New paper from Rederico Salas-Lucia of Bianco's team doi.org/10.3389/fendo.2022.... . This is a well written review which is a comparatively easy read of this complex subject.
I think it misses the point we can perhaps use EEC to monitor brain response to T3 and ankle reflex is also an objective measure of T3 activity. Seems to concentrate a little too much on using blood to determine T3 content rather than looking for other markers of thyroid hormone action (such as asking the patient). Nonetheless I think it is a good paper.
Written by
jimh111
To view profiles and participate in discussions please or .
I'm afraid that Bianco and his coworkers are distinctly hostile to our group. Note no references of our work whatsoever - he's tried hard to be partial. The basic situation as I see it is this. He wants to revisit and refine diagnosis and treatment to include T3 combination without letting go of "TSH must be in the healthy range" as a prime requirement. He also obstinately refuses to acknowledge (or can't understand) the absolutely key controlling role direct thyroidal T3 has in health and disease (accepting this destroys the TSH paradigm). I'd also comment that he was one of the authors of the US recommendations for hypothyroid treatment whose content he now derides. You can't ride two horses going in opposite directions. A very good example of "I want to be first and don't care how I get there". He uses mutation of deiodinases as a key factor when it is a factor but not a deciding one.
Bruce Charlton in the Journal ‘Medical Hypotheses.’ It was written in 2008:
‘Zombie science: a sinister consequence of evaluating scientific theories purely on the basis of enlightened self-interest.’
Quoted in quite an interesting blog from Dr Malcom Kendrick (I don't agree with everything he says, but he’s often spot on) as soon as I read the above, Bianco sprung to mind. I wonder why.
The review has one silver lining, the comment 'is it possible that "defects" in D2 could compromise the effectiveness of therapy with LT4 in restoring T3 homeostasis in the brain?'. They fail to make the deduction that with such defects restoring serum fT3 (with liothyronine or NDT) will not be sufficient to restore brain T3, the defect is still there. I've e-mailed Frederico about this and await his reply. I've a feeling there is a strong emotional attachment to serum hormone levels that does not allow them to contemplate the need for abnormal levels in certain cases.
thank you Diogenes for this comment…. I have read Bianco’s new book and the one glaring thing that I just could not understand was why he persisted in agreeing ( with absolutely no explanation) with the requirement for TSH to be within the reference range. Has he ever explained this? He questions every other assumption made, but steadfastly insists on this. Weird!
Tissue T3 content reflects circulating T3 levels and faithfully informs about TH signaling in most tissues (except for the brain and pituitary gland). The knowledge that in LT4-treated patients serum T3 levels might not be fully restored, raises the concerning possibility that TH signaling in these patients (in most tissues) might also not be fully normalized. Clinicians could consider the potential usefulness of measuring serum T3 levels to monitor the effectiveness of therapy with LT4. Future clinical trials should aim at correlating clinical outcomes with serum T3 levels.
"the concerning possibility" which has been wantonly ignored for decades. Not because patients have not been shouting from the rooftops.
"consider the potential usefulness of measuring serum T3" which is next to impossible in a system wherein lab staff impose their views on which tests should be done, on which patients and in which circumstances. It has been obvious for decades that not doing THS+FT4+FT3 as standard has been pouring potentially vital information down the lavatory.
I'd also ask whether, if the "low-affinity high-capacity T3-binding cytoplasmic proteins" have such an impact, could they undermine Bianco's poly-zinc-liothyronine approach? That they themselves effectively slow the impact of the T3.
And could differences in them be part of the reason some do well on once-daily T3 dosing while others seem to need split-dosing?
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
Thyroid Glandular not helping T3 levels
Thyroid hormone levels
Is it useful to determine thyroid hormones T3 and T4 in 24 hour urine?
thyroid hormone resistance? not getting better on t4 alone or t4/t3 
