Thyroid test results, possible hyperthyroid?

[maduro_plantains]

My TSH is near the lower end of the range.
But seems that my T3 and T4 are within the normal range so would this rule out hyperthyroid?
I  have lower range of the testosterone also around 300's.


THYROID PANEL
T3 UPTAKE 34 22-35 %
T4 (THYROXINE), TOTAL 8.5 4.9-10.5 mcg/dL
FREE T4 INDEX (T7) 2.9 1.4-3.8
TSH 0.57 0.40-4.50 mIU/L
T4, FREE 1.2 0.8-1.8 ng/dL
T3, FREE 3.6 2.3-4.2 pg/mL
T3 REVERSE, LC/MS/MS 19 8-25 ng/dL

[Flyingfool]

The most important question is do you have hyperthyroid symptoms??

Secondly, are you taking thyroid medication?  If so what medication and what dose.

Third. If you are taking thyroid meds, did you take your thyroid pills before having the blood drawn?  As that can cause false high results.

The free T4 and free T3 are about perfect as far as a rule of thumb is concerned. As far as the numbers go.

You are about dead center 50% of range on free T4 which is great. And free T3 which is the active form you are at 68% of the range. The rule of thumb is 50% to about 67% for free T3.

TSH is a poor screening test. How you feel is the most important.

[Cataceous]

Reverse T3 is somewhat on the high side. In some cases it may outweigh mid-range T3, causing symptoms. But these would be more hypothyroid-type effects.

[Kierkegaard]

TSH isn't a thyroid hormone, so you shouldn't use it to determine thyroid function, generally speaking.  Primarily go by free T3 and how you feel. 

[Kierkegaard]

Reverse T3 is somewhat on the high side. In some cases it may outweigh mid-range T3, causing symptoms. But these would be more hypothyroid-type effects.

C, have you come across any more info on the reverse T3 "clogging up" T3 receptors hypothesis?  I've only found scanty stuff, but I don't really know why people who take T4 meds would feel worse unless it were due to this. 

[Osprey]

Reverse T3 is somewhat on the high side. In some cases it may outweigh mid-range T3, causing symptoms. But these would be more hypothyroid-type effects.

C, have you come across any more info on the reverse T3 "clogging up" T3 receptors hypothesis?  I've only found scanty stuff, but I don't really know why people who take T4 meds would feel worse unless it were due to this.

I've been reading "The Thyroid Patient's Manual" by Paul Robinson. In it he cites this study https://www.ncbi.nlm.nih.gov/pubmed/6707210 as showing that rT3 blocks T3 receptors. I haven't had a chance to read the whole thing yet though.

As far as why taking T4 makes some people feel worse he says that it is because taking T4 lowers TSH and lowering TSH will cause your own thyroid to produce less  T4 and T3. He also states that lower TSH directly results in a lower conversion rate from FT4 to FT3 based on these studies. https://www.ncbi.nlm.nih.gov/pubmed/3010024 and https://www.ncbi.nlm.nih.gov/pubmed/4058310

[Cataceous]

Reverse T3 is somewhat on the high side. In some cases it may outweigh mid-range T3, causing symptoms. But these would be more hypothyroid-type effects.

C, have you come across any more info on the reverse T3 "clogging up" T3 receptors hypothesis?  I've only found scanty stuff, but I don't really know why people who take T4 meds would feel worse unless it were due to this.

No, I think I've mentioned that there is some skepticism regarding the receptor-clogging hypothesis. ZRT says "Since high rT3 is linked with conditions associated with slow metabolism, it has been claimed in internet articles, but not in peer-reviewed papers, that rT3 causes a slowing in metabolism by blocking or obstructing the nuclear thyroid receptors. These receptors are the target sites where the primary active thyroid hormone, T3, binds, triggering its actions to drive cellular metabolism and maintain body temperature. Yet there is no credible scientific evidence that rT3 even enters the nucleus of the cell. While rT3 does not bind to, and has no known transcriptional activity at, the thyroid receptor, it does have potent non-genomic activity, mediated by binding to a specific thyroid receptor in the cytoplasm, as an initiator of actin polymerization in astrocytes in the brain [8][9]. ..."

The link from Osprey is very interesting. It says "The 5'D-II [secondary T4->T3 enzyme path] in brain, pituitary, and brown adipose tissue was reduced to less than or equal to 60% of control by 30 micrograms/100 g bw reverse T3 (rT3), an effect that lasted for at least 3 h after rT3 had been cleared. In rT3-pretreated thyroidectomized rats, the generation of [125I]T3 from tracer [125I]T4 was reduced in the serum: 6 +/- 1 vs. 12 +/- 1 X 10(-3)% dose/ml, P less than 0.01, during this 3-h period."

So maybe it can be inferred that high reverse T3 can result in local T3 deficiency in certain tissues. I've been wondering what causes the possible subjective improvements I've seen in taking 10 mcg liothyronine qd. This apparently resulted from cutting rT3 in half, while free T3 didn't move, and free T4 moved lower.

[Flyingfool]

Cat said: “I've been wondering what causes the possible subjective improvements I've seen in taking 10 mcg liothyronine qd. This apparently resulted from cutting rT3 in half, while free T3 didn't move, and free T4 moved lower.”

Could this be because no additional rt3 was created (or very lottle). But the additional t3 added allowed an abundance of ft3 available in the. Mood and rhat the dr3 stuck in the receptors was in fact cleared out?

Rt3 is only made via conversion from T4. With no additional t4 no additional rt3 was manufactured. So ft3 was ready and available to plug any rt3 that cleared a receptor. But in the absence of sufficient ft3, the rt3 is able to take the vacancy first. But in presence of sufficient ft3 wins the battle and race to fill the receptor site before rt3 does.

Common treatment to reduce rt3 is to go to T3 only protocol, severely reducing the amount of T4 and thus any available “stock” to convert wrongly into rt3. So what is left is a bunch of available ft3 and significant reduction in ft3, and the patient feels better.

The patient has to be extremely away that as the rt3 decreases, it is possible to go quite quickly from hypo, to hyper. And at first signs of hyper, to reduce T3 dosage.

If rhe receptor plugging theory doesn't work?  Why does adding T3 and limiting T4 seem to work when rt3 is high?

[Cataceous]

...
Could this be because no additional rt3 was created (or very lottle). But the additional t3 added allowed an abundance of ft3 available in the. Mood and rhat the dr3 stuck in the receptors was in fact cleared out?
...
If rhe receptor plugging theory doesn't work?  Why does adding T3 and limiting T4 seem to work when rt3 is high?

The references I cited offer some ideas, including the so-called "non-genomic" activity of rT3 in the brain, along with the possibility of local T3 deficiency, which is not reflected in plasma levels.

[Kierkegaard]

C,

Did you see this thread I put up a while back? https://www.peaktestosterone.com/forum/index.php?topic=15110.msg135928#msg135928

Scanty but seems to provide some possible evidence of the rT3 "clogging" hypothesis, though how much we can generalize given the study involved choriocarcinoma cells.

[Cataceous]

C,

Did you see this thread I put up a while back? https://www.peaktestosterone.com/forum/index.php?topic=15110.msg135928#msg135928

Scanty but seems to provide some possible evidence of the rT3 "clogging" hypothesis, though how much we can generalize given the study involved choriocarcinoma cells.

Thanks, K. I hadn't read that thread. It was before I started taking more of an interest in thyroid issues.

[Kierkegaard]

C,

Did you see this thread I put up a while back? https://www.peaktestosterone.com/forum/index.php?topic=15110.msg135928#msg135928

Scanty but seems to provide some possible evidence of the rT3 "clogging" hypothesis, though how much we can generalize given the study involved choriocarcinoma cells.

Thanks, K. I hadn't read that thread. It was before I started taking more of an interest in thyroid issues.

Totally understand.  I'm just trying to figure out, like you, why some people feel worse on T4-only meds, including myself.  Let me know what you think when you get a chance to read the study.

[AWesker]

I've been reading "The Thyroid Patient's Manual" by Paul Robinson. In it he cites this study https://www.ncbi.nlm.nih.gov/pubmed/6707210 as showing that rT3 blocks T3 receptors. I haven't had a chance to read the whole thing yet though.

I don't think that is the correct conclusion in that first study - it looks like this:

The 5'D-II in brain, pituitary, and brown adipose tissue was reduced to less than or equal to 60% of control by 30 micrograms/100 g bw reverse T3 (rT3), an effect that lasted for at least 3 h after rT3 had been cleared. In rT3-pretreated thyroidectomized rats, the generation of [125I]T3 from tracer [125I]T4 was reduced in the serum: 6 +/- 1 vs. 12 +/- 1 X 10(-3)% dose/ml, P less than 0.01, during this 3-h period"

Says that Reverse t3 inhibits D2 activity, which converts t4 to t3. It doesn't say anything about rt3 blocking t3 receptors. So if you still have healthy t3 levels, rt3 shouldn't be a problem in normal amounts.

[AWesker]

I've been wondering what causes the possible subjective improvements I've seen in taking 10 mcg liothyronine qd. This apparently resulted from cutting rT3 in half, while free T3 didn't move, and free T4 moved lower.

did you measure total t3/total t4 levels at that time in addition to the free levels?
Here's a possible explanation:
-T3 itself stimulates D1/D2 activity, which convert rt3 to t2, hence lowering your rt3 levels in your labs.
-T3 inhibits TSH, lowering your bodies production of t4, hence lowered free t4.
-Either D1 or D2, I forget which, is mainly responsible for conversion of t4 to t3 in your liver, thyroid, etc, where the resulting t3 ends up in your plasma - and is picked up by blood labs. The other deiodinase is mainly responsible for converting t4 to t3 intracellularly. The t3 resulting from this conversion would *not* be picked up on blood labs. So taking t3 could increase your conversion of intracellular t4 to t3, helping you feel better but not being reflected in your free t3 labs.

[Cataceous]

I've been wondering what causes the possible subjective improvements I've seen in taking 10 mcg liothyronine qd. This apparently resulted from cutting rT3 in half, while free T3 didn't move, and free T4 moved lower.

did you measure total t3/total t4 levels at that time in addition to the free levels?
...

Only total T4, which probably also went down along with free T4 (to 3.8 ug/dL (4.5-12.0)).

A subsequent test a couple hours after dosing shows there's temporarily a decent boost in T3 (4.0 pg/mL (2.0-4.4)).