Hormone Reception Hidden From Thyroid Tests?

[Guest guest]

Sheila,

You wrote:

>

> Chuck, Bob etc,

> where are you please?

I have fairly minor quibbles with several things in the paper. First, he

states,

> ... And reverse T3 doesn’t have metabolic activity; it doesn’t

> have any effect on the cell membrane or the mitochondria....

It would be more accurate to say it has very little activity. It does

lower TSH, which can create the illusion of hyperT or euthyroid, when

the symptoms are still hypoT.

>....The reverse T3 rapidly breaks down to its component parts – the

> thyronine and iodine, which are thus re-cycled and stored, until more

> thyroid hormone is required. So, you see rT3 is a way of disposing of

> excess thyroid hormone.

It is much more, and RT3 does not break down any more rapidly than T3.

Rather, they both get turned into T2 by the same deiodization enzyme.

RT3 acts much more like a brake on metabolism, rather than just a safety

valve. RT3 blocks the receptors that the T3 would fill, so it actively

subtracts from the effects of T3. It prevents some of the T3 from working.

Poor conversion typically reduces both T3 and RT3. That is why " excess "

RT3 is really a matter of the ratio between them, a distinctive problem.

The litany of causes Dr. P. lists are well recognized. However, his

suggested treatment is contradictory. Specifically, he says,

>

>... Provision of extra T4 or T3 is not an option, because it will mearly

> create more rT3....

The claim that intake of T3 will increase RT3 is patently false,

impossible, in fact. RT3 comes ONLY from the deiodization of T4. If your

only source of thyroid hormone is T3, the system cannot make RT3. The

question is whether intake of T3 only will dissolve whatever condition

was causing the RT3 excess in the first place.

> Questions have been raised concerning the possible role of high rT3 in

> causing receptor resistance in fibromyalgia. My colleague Lowe

> found no evidence of this, and nor have I.

As far as I can tell, this statement is based entirely on one paper,

Lowe, J.C., " Thyroid status of 38 fibromyalgia patients:implication for

the etiology of fibromyalgia, " Clin Bull Myo Ther 197;2:36-41.

Obviously this is controversial at best, probably with too little real

data to tell the difference, but here are two papers that found a

connection:

Tsigos C, Chrousos GP. Hypothalamic-pituitary-adrenal axis,

neuroendocrine factors and stress. J Psychosom Res

2002;53(4):865-71. Review.

D. Brady, " Fibromyalgia syndrome: A new paradigm for differential

diagnosis and treatment, " Journal of Manipulative and Physiological

Therapeutics, Volume 24, Issue 8, Pages 529 - 541.

Chuck