-LABGAB] Hormone Reception Hidden From Thyroid Tests?

[Guest guest]

Interesting

questions and it would be good to get some feedback from the scientists on

this forum on both questions. Chuck, Bob etc, where are you please?

From Dr

Peatfield's paper, he states:

" You

may remember that in order for thyroid hormone to work in controlling our

metabolism it has to be converted from the basic, precursor hormone T4 to the

active hormone T3. You will also remember that the amino acid thyronine (which

is made by two tyrosine molecules coming together) when combined with four

iodine atoms is how thyroxine is formed (which we know for short as T4). Then

one of the three 5: deiiodinase enzymes removes one of the iodiio atoms and

forms T3 (triiodothyronine or liothyronine), which does all the work of

controlling our energy output. This it does by improving the capacity of the

cell membrane to pass into the cell every chemical needed to make our

metabolism work, and to fire up the capacity of the mitochondria within the

cell to produce energy.

But

circumstances may arise where the active T3 becomes unwanted by our metabolic chemistry.

Then the T4 to T3 conversion is sabotaged, and the iodine atom removed from T4

is taken from a different site in the T4 molecule. So the chemistry is the

same, but the layout is subtly different. This differed form of T3 is called

reverse T3 (rT3). And reverse T3 doesn’t have metabolic activity; it

doesn’t have any effect on the cell membrane or the mitochondria.

So,

what is it for?

It

turns out that this is a cunning way of removing excess thyroid hormone, and

preventing too much active T3 from being made.

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.

Certain

circumstances can arrive when removal of excess thyroid hormone is helpful.

Obviously, this process can remove excess T3 if the thyroid gland is producing

too much. This happens in early hyperthyroidism, although the recycling is

fairly limited, and with a thyroid gland thoroughly over the top, is only of

modest effect.

Many

authorities like to test for reverse T3. I don’t find this a particularly

helpful test, but perhaps we can look at how it can be interpreted. A low level

is likely to be found with a hypothyroid state. If thyroid output is lower than

it should be, then rT3 levels will be low since there is less T4 to be

converted into either T3 or rT3. You can then conclude that primary thyroid

output is below normal, or that conversion is limited.

Poor conversion

relates to low adrenal function (adequate cortisone is needed for the

conversion to work properly) or exhaustion or dysfunction of the 5 deiiodinaise

enzyme itself. Diagnostically, poor conversion is usually evident in the serum

tests or the 24-hour urinary thyroid hormone.

Treatment

is of course obvious. Either the provisions of T4 or T3 or both; or the use of

natural desiccated thyroid, once adrenal support is fully in place.

The

pathological finding of increased rT3 means that either more thyroid hormone is

being created than the system needs or can use: or, that there is some

pathological process blocking adequate T3 uptake. Dieting or malnutrition will

have this effect; chronic illness will do the same. Particularly one should

mention the presence of cancer somewhere (especially metastatic cancer, i.e.

when it spreads), a degree of liver or kidney failure, Cushing’s disease,

insulin dependent diabetes, and the post operative state following surgery.

Treatment

has to be, therefore, if appropriate, of the primary cause. Provision of extra

T4 or T3 is not an option, because it will mearly create more rT3. High rT3

means that general health should be considered; and if all is well, one has to

decide whether the provision of any thyroid replacement could be too much, or

there is a processing factor causing a back up of T3 or T4.

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. Receptor resistance may indeed occur, but it is due to other

factors, most commonly adrenal insufficiency.

Luv -

Sheila

The question of " Is Hormone Reception Hidden from

Thyroid Tests? "

hinges upon the behavior of the peripheral metabolism of T4 to T3. My

understanding of this metabolism is that if there is sufficient T3

(what precisely that means, I am not sure, but presumeably in the

blood) then this metabolism strips T4 of a different iodine atom and

creates reverse triiodothyronine (rT3) instead of T3. This regulatory

behavior would then manage the level of T3 in the blood and make the

various levels independent of use, providing that the pituitary is not

responsive to rT3.

This characterization of the peripheral metabolism would create a

physiological barrier between the standard thyroid testing procedures

and all post thyroid hormone deficiencies as free T3 is not tested

either.

The second question is: " Since hypothyroidism and hyperthyroidism are

effectively duals, isn't the not testing T3 for hypothyroidism and

testing T3 for hyperthyroidism contradictory? " It is said by Dr

Garber of the American Association of Clinical Endocrinologists that

T3 need not be tested for hypothyroidism because it " generally "

follows T4. Then would not that statement also be true for

hyperthyroidism. It seems a bit far fetched to me.

Have a great day,