What happens when healthy people overdose Reverse T3? We learned in 1984.

One of the most common myths about Reverse T3 (RT3) thyroid hormone is that it blocks T3, impairs net T4-T3 conversion rates, or functions as a “metabolic brake.” No, that’s a RT3 myth that was debunked long ago, back in 1984.

Introduction

Certain experiments in the laboratory — in vitro — have suggested that RT3 can interfere with T4-T3 conversion. Some of these experiments were conducted before 1984.

However, if RT3 could function like an anti-T3 hormone in real life, in living humans and not just in cell cultures or rats, you’d expect changes to T3, T4, and TSH to follow excess RT3 — I’d expect a reduction in the T3/T4 ratio even if the TSH stayed the same.

Shulkin and Utiger’s 1984 experiment showed that dosing Reverse T3 as a pharmaceutical — to levels that inflated RT3 levels “at least 10-fold” which is 10 times the baseline mean level — did absolutely nothing to circulating TSH, T3, or T4.

RT3 overdose didn’t cause hypothyroidism in healthy people. It didn’t even cause symptoms of hypothyroidism like a lower heart rate. That means that excess RT3 didn’t compete with or counteract thyroid function, T3 or T4 transport, T4 or T3 metabolism, or TSH response to circulating RT3 or other thyroid hormones.

Why didn’t RT3 excess affect any part of their thyroid function, metabolism, or pituitary response? Was something wrong with their experimental design? Was their RT3 pharmaceutical not bioidentical? Read my explanation after you review the summary and analysis of the study itself.

Their abstract

Abstract:

“Serum rT₃ concentrations are often increased in patients with nonthyroid illness. Such elevations could be responsible for some of the alterations in pituitary-thyroid function that occur in such patients, particularly since rT₃ is a potent inhibitor of extrathyroidal T₃ production in vitro.

To evaluate the role of serum rT₃ elevations in the regulation of the hypothalamic-pituitary-thyroid axis, 10 normal subjects were given 3 mg rT₃, orally, in divided doses for 4 days. Serum rT₃ concentrations were elevated at least 10-fold by the end of the first day of treatment.

Mean serum T₄ and T₃ concentrations did not change, nor was there any change in basal or TRH-stimulated serum TSH concentrations. There was, likewise, no change in serum binding of T₃ or T₄.

These results show that rT₃, given orally, has no detectable activity in normal subjects, and hence, elevations in serum rT₃ concentrations per se do not contribute to other abnormalities in thyroid function found in patients with nonthyroid illness.”

For your convenience and verification, here it is, in the original font with my underlining for emphasis.

As you can see, the question was about the power of RT3 hormone to reduce T4-T3 conversion. High RT3 was unable to change to the major biomarkers that WOULD be expected to change if RT3 excess had the ability to inhibit T3 production:

• no change in the T3/T4 ratio or levels,
• no change in T3 signaling or TRH signaling in the regulation of TSH,
• no change in free vs. bound fractions of T3 or T4 in blood.

As a result, oral RT3 that huge increases RT3 levels in blood do not have detectable effects on the pituitary-thyroid system. Therefore, the rise of RT3 “does not contribute,” does not cause or drive in any way, the losses of T3 and failure of TSH to rise during “nonthyroid illness.”

More about nonthyroidal illness will be revealed as you read on.

The motivation for the study

Utiger was a leading thyroid scientist, the father of the TSH test. In this article, published in a leading thyroid journal (The Journal of Clnical Endocrinology and Metabolism), they laid out what was already understood about Reverse T3 hormone:

“PATIENTS with nonthyroid illness have a variety of abnormalities in thyroid function. Perhaps the most characteristic of these abnormalities are reduced serum T3 and increased serum rT3 concentrations accompanied by normal serum T4 and TSH concentrations.” (Intro, Para 1.)

The main interest in RT3 has been in the context of severe illness, when the relationships among thyroid hormones and TSH become deranged. This is commonly known today as “nonthyroidal illness syndrome” (NTIS). The term “nonthyroidal” primarily distinguishes the syndrome from a thyroid disease such as primary hypothyroidism (thyroid gland failure or surgical removal), and “illness” names the real driver of the metabolic derangement. Of NTIS can also happen during treatment for a thyroid disease (see Wadwekar, et al, 2004) — but it can happen to anyone who is severely ill.

To the eyes of Shulkin & Utiger, before the discovery of what alters deiodinase enzyme behavior in illness, the puzzling thing was what caused RT3 to rise while T3 fell? These were patients with otherwise healthy and normal thyroid function. Then a crisis like a heart attack, car accident, or even a severe chronic a disease in a major organ or system, would raise RT3 and lower T3, surprisingly while keeping T4 and TSH normal as if nothing is going wrong with T3 signaling. But if nothing is going wrong, why is there such a strong association between low T3 and mortality in illness?

Some mechanisms were known in 1984, but others still unknown:

“Serum T3 concentrations decline because extra thyroidal T3 production is diminished, and serum rT3 concentrations rise because its clearance is diminished. The biochemical mechanisms that cause these abnormalities are not known.” (Para. 1)

That’s an important fact many forget about why RT3 rises — RT3 rises not just because more is created from T4, but also because the RT3 clearance rate is slowed down by illness. Now we know what they didn’t — that illness handicaps DIO1 (deiodinase type 1) enzyme that clears RT3 to inactive T2. DIO1 is also weakened by the loss of circulating T3 that normally upregulates DIO1 in the thyroid gland and liver.

But at that time, without knowledge of the mechanisms of DIO3 and DIO1, people were worried because of prior studies that hinted of RT3 activity:

“While rT3 is generally considered biologically inactive, both thyroid hormone agonist and antagonist properties have been reported for it (see below and Discussion). One possible explanation for decreased T3 production is that extrathyroidal conversion of T4 to T3 is inhibited by rT3, since rT3 is a potent inhibitor of the conversion of T4 to T3 in rat liver and kidney homogenates and rT3 reduces serum T3 concentrations when infused into rats (1-3).”

There were already studies in living rats and in cell cultures (homogenates) that suggested RT3 was not entirely inactive. So what about humans?

For the good of all patients, they needed to create a safe experiment to discover whether high levels RT3 hormone intrinsically had the power to inhibit T4-T3 conversion in vivo, in living human beings. Was RT3 an anti-T3 hormone, a toxin, or not? (The answer was, no, RT3 is not a competitive antagonist in vivo).

Utiger, as a champion of the TSH test, was most of all puzzled how a prior study showed that “short term RT3 administration did not inhibit TSH secretion in humans (5).” Reference 5 was this study in 1976, which influenced their study design: Nicod P, Burger A, Strauch G, Vagenakis AG, Braverman LE. 1976. The failure of physiologic doses of reverse T3 to effect thyroid-pituitary function in man. J Clin Endocrinol Metab 43:478

How they designed the RT3 dosing experiment

Shulkin and Utiger borrowed some strong features from the prior 1976 study of RT3 dosing, and added some new features:

• Both studies began by isolating RT3 from illness as a contributing cause. Only by observing RT3 in healthy subjects would it would be clear whether RT3 itself — rather than illness that drives up RT3 — could be the cause of T3 losses.
• Both studies examined a small group of human subjects. That’s okay in this case because they were studying cellular mechanisms, not probabilities within a population. This experiment had a lot of complex variables and tools and was likely very expensive per participant. The 1976 study only enrolled 5 men; this one enrolled 5 women as well as 5 men, aged 22 to 28 years old, with normal body weights. They had a healthy pituitary with a normal TSH response to TRH stimulation before the study.
• Like Nicod’s 1976 study, the 1984 researchers studied not just basal TSH but hypothalamic TRH-stimulated TSH. That was mainly because the TSH test wasn’t yet sensitive enough without this method of amplification. The third-generation TSH test was launched in 1988.
• Both studies measured T3 and T4 concentrations to see if their ratios and levels changed.
• Before running the experiment, they cross checked the quality of their RT3 pharmaceutical and hormone assays. They used the highest quality “liquid chromatographic”* methods available to ensure that the RT3 pharmaceutical was pure, not contaminated with T4, and that their detection of Total T4, Total T3, and Total RT3 did not confuse RT3 with any other hormone. They checked their T3 and T4 assays by ensuring that RT3 in serum obtained from normal individuals didn’t skew T4 or T3 results.
  • *NOTE: How do we know the RT3 in the tablet was bioidentical to naturally produced Reverse T3? Liquid chromatography can distinguish bioidentical levo-isomers (L-thyroxine, levothyroxine) from inactive dextro-isomers (D-thyroxine, dextrothyroxine), both produced during synthetic thyroid hormone manufacturing. D-RT3 would appear with a double peak or delayed peak, similar to the delayed peak of D-T4 (Hay et al, 1981)

In that prior study in 1976, they had studied “physiologic doses of RT3.” But now in Utiger’s study, they studied huge supraphysiologic doses. Their dosing protocol was as follows:

• They administered RT3 in 3 huge doses per day: “1.0 mg rT3, orally, every 8 h for 4 days for a total of 13 doses” starting and finishing with a morning dose after an overnight fast. 1.0 mg is 1,000 micrograms, so this was a dose totaling 3,000 mcg RT3 per day.
• Before each dose, blood samples were drawn to measure T3, T4, RT3 and TSH.
• They also administered a 400 mcg TRH–stimulated TSH test under the burden of RT3 in serum. This would stimulate pituitary TSH and magnify the basal TSH. This was a common technique at the time and in Utiger’s publications; they wanted to see if the TRH-stimulted TSH response was within the expected parameters in healthy subjects.

Results

• RT3 levels at baseline averaged 36 ng/dL. After the first day of 3 doses, “the nadir levels preceding the next rT3 dose were 10-fold higher than the basal concentrations.” By the end of the dosing experiment, the lowest Total RT3 level in blood had reached a mean of 526 ng/dL before the final dose. That is 14.6x higher than baseline, to be specific.
• How high did the peak RT3 go? “The peak serum rT3 concentration (mean, 2607 ng/dl; range, 1050-5068 ng/dl) occurred 110 min after rT3 administration, and thereafter, serum rT3 declined gradually.”
• How much did T3, T4, and TSH change?
  • Mean T4 held steady at 7.7 mcg/dL at baseline and at the end of the experiment.
  • Mean T3 changed from 117 to 115 ng/dL.
  • Mean TSH was 2.5 and then 3.1 mcU/mL, but this difference occurred because the TSH maintained its healthy rhythm of a rise overnight. Under TRH stimulation, TSH was 16.9 at the beginning of the experiment and 19.9 mcu/mL at the end.
  • Overall, within the range of error expected on their assays, this counted as virtually no change, despite 10-fold elevations in RT3.

• What else did they find?
  • No differences between men and women.
  • No symptoms except transient nausea in 2 out of 10 subjects.
  • No change in heart rate, blood pressure, or weight.

The researchers’ discussion of the experiment

In the discussion section, Shulkin and Utiger marvelled at the lack of change in T3, T4, and TSH “despite sustained 10-fold or greater elevations in serum rT3 concentrations and peak levels approaching 100 times basal values.” Nobody with illness-induced high RT3 ever has levels this high. Sometimes in people with kidney diseases, RT3 doesn’t rise above range at all during NTIS. Therefore, there were only 3 limitations they observed in their methods:

“Thus, impaired extrathyroidal T3 production in patients with nonthyroid illness cannot be ascribed to inhibition of T3 production by rT3 unless

• more prolonged rT3 increases are required,

• sufficient rT3 did not gain access to the intracellular site(s) of T3 production, or

• rT3 has actions in patients with nonthyroid illness that do not occur in normal subjects.”

They discussed each of these possibilities in turn.

• A more prolonged RT3 increase shouldn’t be required for this experiment because “reduced serum T3 and increased serum rT3 concentrations occur within 24h after the onset of various conditions, such as starvation, infection, or surgery, whose onset can be precisely defined (11).”
• While they couldn’t measure T4-T3 deiodination directly in 1984, they compared the observed lack of effect to studies of RT3 in living rats that clearly impaired their T3 concentrations after only a 4 hour infusion of RT3. This study showed no reduction in T3.
• They also compared their study to a prior experiment that showed an impact of reduced metabolic rate in treated hypothyroid and hyperthyroid patients when they were administered 300x to 1200x more RT3 than T4 or T3 — but while “very large quantities of rT3 may have in vivo actions,” what kind of RT3 actions did that experiment reveal? It didn’t answer the question about whether high RT3 could interfere with the pituitary-thyroid axis via T3, T4, and TSH.

My thoughts as a thyroid patient mentor and educator

People who continue to fear RT3 or spread fear of RT3 to others are probably unaware of this study. It exonerates the hormone RT3 from being blamed for a host of evils.

Anyone who knows this study should think twice when they see or hear internet myths like these:

• “RT3 is a metabolic brake” — No, DIO3 enzyme, which happens to make RT3, is a metabolic brake because it breaks down T3.
• “Excess conversion of T4 to RT3 causes less T4 to convert to T3” — No, that’s not how the cause and effect works.
• “Higher RT3 causes poorer T4-T3 conversion” — Not in living humans. Only if you isolate cells in a petrie dish or study rats.
• “High RT3 causes hypothyroid symptoms” — No, because loss of T3 signaling causes hypothyroidism, and RT3 can’t interfere with T3 hormone’s pathway.
• “RT3 can impair T3 uptake into cells and cause “T3 pooling” — No, most transporters on cell membranes prefer to carry T3 and T4 into cells, regardless of how much RT3 is in blood.

Why would anyone continue to blame high-normal or mildly high RT3 for symptoms in hypothyroid patients when RT3 levels hundreds of times as high did NOT cause any symptoms or signs of poor T4-T3 conversion, T3 inactivation, or impaired T3 uptake or T3 signaling in tissues?

Dosing studies can provide a lot of insight into mechanisms because they isolate a substance from the natural causes that elevate it. These 10 people dosed RT3 the same way we hypothyroid patients dose synthetic T3 and T4. Hypothyroid patients know by experience that synthetic LT3 and LT4 dosages are very potent; they can suffer when underdosed or overdosed even a little bit below their individual optimal zone, even if their TSH is normal. In contrast, this huge RT3 overdose was incredibly powerless.

Why didn’t sky-high RT3 levels harm these 10 healthy people?

In short, because A) Their high RT3 was not driven by illness, but most of all — B) they didn’t have a T3 deficiency induced by hypothyroidism and/or illness.

When you see RT3 rise per unit of T4 — AND — T3 fall per unit of T4, this inverse shift is the classic signal of nonthyroidal illness syndrome (NTIS). The root cause of any hypothyroid symptoms resulting from T3 losses is not the RT3 hormone– the root cause is the illness that upregulates DIO3 enzyme while impairing peripheral DIO2 and DIO1.

Various health disorders increase inflammatory cytokines and/or drive tissue hypoxia and oxidative stress. These intracellular signals have the power to upregulate the DIO3 (deiodinase type 3, D3) enzyme inside cells.

• DIO3 is the unseen enzyme that creates RT3 from T4 and inactivates T3 at the same time.
• DIO3 has higher affinity for T3 than T4. It prefers to inactivate T3 — more T3 hormones “die” than RT3 hormones are born in cells that are DIO3-rich.
• What is the byproduct of T3 inactivation? 3,3′-T2, an inactive T3 metabolite. You can think of this as “Reverse T2.”
• Why don’t we have blood tests that measure 3,3′-T2 hormone? Because this form of T2 has a faster clearance rate than T3 itself — it becomes deiodinated to T1 and then to T0 – T zero, a tyrosine framework without any iodine atoms left.

But these 10 “healthy subjects” overdosing RT3 had a normal DIO3 enzyme because they lacked any health condition that would have upregulated it. So having tons of RT3 in blood from RT3 tablets did no harm to them. No illness interfered with their T4-T3 conversion or T3 signaling in the pituitary and hypothalamus, which powerfully regulates TSH.

Causes come before effects. High RT3 is not a cause. It’s an effect.

1. In the example of acute nonthyroidal illness, does RT3 rise first?

Acute illness shows this. It’s not easy to see causation over time in insidious chronic diseases like cancers or heart failure, even if they also drive up RT3 per unit of FT4 and cause T3 losses per unit of FT4. But in most cases in acute illnesses like heart attacks, the series of cause and effect over time is clear.

1. First T3 and RT3 are normal. Then the heart attack occurs.
2. Then within 24 hours after the heart attack, RT3 skyrockets and TT3 plummets (Wiersinga et al, 1981).
3. The rise of RT3 does not occur before the loss of T3; they both occur together. They are both effects.

2. During recovery, does RT3 fall first?

If RT3 was the cause of T3 losses, you’d expect RT3 to come down before T3 rises during recovery. However, that’s not what happens.

The first sign of recovery is a rise of TSH above normal range, which kicks a healthy thyroid into gear to first prevent further T3 losses, and then replenishes T3. This T3 turnaround occurs before the RT3 returns to normal levels. Patients are already out of danger while RT3 remains high. The high RT3 is so weak that it fails to prevent the recovery of T3.

What’s more associated with mortality, a high RT3 or a low Total T3?

In the RT3 literature, mortality during illness is not strongly associated with the height of RT3 levels, but rather with low Total T3 (in people NOT dosing T3). See Kang et al, 2018 who studied TT3 and FT4 in heart failure. They stated:

“Although the lowering T3 is commonly interpreted as adaptive and beneficial in acute stage of the conditions, the persistently lasting low T3 levels might contribute to the progressive deterioration of cardiac function and myocardial remodeling process [4].”

Warner & Beckett (2010) explain the increased mortality risk this in a graphic:

But you don’t need to measure RT3 or Total T3 to know that NTIS is mild or moderate or severe (if you’re not dosing any T3) — There’s a more accessible set of blood tests that tells you a lot. All you need to see is the low FT3/FT4 ratio that widens as you move from mild to moderate, and see both FT3 and FT4 fall as you transition to “severe.”

Here are some explanations for some of the changes in the graphic:

1. A low TT3 may eventually be followed by a low Total T4 if your illness worsens, because DIO3 enzyme inactivates both T4 and T3, while TSH will not rise until the recovery phase.
2. In NTIS, why does FT4 rise, and why doesn’t FT3 fall as low as TT3? Illness causes T4 and T3 to have reduced affinity to binding proteins such as TBG increasing the % free. Also, we often lose albumin during illness, and albumin binds 10-20% of T3).
3. In NTIS, why doesn’t TSH rise as soon as TT3 falls? 1) because FT4 often inflates (see point #2), and 2) while DIO1 and DIO2 are oppressed in peripheral tissues, the hypothalamus and pituitary may experience a local boost or maintenance of in DIO2-driven T4-T3 conversion rates.
4. The TSH may also fall low if you fail to recover from NTIS. When FT3, FT4 and TSH are concurrently low or low-normal, the thyroid status is similar to central hypothyroidism (pituitary TSH secretion failure). A low TSH fails to drive thyroidal secretion and T3 and T4 recovery. This phenomenon should naturally raise questions about the vulnerability of people with central hypothyroidism during illness, and the vulnerability of people who lack a thyroid that can be stimulated by TSH, if they don’t have access to LT3 dosing to replenish T3.

What’s more harmful, RT3 gains, or T3 losses?

I hope you’ll answer intelligently now — hidden intracellular T3 losses are more harmful than visible RT3 gains.

It’s a common fallacy to think that the most abundant or excessive blood level is the driver, the cause, the powerful actor in one’s current distress.

If the overabundant hormone is one of the least powerful thyroid hormones we know of, it’s not the root cause of your problem. Not even an acute overdose of RT3 in this experiment caused any harm or metabolic imbalance.

Here’s a similar question: In untreated hypothyroidism, what’s more harmful, a high TSH or a low FT4 and/or FT3? We all know that when TSH is very high, it is the result of hypothyroidism, not the cause of it. When we feel symptoms and TSH is higher than it should be, it’s not because too much TSH is entering TSH receptors, it’s because too little T3 is entering T3 receptors.

Here’s a financial analogy to put this RT3 experiment in a nutshell:

• You’re not rich even if you have a huge bucket full of pennies. Pennies are not worth much in a dollar-based economy. They’re relatively powerless.
  • In a similar way, having 10-100x the normal level of RT3 in blood is neither very significant nor very harmful in the thyroid hormone economy. Why should one obsess over RT3? It naturally rises in tandem with FT4 in health, and escalates per unit of FT4 in illness, but RT3 doesn’t oppress or interfere with T3 in any meaningful way.
• In contrast, you’r rich if you have many 100-dollar bills. They aren’t bulky. They could be hiding in your purse or pocket.
  • In a similar way, having healthy levels of the most powerful thyroid hormone, T3, even if unmeasured, can make you very rich and powerful in health.
• Losing $100 dollars at a time from your bank account at a faster rate than usual might not cause an immediate crisis. But over time, you’ll need to stop the losses and replenish what you’ve lost, or you’ll be in financial trouble.
  • Swift T3 losses in blood won’t cause instant death, but if you fail to recover from a T3 deficit in a timely manner, you could be very disadvantaged when recovering from illness.

So let’s not continue to blame excess RT3 for symptoms and illnesses. Now you know RT3 by itself can’t cause T3 losses or illnesses, but RT3 is a side effect of DIO3 upregulation and DIO1 downregulation in illness. Obsessing over high RT3 levels is beside the point — illness naturally inflates RT3 per unit of FT4. Your RT3 is not harming you as much as a renegade DIO3 enzyme that is taking apart your T3 at a faster rate.

Instead, focus on maintaining T3 sufficiency in health and illness. In people not dosing any T3, chronically low TT3 and low FT3/FT4 ratios are associated with mortality during illness (Ataoglu et al, 2018). Unseen intracellular T3 losses in the presence of low-normal FT3 or low TT3 can drive up health risks. So if you’re ill, work on treating the real cause of the illness while avoiding dangerously low TT3 and FT3 levels, if you can.

References

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Baloch, Z., Carayon, P., Conte-Devolx, B., Demers, L. M., Feldt-Rasmussen, U., Henry, J.-F., LiVolsi, V. A., Niccoli-Sire, P., John, R., Smyth, P. P., Spencer, C. A., & Stockigt, J. R. (2003). Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. Thyroid, 13(1), 3–3. https://doi.org/10.1089/105072503321086962

Garnick, R. L., Burt, G. F., Long, D. A., Bastian, J. W., & Aldred, J. P. (1984). High-Performance Liquid Chromatographic Assay for Sodium Levothyroxine in Tablet Formulations: Content Uniformity Applications. Journal of Pharmaceutical Sciences, 73(1), 75–77. https://doi.org/10.1002/jps.2600730120

Hay, I. D., Annesley, T. M., Jiang, N. S., & Gorman, C. A. (1981). Simultaneous determination of D- and L-thyroxine in human serum by liquid chromatography with electrochemical detection. Journal of Chromatography, 226(2), 383–390. https://doi.org/10.1016/s0378-4347(00)86072-7

Kang, M. G., Hahm, J. R., Kim, K.-H., Park, H.-W., Koh, J.-S., Hwang, S.-J., Hwang, J.-Y., Ahn, J. H., Park, Y., Jeong, Y.-H., Park, J. R., & Kwak, C. H. (2018). Prognostic value of total triiodothyronine and free thyroxine levels for the heart failure in patients with acute myocardial infarction. The Korean Journal of Internal Medicine, 33(3), 512–521. https://doi.org/10.3904/kjim.2016.292

Nicod, P., Burger, A., Strauch, G., Vagenakis, A. G., & Braverman, L. E. (1976). The failure of physiologic doses of reverse T3 to effect thyroid-pituitary function in man. The Journal of Clinical Endocrinology and Metabolism, 43(2), 478-. https://doi.org/10.1210/jcem-43-2-478

Shulkin, B. L., & Utiger, R. D. (1984). Reverse triiodothyronine does not alter pituitary-thyroid function in normal subjects. The Journal of Clinical Endocrinology and Metabolism, 58(6), 1184–1187. https://doi.org/10.1210/jcem-58-6-1184

Warner, M. H., & Beckett, G. J. (2010). Mechanisms behind the non-thyroidal illness syndrome: An update. The Journal of Endocrinology, 205(1), 1–13. https://doi.org/10.1677/JOE-09-0412

Wadwekar, D., & Kabadi, U. M. (2004). Thyroid hormone indices during illness in six hypothyroid subjects rendered euthyroid with levothyroxine therapy. Experimental and Clinical Endocrinology & Diabetes: Official Journal, German Society of Endocrinology [and] German Diabetes Association, 112(7), 373–377. https://doi.org/10.1055/s-2004-821012

Wiersinga, W. M., Lie, K. I., & Touber, J. L. (1981). Thyroid hormones in acute myocardial infarction. Clinical Endocrinology, 14(4), 367–374. https://doi.org/10.1111/j.1365-2265.1981.tb00622.x