Bianco et al paper on DTE (NDT) and comibnation therapy

[diogenes]

This recent paper discusses the use of DTE (NDT) and T4/T3 comibnation therapy

Thyroid

©

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DOI: 10.1089/thy.2020.0153

1

LIOTHYRONINE AND DESICCATED THYROID EXTRACT IN THE TREATMENT OF HYPOTHYROIDISM

(DOI: 10.1089/thy.2020.0153)

LIOTHYRONINE AND DESICCATED THYROID EXTRACT IN THE TREATMENT OF HYPOTHYROIDISM

Thaer Idrees, Scott Palmer, Rui M. B. Maciel, Antonio C. Bianco

[dolphin5]

Thanks, will look that up. X

[Hidden]

Excellent! But try telling the "Establishment" that!

But one presses on...

[linda96]

Thank you, definitely more positive.

There’s a reference to a paper from 1977. A study that took place in Brazil, where the study subjects took T3 only for a year - and were fine.

I can’t locate it?

[humanbean]

For those who don't know :

DTE = "Dessicated Thyroid Extract"

NDT = "Natural Dessicated Thyroid"

DTE is the name usually used by the medical profession, when they acknowledge it exists at all.

Patients use the name NDT as I'm sure everyone on here already knows.

[helvella Administrator]

Link to abstract:

liebertpub.com/doi/abs/10.1...

Liebert want 51 US dollars to access the full paper.

[helvella Administrator]

The conclusion is ridiculous.

Conclusions: Newly diagnosed hypothyroid patients should be treated with LT4. A trial of combination therapy with LT4+LT3 can be considered for those patients that have unambiguously not benefited from LT4.

a) Why the assumption that newly diagnosed hypothyroid patients should be treated with LT4?

Yes, it might be simpler, cheaper, more readily manageable, adequate. But unless and until demonstrated to a high degree of confidence, it is stilll just that. Assumption.

b) Why the need for the patients to unambiguously not benefit from LT4?

Many, many hypothyroid patients gain some benefit from LT4. This statement seems to say that even the tiniest benefit rules out consideration for LT4+LT3. Whereas we often see that it is the last 5, 10, 20, 50% of recovery that LT4-only patients struggle with.

[diogenes Remembering in reply to helvella]

I've sent the whole paper to Louise Roberts at TUK.

[helvella Administrator in reply to diogenes]

Thank you.

[diogenes Remembering in reply to helvella]

I find it interesting that Bianco and co bust a gut trying to keep us out of the picture. No references for our work. A pitiful jealous performance unworthy of proper science and evenhanded attribution of work done.

[helvella Administrator in reply to diogenes]

I also notice that:

AB is a consultant for Allergan Inc and Synthonics, Inc.;

Allergan now own Armour Thyroid.

Synthonics

October 12, 2018

Novel coordination of thyroid hormone with zinc promotes slow release of active hormone to supplement standard therapy

A new “metal-coordinated” drug-delivery technology potentially could be used to supplement the standard therapy for hypothyroidism, which affects nearly 10 million Americans, and many more patients worldwide, according to results of a study published in the journal Thyroid this month.

[vocalEK in reply to helvella]

Hmmmmm.

[jimh111]

Thanks for posting. A few points.

They recommend that 'serum T3 levels' are measured by while patients are fasting about 3 hours post-dose. L-T3 is highly absorbed and blood levels peak after about 3 hours. There's no evidence I know of to show that post-dose fasting affects fT3 levels of patients taking L-T3. Even if it did it would make sense for patients to eat or fast as they normally do, so results reflect normal levels. We don't know how serum fT3 levels affect thyroid hormone action. Is gene expression determined by minimum fT3, maximum fT3 or the area under the curve (AUC)? In-vitro experiments show that gene expression requires several hours T3 saturation. Thus, measuring peak fT3 is likely to give false information. I'd take the blood around half-way between doses as a very rough reflection of AUC. This may prove to be wrong but it my best guess.

The paper correctly points out that most T3 comes from type-2 deiodinase (D2). If the patient has low fT3 (after supplying a little L-T3 to replace T3 from the thyroidal secretion and deiodinase) then it is likely due to impaired D2 activity. The current approach is to give sufficient L-T3 to normalise fT3. This is wrong. D2 regulates local T3 and contributes to circulating T3. If D2 activity is impaired replacing serum T3 will do little to compensate for reduced local T3 in tissues dependent upon D2. An analogy is the monitoring of patients with dehydration, their urine output is measured. The nurse could compensate for reduced urine volume by adding some of their own urine thus correcting the volume. This doesn't help the patient. The same applies to reduced D2 activity, restoring serum fT3 does not restore tissue hypothyroidism in those tissues such as the brain that depend on D2 for euthyroidism. I would expect Tony Bianco's team to recognise this!

This and similar papers address cases where patients have had their serum thyroid hormone levels restored to normal levels but are still exhibiting signs and symptoms of hypothyroidism. In many such cases they recover when their medication is adjusted, often putting one or more of TSH, fT3, fT4 out of their reference intervals. Many endocrinologists are now able to accept that it is not sufficient to bring blood tests 'within range', patients may be in the wrong part of the 'range' or even need to be outside the 'range'. With a perfectly straight face endocrinologists state that a patient cannot be hypothyroid because 'their blood tests are in range'. Two patients with identical signs, symptoms and blood tests are given different diagnoses because one happened to have an elevated TSH that was meassured sometime in the past. A corollary is that in both cases the hypothyroidism is unlikely to be due to imperfect serum hormone levels, the underlying cause will lie elsewhere. Perhaps we should stop trying to perfect serum hormone levels and seek the real causes of severe tissue hypothyroidism in patients who have decent circulating hormone levels.

[shaws Administrator]

Thanks diogenes and how I wish that those who should know better read this article. How is it that they seem to know little at all about the various needs that patients with a dysfunctional thyroid gland need to know in order to recover their health. They also seem not to read, nor care, or take any notice of Research results. They just bury their heads in the sand.

[Hidden]

This leaves me conflicted - good to see any research happening but it smacks of yet more craven appeasement to ‘established‘ thinking and norms. What is the point of medical research if its not towards curing or alleviating the symptoms of ALL those affected? Writing off existing patients boggles the mind!