enables local regulation of T3 levels indepent of blood levels. My view is that if this local conversion is down-regulated then restoring normal blood fT3 is not enough to compensate for the loss of local T3. This would explain why some patients need higher serum fT3 to overcome brain fog. This is undesirable as there may be too much serum fT3 for other tissues such as the heart. For now we have to give these patients the higher T3 levels but there should also be urgent research into trying to discover the causes of impaired conversion and finding cures.

[tattybogle in reply to jimh111]

thankyou

[Joyya in reply to jimh111]

Thank you. This is very helpful.

[Joyya]

Thanks for the sketch from memory.