Download T4 to be maintained at a reasonable level

T4 to be maintained at a reasonable level.
You must maintain your FT4 at a reasonable level because it is the reservoir for thyroid
hormone. The first level response to the use of thyroid hormone is for the bound form to come
into the free form and for the T4 to be converted to produce T3. If you do not have the store
of T4, you have no short term source and rely entirely on the T3 you are taking each day. This
is problematic because the level of T3 in this circumstance would fluctuate quite significantly
over each day of the year.
T4 does nothing in respect of the binding of TSH. Low levels of T4 do cause the pituitary to
produce higher levels of TSH via the binding of T4 to receptors in the hypothalamus. The cells
of the hypothalamus are particularly sensitive to T4 because brain cells have a particular form
of deiodinase (Type II) which only produces T3 from T4. It produces no R-T3.
Treating R-T3 is a bit of a furphy. R-T3 is a product of Deiodinase I which produces both T3
and rT3 . This deiodinase’s most vigorous reaction is to turn rT3 into T2. It second most
vigorous reaction is to turn T4 into T3. Its third most vigorous reaction is to turn T4 into rT3.
The third reaction is much less vigorous than the second which is only slightly less vigorous than
the first. In normal circumstances then, the body produces a lot of T3 and a little rT3 which is
very quickly converted into T2. If the amount of deiodinase I declines, all these reactions slow
down, but the impact is felt mainly by the most vigorous reaction – ie the breakdown of rT3
slows the most. This is what results in a build up of rT3 and a decline in T3.
The deiodinase I reactions are partly mediated by T3 so that the reduction in T3 feeds back
positively to further slow down the production of T3. The reaction is therefore quite sensitive.
This well defined process is what drives the ‘logic’ behind the proponents of Wilson’s Syndrome.
Their response is to pump up the T3 levels to push up the conversion rate. The catch of course
is that the T3 mediation is only one of the elements affecting the amount of Deiodinase I and
its vigour.
I have a very simple approach which is that the idea is to have the hormone levels as close to
the ‘normal’ values as possible. If you are taking combination T4/T3, this means having readings
close to the ‘normal’ averages. If you are taking T4 alone, you need to push the T4 level higher
than the ‘normal’ average to compensate for the lack of T3 production by the thyroid. The rule
of thumb here is that you need the T4 reading in the upper third of the reference range. This
should then produce mid range T3, but will of necessity produce a low normal or suppressed
TSH.
( Alun Stevens MSc FIAA )
There is no question that T3 is an active, effective thyroid hormone. However, in most vital
organs, much of the T3 is produced by removal of an iodine atom from T4 delivered by the
blood to sites of thyroid hormone action. The extent of T4-to-T3 conversion varies from one
organ to the other, but in some organs, like the brain and pituitary, this process provides most
of the T3. Treatment with T3 produces an unnaturally large amount of T3 in some organs. This
may be inappropriate, especially in times of illness or nutritional deficiency. Long-term T3
treatment may cause harm. Excessive T3 treatment can greatly affect the heart and skeleton
aka, Osteoporosis. These effects can be serious and even life-threatening.
( Extract- American Thyroid Association Statement ALERT on "Wilson's Syndrome" November
16, 1999)
Thyroid Physiology:
(1)
•
THE THYROID ABSORBS IODINE AND USES IT TO MAKE
– T4 (THYROXINE)
– T3 (TRIIODOTHYRONINE)
•
•
THYROID PRODUCES MUCH MORE T4 THAN T3 ~40:1
T3 PRIMARY ACTIVE HORMONE (4 times as potent)
•
T3 BINDS TO RECEPTORS IN CELL NUCLII AND TRIGGERS METABOLIC
PROCESSES, NERVE DEVELOPMENT AND GROWTH *
*This does not happen properly in a small number of people as they have malformed
receptors due to genetic problems. Thyroid Hormone Resistance pre exists the Thyroid
condition.