On today’s episode of The Modern Vital Podcast, we’re gonna talk about rT3.

Is it a myth? Is it important in the diagnosis and treatment of thyroid disease? 

Our Modern Vital Fact of the Day is that the thyroid is the only known organ in the body that can absorb and use iodine, which is a crucial mineral required for the production of thyroid hormone. 

Thyroid hormone is key to the regulation of metabolism, growth and development, even when the diet is deficient in iodine, unlike diets which contain a lot of seaweed. 

The thyroid can still absorb and concentrate iodine from the bloodstream. Interestingly, iodine is the key mineral in the conversion of T4 to T3. T4 simply means that there are four atoms of iodine attached, and then one is cleaved with the help of an enzyme called a deiodinase.

Then T4 becomes t3, and this happens from outside the cell to within the cell. T4 is converted to T3. There are four types of deiodinases: D1, D2, D3, D4. D2 is the main deiodinaes enzyme actively involved in converting T4 to T3 and D3 is actively involved in converting T4 to rT3. Which brings us to our topic du jour, the myth of rT3.

Is it necessary to run rT3? 

Our thyroid gland is incredibly sensitive. I think of it as like a butterfly shaped antenna, which is picking up all the signals of oxidative stress and inflammation throughout our body, and relaying these messages back to our brain so as to make any refinements necessary to metabolism.

Hence, when the thyroid becomes imbalanced, we need to assess the body for oxidative stress and inflammatory markers, so as to potentially identify the root cause or causes of the thyroid imbalance in the first place. Causes such as chronic infection like mold or Epstein Barr, nutrient deficiencies like iron and selenium, stress, and insomnia.

Approximately 5% of those in the US have hypothyroidism, which is over 15 million people. The thyroid gland is the metabolic director of the body. 

A typical thyroid blood test involves just one or two markers, a TSH, and maybe a FT4. Oftentimes, the TSH is ordered with a reflex to FT4, meaning that if the TSH results are abnormal, then the FT4 will be ordered.

But naturopathic doctors and other integrative medicine specialists like to order a full, comprehensive thyroid panel, which includes TSH, FT4, FT3, rT3, and also thyroid antibodies like TG and TPO antibodies. 

So there’s a lot of talk about rT3 and whether it’s important or not.

Many studies do not appear to indicate that it is necessary to run in most cases. But I am going to posit that the reason this is so is because a root cause approach is not usually the kind of approach evidence-based researchers are taking because it’s very difficult to put together a randomized control trial proving that rT3 is worth running when the root causes throwing reverse T3 off vary so widely

What I mean to say is that rT3 can give the skilled practitioner information in the light of the individual case, but without knowing the case, it may not be helpful and probably isn’t. It gives us a lot of information about that person’s thyroid and in particular about their health and life and the context of all the variables that make up their picture.

So a quick summary: TSH is thyroid stimulating hormone. It’s released by the anterior pituitary gland in the brain. It sends a signal immediately to the thyroid gland, telling it how much thyroid to make. The thyroid gland makes FT3 and FT4, but only about 10 to 20% of the body’s free T3 is actually made there.

This is the active thyroid hormone made in the thyroid gland. The rest is converted from FT4 in the peripheral tissues such as the liver, the gut, the kidneys. And this is another reason why things like liver inflammation or gut issues like intestinal permeability can potentially significantly impact thyroid metabolism and function because so much conversion takes place in those tissues of FT4 to FT3.

In other words, if the body is having a hard time with conversion, then symptoms will ensue. Symptoms such as brain fog, fatigue, depression, constipation, et cetera. Of course, these are mere symptoms of hypothyroidism. 

By the way, some nutrients associated with improved conversion of FT4 to FT3 include selenium, zinc, iodine (of course), B2 (which is riboflavin), B3 (which is niacin), B6 (which is pyridoxine), and even the herb Ashwagandha. Iron is another important nutrient that plays a significant role.

The fact is about 80% of the body’s FT4 is converted to FT3 and maybe 20% or so (studies differ on what this amount actually is) but let’s call it 20% or one fifth is converted to a kind of storage form called rT3. Now, I don’t like calling it a storage form necessarily because it’s not really converted back to FT3.

A key point though is that our body needs rT3 as well. We just don’t know very much about it. 

Now, some things that can drive up reverse T3 include physical and emotional stress, low cortisol, chronic infections, eating disorders, starvation, Graves disease, nutrient deficiencies, and much more. 

Thus, if I suspect that my patient is low in glutathione, or let’s say that I’ve tested their glutathione levels and found that they’re low… Now remember, glutathione is the body’s most important antioxidant. Glutathione is a selenium dependent antioxidant. In other words, it depends on the mineral selenium in order to be made in the body.

Now, I may then suspect that my patient is also selenium deficient if they’re glutathione deficient. And we do know that selenium deficiency can be a root cause of high rT3. This association, and I would posit it that also a causation has been confirmed by studies. My point is that testing comprehensive thyroid labs is a root cause approach.

I like to think of rT3 as like a nut that a squirrel stores away for the winter, particularly when the squirrel thinks that the winter is gonna be long and hard, but the nut actually will never be used to be made into energy, by storing it away. The body ensures that the free T4 that is then converted to reverse T3 will not be used by the body.

The nut will not be used to make energy even though it is stored. I have not found studies showing that cT3 can be converted back to T3. 

It doesn’t take much digging to find hundreds of practitioners, particularly functional medicine practitioners, integrated medicine practitioners, naturopathic practitioners stating that rT3 can turn off thyroid receptors by binding to them, and thereby they can keep T3 or the active thyroid hormone from having an action on those receptors. 

Just a quick review, T3 is the active form of thyroid hormone, and hormones have their action in the nuclei of our cells where they can trigger gene transcription and translation, turning on and off genes, and then eventually having proteins being manufactured in the cells.

T3 makes its way into our cellular nuclei and then interacts with thyroid hormone receptors. However, after combing through the research and the literature, I can’t find studies confirming that rT3 can actually get into the nuclei of our cells and block those thyroid receptors. Now, somebody can try to prove me wrong, but I cannot with confidence agree that rT3 blocks thyroid receptors If I can’t find literature poving that it is so.

It does make sense because the rT3 is like the mirror image of T3, and so it could actually fit right into that receptor, yet not have an action. However, I can’t find evidence that rT3 is actually in the nuclei of our cells. It may happen by some other unknown mechanism indirectly.

It seems to be that people who are not clinicians, but rather researchers and scientists are saying not to test rT3, it’s not important. And then most integrative medicine practitioners are saying, Hey, it’s a really good idea in many cases to test rT3 as part of a comprehensive thyroid panel.

I happen to fall more in the latter category, but I disagree with these clinicians who are saying that rT3 blocks thyroid receptors because I can’t find that evidence. 

It may be so, but we don’t actually have the evidence, so why say it if we actually don’t have the evidence yet? We could say that we suspect it.

We do know that rT3 appears to be associated with states where metabolism is greatly slowed down since thyroid hormone is the metabolic director of the body. Interestingly, hibernating bears have been shown to have low rT3, which speaks to a role that it may be playing in down-regulating metabolism.

It has even been referred to as the hibernation hormone. Ironically, in states of starvation though, in humans, rT3 usually will climb. 

Now, one other point that I wanna bring up is important. The ratio of T3 to rT3 is associated with insulin resistance. Of course, it’s an association, not necessarily a causation, but it does show a metabolic link between our insulin receptors being resistant to insulin’s directive to push that blood sugar into our cells and thyroid metabolism. 

Some doctors suggest that we wanna see a ratio above 10. In other words, we wanna see above 10 parts T3 to one part rT3 in the blood. I think that’s a little bit high, but I do think that there’s a lot to be said for this, and studies do support. It. They support the link in the association.

The point is that we wanna monitor the ratio and some doctors refer to a ratio below 10 as consistent with reverse T3 syndrome. That’s not really that helpful either because syndrome just means a bucket in which we dump a bunch of symptoms or findings. It doesn’t really explain a root cause. The moral of a story is we don’t want rT3 or this ratio in particular to be too high or too low, and we wanna assess what might be causing it to be off when it’s off.

What’s my overall point? My point is that the thyroid is incredibly sensitive to environmental factors and testing rT3 is an important part of a comprehensive hormone panel, particularly with regard to a holistic root cause approach to each individual. 

That concludes episode #6 of The Modern Vital Podcast.

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