The difference between producing and taking thyroid hormones?

The difference between producing and taking thyroid hormones?

This is the first time I have noticed a suggestion in a paper that there could be a fundamental difference between producing adequate thyroid hormone in your own thyroid and taking it as a tablet. On that basis alone it is interesting. And it does not need there to be any difference in the chemical substance.

The underlined sentence is what I see as the bit that is highly relevant to the group.

The paper is very speculative.

BioMed Research International

Volume 2013 (2013), Article ID 503419, 5 pages

Clinical Study

Endometrial Polyps in Women Affected by Levothyroxine-Treated Hypothyroidism—Histological Features, Immunohistochemical Findings, and Possible Explanation of Etiopathogenic Mechanism: A Pilot Study

Carlo Saccardi,1 Salvatore Gizzo,1 Kathrin Ludwig,2 Maria Guido,2 Mara Scarton,1 Michele Gangemi,1 Raffaele Tinelli,1,3 and Pietro Salvatore Litta1

1Department of Women’s and Children’s Health, University of Padua, 35128 Padua, Italy

2Department of Medical Diagnostic and Special Therapy, University of Padua, 35128 Padua, Italy

3Ospedale San Bassiano, OB/GYN Unit, 36061 Bassano del Grappa, Vicenza, Italy

Received 29 April 2013; Accepted 19 July 2013

Academic Editor: Kyousuke Takeuchi

Copyright © 2013 Carlo Saccardi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The aim of the study was to investigate the possible overexpression of estrogen (ERs) and progesterone (PRs) receptors both in EPs glandular and stromal cells in postmenopausal women with levothyroxine-treated hypothyroidism in comparison to EPs detected in women with physiological thyroid hormone levels. During the study period (January-February 2013) 22 patients were eligible (12 treated, 10 controls). The two groups were homogenous for general, EPs sonographic and hysteroscopic features. None of the cases of atypia was found. Immunohistochemistry showed that the two groups were similar for ERs and PRs intensity rates in EPs glandular cells despite a trend of ERs percentage expression more than 60% in 2/3 of treated patients versus 1/3 of controls. In stromal EPs components, ERs intensity was high positive in 10 (83,3%) treated cases while it was high positive in 1 control (10%). Percentage of ERs stromal expression showed a different trend between the two groups despite a borderline statistical significance. Our hypothesis is based on a possible double action of hypothyroidism and thyroxine intake: the subclinical TSH increased levels and its possible circadian oscillation could stimulate the endometrial TSHRs (increasing type 2 DIO activity); the circulating levels of exogenous thyroxine could be locally metabolized in active form by type 2 DIO stimulating ERs.

Full paper available at link above.


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9 Replies

  • It's a bit too much for me to get my head around

  • me to to many big words lol

  • Are they saying that the endometrium has more than usual number of receptors for oestrogen and progesterone due to not following circadian rythem of normal thyroid hormone production? what does that mean for our endometriums-doesnt sound good. Too much oestrogen can cause endometrial cancer, so does this mean that hypothyroidism and thyroxine can cause endometrial cancer? In that case we should all be aware so that we can make sure to have regular ultra sounds.


  • I read it as TSH-receptors rather than oestrogen and progesterone receptors.

    Though I am more than willing to accept that I might be wrong!


  • This paper throws up some interesting reading but if your not used to complex scientific paper it is quite a difficult read. What i found interesting is that there is a marked difference in endometrial polyps in women with hypothyroidism that those with normal thyroid function. Also the fact that there are tsh receptors in the endometrium resulting from thyroid hormone production independent from the thyroid. As wel as the competition between oestrogen and thyroid hormone for one receptor i would love to read their full study once completed as this was a pilot watch this space... I would love to read some of the research they make reference to.

    Thanks rod absolutely fascinating

  • Help! I've read this 3 times and still can"t understand it - only that there are differences in type 2 DIO activity - but what is this???


  • There are three enzymes that convert thyroid hormones within the body - Deiodinase 1, 2 and 3 - often called D1, D2, and D3. But sometimes called 2 DIO or something else!

    What is being said is that the rate at which D2 is operating changes and might be having its own somewhat odd effect.

    While not being perfect, this Wiki article is not too bad as a starting point:

    It is very much a difficult thing to get your head round - not sure I have managed yet! But the issue is that the frequently repeated claim that taking a little white pill makes you exactly the same as anyone without thyroid disease might have been disproved. At last.

    And once one place has been found where it isn't true, we might then see others. Resulting, in time, in an explanation of what causes the differences.


  • Thanks Rod - I'll have a read of the link. It's interesting that the circadian rhythms are believed to be involved. Maybe the continual affect of non-circadian delivery of the replacement thyroxine 'confuses' the receptors in the body?

    The plot thickens...


  • That struck me as well.

    From my earliest involvement with things thyroid I have wanted to see at least some experimentation with automated delivery - maybe using an implanted device. After all, such things have been done in other areas of medicine.


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