Defend our plasma T3. Today.

Defending T3 is a biological priority-500


Abdalla, S. M., & Bianco, A. C. (2014). Defending plasma T3 is a biological priority. Clinical Endocrinology, 81(5), 633–641.

In this ground-breaking article with a profound title, Abdalla and Bianco explain that human biology is set up to carefully protect and defend optimal thyroid T3 hormone levels in our bloodstream (plasma).

This is why we should all be willing to defend human Plasma T3 when it is at risk.

Dear Canada,

Please help us defend access to the T3-based medications that have been experiencing drug shortages.

Our Petition is open for e-signatures until December 25, 2018.

Canadians with healthy thyroid glands CAN turn up their “thyroid thermostat” whenever their body needs to raise its metabolic rate, whether during exercise, during exposure to cold climate, or to kick-start their recovery from a temporary low-T3 state caused by a serious illness.

However, patients with lifelong, chronic hypothyroidism are NOT able to naturally defend this crucial cellular energy source, T3.

How could we possibly suffer a T3 defict while taking thyroid hormones?

Too many of us on the standard T4 therapy fall far short in our T3 levels compared to healthy people, as Abdalla and Bianco explain at the end of their article.

Suboptimal T3 could well be the main reason why so many thyroid patients are fatigued, suffering cognitive and emotional difficulty, or chronically ill and taking other medications.

Nothing in our diet or lifestyle can supply thyroid patients with T3 hormone. It can’t be fixed by exercising or eating healthier.

No, you just can’t get T3 from muffins.

T3 is necessary in recovery from severe illness.

The TSH-T3 response is the first step in the natural recovery process in severe illness, which often causes “low T3 syndrome” even in people with healthy thyroid glands.

For decades, researchers have performed clinical trials to see if T3 medication can help people with normal thyroid glands recover from low T3. Recently, the methodologies are showing some promise.

If even people with normal thyroid glands benefit from T3 therapy in recovery, can thyroid patients recover without it?

Abdalla and Bianco wonder the same thing in this article under their heading “How well defended is serum T3 in the absence of a functional thyroid gland?”

Nobody has a definitive answer to this important question yet. People without thyroid glands are excluded from research on Low T3 syndrome.

But why are we even asking if a _chronic_ state of low, or even suboptimal T3, possibly maintained for decades, is harmful to human health?

It’s like thyroid medicine is trapped in the days before smoking tobacco was declared unhealthy, when people were still saying there was “not enough research” — How much knowledge of T3’s vital importance and power will be enough? We have known since the discovery of T3 hormone in 1952 that it is the most important and active thyroid hormone, and we know extreme T3 deficiency can and does kill people. It’s called myxedema coma. And a sustained Low T3 level in blood in the intensive care ward is the most powerful predictor of death and continued morbidity.

In this article, scientists point out that the patient with a compromised thyroid axis simply does not have the biological equipment to defend T3, and the standard T4 medication does not always defend it.

The health implications of chronic T3 deficiency may be significiant, both to the individual and our population at large.

Our thyroid levels are locked in place.

T4 therapy is also currently designed to _prevent_ changes in TSH and our T4 hormone levels. Even if our TSH or T4 were able to temporarily soar above the normal range in a situation when we needed extra T3, neither TSH nor T4 may be able to stimulate a handicapped thyroid metabolism to increase plasma T3 levels (see Abdalla and Bianco’s explanation of the deiodinases D1, D2 and D3).

We thyroid patients cannot simply raise our pituitary TSH or our T4 or T3 — it is generally “locked” in place by our daily dose of thyroid hormone. And it could easily be locked in an unhealthy place and prevented from rising, because doctors are being told _not_ to measure our Free T3 in a simple blood test.

Therapy with T3 hormone offers a direct fix for low T3, no matter what the cause. It is not a simple fix, but it is truly effective in raising plasma T3 levels.

T3 dosing is also sustainable long-term in thyroid therapy, despite these authors’ point about its inconvenience due to T3’s short half-life in serum.

You would take T3 medication if your body needed it, even if it required two or three doses of T3 hormone per day.

We need to keep T3-based meds on the market. We need doctors who can discern and treat chronic low T3.


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