A review paper showing the complex action of T3... - Thyroid UK

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A review paper showing the complex action of T3 on cardiac function

diogenes profile image
diogenesRemembering
13 Replies

REVIEW ARTICLE

Front. Endocrinol., 29 August 2019 | doi.org/10.3389/fendo.2019....

Novel Insight Into the Epigenetic and Post-transcriptional Control of Cardiac Gene Expression by Thyroid Hormone

Francesca Forini, Giuseppina Nicolini, Letizia Pitto and Giorgio Iervasi*

This review is intensely complicated in that it discusses the interaction of T3 with genes that control cardiac function. I don't expect people to read it in full because it is very detailed in genetic analysis. But the summary is that T3 controls gene expression by promoting the altering of gene structure chemically so that they respond differently in different circumstances. Thereby a deficiency in T3 alters gene expression in disease (a phenomenon called epigenetics). This causes an increased likelihood of cardiac disease and failure. I merely put this out as a demonstration that the heart essentially needs adequate FT3 to operate properly, and the mechanisms for doing so. Obviously this knocks on to the essential need for adequate FT3 levels in blood to keep a healthy heart (and other things).

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diogenes
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De8813 profile image
De8813

And FT3 doesn't seem to be getting tested anymore 😔.

Love reading all your amazing information. Thank you diogenes x

ling profile image
ling

What about a high level of T3? Will that also alter gene expression in disease?

Thank you

diogenes profile image
diogenesRemembering in reply toling

It will. Experiments on rats given a high dose of T3 extra to their needs show changes in the makeup of several genes, which doesn't go back to normal when the extra T3 is stopped. Epigenetic changes can be longlived, the longer the situation is maintained.

UrsaP profile image
UrsaP in reply todiogenes

Could that be the same with T4? Could taking T4, say, if it was not being used properly, alter gene expression. Could this result in dio, or other polymorphisms?

diogenes profile image
diogenesRemembering in reply toUrsaP

T3 is the principal controller of these gene changes. No evidece that T4 has any significant effect though there may be minor effects we don't know about.

ling profile image
ling in reply todiogenes

Thank you.

So similarly, high FT3 levels from Graves, will alter gene expression and increases the likelihood of cardiac problems?

Thank you

in reply todiogenes

Thank you once more for the information and the summary of the paper.

Are the low T3 epigenetic changes usually permanent too?

Naomi8 profile image
Naomi8

Wow!thanks Diogenes!

Is there any reliable data on over-range FT3?I seem to need enough T3 to give FT3 results that are at the top or slightly over range.Too much T4(in NDT alone or in thyroxine)gives me ectopic beats & supraventricular tachycardia episodes,so I am adding a little T3 to my NDT .

I have heard so much scaremongering by GPs & endos about osteoporosis.Post-menopausally,this is a worry

diogenes profile image
diogenesRemembering in reply toNaomi8

See my later post on this

Hello Diogenes

I won't attempt to follow that sort of paper as I won't understand it. I will ask though - does it talk about slow or slow and erratic heart rates and/or the need for pacemakers?

diogenes profile image
diogenesRemembering in reply to

No, only talks about biochemistry (TSH).

NWA6 profile image
NWA6

Thanks for the summary 🤗 yep I could’ve told the geniuses this.

Low FT3 - low heart rate, sometimes only 33bpm. I am not an athlete and even when I was fit my heart rate was still 64bpm. So my unusually low heart beat was quite simply for me, low T3

Now I have T3 added I’m back up to a reasonable 66-76bpm

Just read the introduction. It seems to be saying that the epigenetic changes are a partial reversal or switch over to their state during foetal life! Does that mean the body/heart is sort-of trying to renew itself?

I read that some cells (brain? Heart?) of a person who has just died will try to save themselves by reverting to a form more like that of stem cells in an apparent desperate attempt to regenerate. Can't remember any details, so may have got that wrong, but something of the sort. Wow!

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