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Re: RT3

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> Val thinks I may have a problem with RT3, where can I go to read up

Some info from my files:

Small amounts of rT3 are made within the thyroid; however, peripheral

generation from T4 is estimated to account for 95 percent of all rT3

produced.[5] The enzyme responsible for this conversion is 5-

deiodinase and is not believed to be dependent on selenium for its

activity. This enzyme acts on the nonphenolic ring of T4 (the inner

tyrosyl ring) to produce the hormonally inactive rT3. Under normal

conditions, 45-50 percent of the daily production of T4 is

transformed into rT3. Substantial individual variation in these

percentages can be found secondary to a range of environmental,

lifestyle, and physiological influences.

Causes of decreased T3 and increased rT3:

Aging [12]

Burns/thermal injury[63]

Caloric restriction and fasting[64-66]

Chemical exposure[67]

Cold exposure[68]

Chronic alcohol intake[69]

Free radical load[30]

Hemorrhagic shock[70]

Insulin-dependent diabetes mellitus[71]

Liver disease[31]

Kidney disease[72,73]

Severe or systemic illness[74]

Severe injury[76]

Stress[77]

Surgery[15,78-80]

Toxic metal exposure[26-29]

Changes in 5'-deiodination occur in a number of situations, such as

stress, poor nutrition, illness, selenium deficiency, and drag

therapy. Toxic metals such as cadmium, mercury, and lead, have been

associated with impaired hepatic 5'-deiodination in animal models.[26-

29] Results suggest free radicals are also involved in inhibition of

5'-monodeiodinase activity;

Drugs that increase RT3:

Drug (use/class) rT3

Dexamethasone (corticosteroid)[81] increase

Propylthiouracil (thiourylene)[82] increase

Iopanic acid (radiographic contrast agent)[83] increase

Sodium Ipodate (radiographic contrast agent)[84] increase

Amiodarone (antiarrhythmic/antianginal)[85] increase

Propranalol (beta blocker)[86] increase

Elevations in cortisol,[13,14] catecholamines,[15] and some cytokines

(IL-6, TNF-[Alpha], and IFN-[Alpha]),[18-20] and low serum albumin

levels[12] have been associated with low T3 syndrome. It has been

suggested that high levels of cortisol might be responsible for the

altered T4 peripheral metabolism to T3 and rT3 in these patients.[76]

Soy protein consumption also was found to contribute to age-related

alterations in thyroid hormone in animals.[132] These alterations

included a decline in T4, fT4, T3, and 2,3'-T2 and an increase in rT3.

[132]

Because of its role as a cofactor for type I 5'-deiodinase,

selenium's influence on deiodination is the best characterized of any

nutrient. While a selenium deficiency does not seem to result in a

decrease in the production of T4 or T3 within the thyroid gland,

deficiency substantially alters the conversion of T4 to T3 in

peripheral tissues such as the liver and kidney. This is generally

accompanied by reduced T3 and an increased rT3 in the circulation.

Zinc deficiency appears to strongly inhibit type I 5'-deiodinase in

animal models; however, the mechanism for this effect is not

understood and it is currently not clear if a similar role for zinc

exists in humans.

A little long, I know, but probably beneficial reading for quite a

few here.

Barb

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Great! Do you have a link to the original paper?

I'm saving this info!

sol

Barb wrote:

> Some info from my files:

> Small amounts of rT3 are made within the thyroid; however, peripheral

> generation from T4 is estimated to account for 95 percent of all rT3

> produced.[5] The enzyme responsible for this conversion is 5-

> deiodinase and is not believed to be dependent on selenium for its

........................

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