Weird reaction to Levothyroxine and reverse T3 issues

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I was diagnosed with sub clinical hypothyroidism around 6 months ago, I was very much symptomatic despite only having a TSH of 3ish and low but in range T3 and T4 levels. I was initially put on NDT (NP thyroid but that did little to change any of my symptoms, doctor put me on Levothyroxine instead.

Literally the same day I started Levothyroxine went hyper on a dose of 50mcg so I stopped for a few days. Trialed a dose of 25mcg per day and I felt amazing and back to 100% for about 3 days before it tapered off and I went back to feeling hypo once again but I figured I'd stick it out for 6 weeks and get blood work done. These few days my hair stopped failing out, brain fog was eliminated, I felt like my muscles were full of glycogen for the first time in a long time, ED was resolved and libido was great, but it all subsided after a few days.

Pulled bloods after the 6 weeks on 25mcg per day and TSH was 0.5, T4 of 1.54, T3 of 4.0, but my RT3 is 29 which is obviously quite high. So everything aside from RT3 is great. Cortisol is upper mid range, iron is all on the upper mid end of the range, ferritin is a little high at 250, all my inflammation markers are great, so l'm not sure what is causing this?

The weird part for me is that T3 essentially does nothing for me, I’ve taken 75mcg of T3 in a single day and I essentially had no reaction to it aside from feeling a touch warmer, it was nothing like how I felt hyper from a 50mcg dose of Levo. I know someone will inevitability ask if I’ve mixed up my T3 and T4, and that’s not the case. It feels like I have some sort of resistance to T3, I legitimately can’t go hyper with it regardless of how much I take.

Any idea what could be causing a near instant reaction to T4 only to have it all go down the RT3 path and leave me feeling Hypo again? And why T3 does nothing for me as well?
Defy Medical TRT clinic doctor


Any idea what could be causing a near instant reaction to T4 only to have it all go down the RT3 path and leave me feeling Hypo again?
Thyroids resistance, resistance at the receptor. I knew two women with the same problem, only neither responded at all to thyroid hormones, T3 or T4.

All that T3 and T4 floating around in the body not doing anything.
I don’t believe I have a total resistance to thyroid hormone, I’m more inclined to believe this is caused by RT3.

I’m certainly no expert, but my response to Levothyroxine working for a few days only to have it slowly stop working again seems to me that T4 increases upon starting Levo, only to have it go down the T4 > RT3 path due to increased DIO3. Only thing is I’ve ruled out all the typical causes for increased RT3 being liver, cortisol, inflammation and iron.

So I’m looking for some more uncommon causes of increased RT3.

In the interim, I’m dropping HCG which I’ve been taking for 4 years as part of my TRT protocol. I know HCG has the potential to cause thyrotoxicosis in some people as it weakly increases T4 and T3 serum. I found some studies indicating that RT3 correlates with the rise in HCG in pregnant women, so this might have something to do with it


I don’t believe I have a total resistance to thyroid hormone, I’m more inclined to believe this is caused by RT3.
I think you may be right, after more research I found this -> Reverse T3 and Reverse T3 dominance

Reverse T3 dominance, also known as Wilson’s Syndrome, is a condition that exhibits most hypothyroid symptoms although circulating levels of T3 and T4 are within normal test limits. The metabolism of T4 into rT3 is in excess when compared to T3 therefore it is a T4 metabolism malfunction rather than a straight forward thyroid deficiency. Periods of prolonged stress may cause an increase in cortisol levels as the adrenal glands respond to the stress. The high cortisol levels inhibit the 5-deiodinase enzyme Type 1 and thus the conversion of T4 into T3 thus reducing active T3 levels. The conversion of T4 is then shunted towards the production of the inactive rT3 via the 5-deiodinase enzyme Type 3. This rT3 dominance may persist even after the stress passes and cortisol levels have returned to normal as the rT3:T3 imbalance itself may also inhibit the 5-deiodinase enzyme Type 1 thus perpetuating the production of the inactive rT3 isomer. There is some argument to this last point with some research indicating that the elevated rT3 is only temporary and not a permanent condition and in most healthy people this may well be the case. We have however found that in many patients suffering from a range of hypothyroid symptoms do indeed have prolonged elevated rT3 levels which respond favorably to this treatment. Many medical practitioners do not accept rT3 dominance theory and thus many doctors will refuse to treat this condition despite the fact many suffers have been successfully treated. See below for the evidence in the references.

Other causes of reverse T3 dominance include: leptin resistance, inflammation (NF kappa-B), dieting, nutrient difficiencies such as low iron, selenium, zinc, chromium, Vit B6 and B12, Vit D and iodine, Low testosterone, low human growth hormone, Insulin dependent Diabetes, Pain, Stress, environmental toxins, Free radical load, Hemorrhagic shock, Liver disease, Kidney disease, Severe or systemic illness, severe injury, Surgery, Toxic metal exposure.
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