T4 not converting to T3: impaired conversion as an overlooked cause
Your TSH is fine, your fT4 is high, and yet your metabolism feels as if the handbrake were on. Here you will learn what can slow the conversion into active T3 and why more levothyroxine does not always help in that case.
All guides from the thyroid cluster
A lab value can be right without the hormone arriving where you need it. T4 is the key blank, T3 the key. If you only count the blanks, you can sometimes overlook the workshop.
“I'm taking more hormone than ever and feel worse than ever”
I know this pattern very well. A man has been taking levothyroxine for years and is under constant pressure at work. Because the fatigue persisted, his dose was increased several times along the way.
When we went through his results together, a pattern stood out. His TSH had become very low by then, and his free T4 was at the upper limit. His free T3, by contrast, was at the lower limit. On top of that came low iron stores, a long phase of eating very little to lose weight and hardly any restful sleep.
The turning point was a different question. No longer: how much more hormone does he need? But rather: what is slowing the conversion? In agreement with his family doctor, the dose was not raised any further. Instead, food, sleep, iron and his stress load moved to the center.
A few months later, he described himself as more alert and less sensitive to cold. His free T3 was higher than before, even though the tablet had stayed the same.
I cannot claim causality, but I document the temporal connection. A lot changed at the same time during this period. A single course does not allow any conclusion about you.
The lesson: More blanks do not automatically mean more matching keys. Sometimes the bottleneck is in the workshop, not in the warehouse.
Maybe you recognize yourself in this. You take your tablet every morning, on time and on an empty stomach. Your doctor says your levels are good. And yet you are exhausted, you feel cold and you think as if through a fog.
This is not your imagination. Nor does it mean that anyone did a bad job. For most people with hypothyroidism, levothyroxine is a reliable treatment. For some, though, a gap remains. One possible cause of this has an unwieldy name: T4 to T3 conversion disorder.
In this article, we look at what is behind the term and how you can recognize the pattern in your lab results. After that, we turn to five brakes that can slow the conversion. And to the honest question of what studies show about combining with T3. You will find how the three enzymes of conversion work in detail in the article From T4 to T3: the conversion and its enzymes.
What you will learn in this article
- What “conversion disorder” means and what it does not
- How you can recognize the pattern in your lab results
- The blind spot of T4-only therapy
- Brake 1: energy shortage and diets
- Brake 2: chronic stress and cortisol
- Brake 3: inflammation
- Brake 4: missing building blocks
- Brake 5: genes
- What studies show about combining with T3
- Three levers for your next doctor's appointment
What “conversion disorder” means and what it does not
Maybe you read the term in a forum, and at your doctor's office it was met with a frown. Both reactions are understandable. The term describes something measurable, but it is not an official diagnosis.
Imagine T4 as a key blank. It carries four iodine atoms and barely fits the lock, that is, the receptor of your cells. Only when a workshop files off one iodine atom at the right spot does T3 come into being. This key unlocks the door and gets metabolism, warmth and energy going inside the cell.
If the filing happens at the wrong spot, reverse T3 is created. It looks almost the same but practically unlocks nothing. The workshops are three enzymes, the deiodinases. D1 and D2 file the matching key. D3 turns T4 into the inactive reverse T3 and breaks T3 down again.
A team in Pisa led by A. Pilo used labeled hormones in 1990 to track where in the body T3 is made. In 14 investigations in healthy people, the thyroid supplied 3.3 micrograms of T3 per day per square meter of body surface area, while conversion in the tissues supplied 12.7 micrograms. So roughly four fifths of the active hormone came from outside the thyroid.
What this means for you: how well you feel depends not only on how much your thyroid or your tablet supplies. It depends just as much on how well your workshops are working.
Pilo A et al. Am J Physiol. 1990. DOI: 10.1152/ajpendo.1990.258.4.E715A team led by Ana Luiza Maia from Porto Alegre measured the work of the enzymes in cell cultures and extrapolated it to human liver and muscle. According to these calculations, D2 produces about 29 nanomoles of T3 a day in healthy people, D1 about 15 nanomoles. The authors suspect that a throttled D2 is the main reason for the low T3 seen in severe illness.
What this means for you: type 2 deiodinase is probably the most important source of the T3 in your blood. Whatever slows it down can show up directly in your fT3.
Maia AL et al. J Clin Invest. 2005. DOI: 10.1172/JCI25083One more important clarification. In psychiatry, the term conversion disorder refers to something entirely different, namely losses of bodily function for which no organic cause can be found. That has nothing to do with the thyroid. Instead, the thyroid literature speaks of reduced conversion efficiency and a low T3 to T4 ratio. In severe illness, the picture is called low T3 syndrome.
Seen through the KPNI lens, conversion is a junction of all four systems. The hormonal system provides the blank. The nervous system reports via stress hormones whether danger is present. The immune system cuts in with messenger substances when it is fighting inflammation. And metabolism decides whether enough energy and building blocks such as selenium, iron and zinc are available.
Slowed conversion is often not a defect but an adaptation. Your body turns down the heating when it senses hunger, danger or inflammation. In times of scarcity, that can be wise.
So the crucial question is not only: how much hormone is missing? But also: which reason for the energy-saving mode is still there?
And now you know why a good value for the blank does not yet tell you whether enough keys are arriving in your cells.
How you can recognize the pattern in your lab results
You are holding your lab report and see nothing but numbers without arrows. Everything in the normal range, so everything is fine? Not necessarily. It gets interesting when you put the values side by side.
TSH is the signal from the pituitary gland to the thyroid. Free T4 shows the blank in your blood, free T3 the finished key. For the question of conversion, what matters most is how fT4 and fT3 relate to each other. A typical conversion pattern looks like this: fT4 in the upper range, fT3 in the lower range, TSH normal or low.
Diagram: where the values lie within the reference range
Schematic illustration of a typical conversion pattern, not real measurements. Reference ranges differ depending on the laboratory and the measurement method.
Balanced
- TSH in the target range
- fT4 and fT3 at a similar level within the reference range
- Ratio of fT3 to fT4 within the usual range
Conversion pattern
- fT4 in the upper range, fT3 in the lower range
- TSH normal or low
- more common on levothyroxine
- reverse T3 sometimes elevated
Acute saving pattern
- fT3 clearly low, reverse T3 high
- TSH and fT4 normal or low
- in severe illness, fasting or major energy shortage
And reverse T3? It can round out the picture, but it is not proof on its own. On levothyroxine, more T4 is available, from which more reverse T3 can also be formed. An elevated value then says little about the workshop. I put it in context in detail in the article Understanding reverse T3.
David Halsall and Susan Oddy from Addenbrooke's Hospital in Cambridge summarized what is known about reverse T3. The value rises in severe illness, with medications such as amiodarone and in rare genetic disorders of the deiodinases. In their assessment, the measurement has not yet found a firm use in routine diagnostics.
What this means for you: an elevated reverse T3 is one piece of the puzzle. It does not replace a look at fT3, fT4 and your life situation.
Halsall DJ, Oddy S. Ann Clin Biochem. 2021. DOI: 10.1177/0004563220969150A team led by Yuji Nagayama at the Yamashita Thyroid Hospital in Fukuoka analyzed data from 426 people without a thyroid of their own who were taking a full replacement dose of levothyroxine. Of these, 58 percent had normal fT3 and fT4 levels. Another 21 percent had a normal fT3 with an elevated fT4, and 18 percent a low fT3 with a normal fT4. Those with a low fT3 had, by comparison, a higher body mass index and a higher level of the liver enzyme ALT.
What this means for you: even with an adequate dose, fT3 can be on the low side, and this seems to be linked to metabolic markers. In the authors' view, further studies first need to show whether fT3 should help guide dosing in the future.
Nagayama Y et al. J Clin Endocrinol Metab. 2026. DOI: 10.1210/clinem/dgag220How to make your lab report meaningful
- Have TSH, fT4 and fT3 measured from the same blood draw, not on different days.
- Agree with your doctor whether your blood is drawn before or after your tablet, and keep it the same at every checkup.
- Mention acute infections, fasting phases and very hard training weeks, because they can temporarily lower fT3.
- Compare values over time instead of interpreting a single snapshot.
- Ask about the ratio of fT3 to fT4 and interpret it together. So far there is no generally accepted cutoff for it.
“In the normal range” means: your value lies where the large majority of healthy people lie. It does not mean that exactly this value is right for you. With conversion, the single number matters less than how the numbers relate to each other.
And now you know why two lab reports full of “normal” values can still tell very different stories.
The blind spot of T4-only therapy
You do everything right. You take the tablet on an empty stomach, keep your distance from coffee and go to every checkup. Your TSH sits in the target range. And yet something is missing that is hard to put into words.
Here lies a point that received little attention in standard therapy for a long time. Besides T4, a healthy thyroid also releases some ready-made T3. Levothyroxine replaces only T4. If your own thyroid is entirely or largely missing, all of your T3 has to come from conversion. If your workshops work well, this usually succeeds. If not, a gap remains.
Damiano Gullo and Riccardo Vigneri from the University of Catania compared 1,811 people without a thyroid of their own with 3,875 healthy comparison participants. All of those treated had a normal TSH on levothyroxine. Even so, their fT4 was higher on average and their fT3 lower. In 15.2 percent, fT3 was lower than in the healthy participants, and the ratios of fT3 to fT4 varied widely.
What this means for you: how well the tablet is turned into T3 varies greatly from person to person. A normal TSH therefore does not show for everyone that enough T3 is reaching the tissues.
Gullo D et al. PLoS One. 2011. DOI: 10.1371/journal.pone.0022552Sarah Peterson, Elizabeth McAninch and Antonio Bianco from Chicago analyzed data from the large US health survey NHANES. Among 9,981 people with a normal TSH, 469 were taking levothyroxine. They had more fT4 and less fT3 than matched comparison participants, and their ratio of T3 to T4 was about 15 to 20 percent lower. Their body mass index was higher, although by their own account they ate fewer calories per kilogram.
What this means for you: even with a good TSH, the hormone balance on levothyroxine differs measurably. Whether this plays a role for you can only be clarified on an individual basis.
Peterson SJ et al. J Clin Endocrinol Metab. 2016. DOI: 10.1210/jc.2016-2660How widespread dissatisfaction can be is shown by an online survey on the website of the American Thyroid Association. The 12,146 participants rated their treatment at 5 out of 10 points on average. Such a survey mainly attracts dissatisfied people and is therefore not representative. But it does show how many people are struggling with their situation.
A normal TSH shows that the control center in the brain is satisfied. It does not always show that every tissue is getting enough T3.
And what happens when the dose is simply increased, as in the story above? That is exactly what two research groups looked at more closely.
Matthew Ettleson and Antonio Bianco from Chicago, together with a Brazilian laboratory network, analyzed the values of 9,850 people on levothyroxine. Up to an fT4 of about 0.7 nanograms per deciliter, T3 rose steadily along with it, after which the curve flattened markedly. TSH, by contrast, fell steeply as fT4 rose. And the higher the fT4, the smaller the share that became T3.
What this means for you: a higher dose can shift TSH and fT4 considerably, but T3 only a little. The lab report then changes more than what arrives in the cells.
Ettleson MD et al. J Clin Endocrinol Metab. 2023. DOI: 10.1210/clinem/dgac725A team led by John Midgley and Rudolf Hoermann, with clinics in Lüdenscheid and Bochum, studied 353 people on levothyroxine and calculated how efficiently they converted. Those who converted most weakly had the lowest fT3 levels despite the highest dose and the highest fT4. Some did not reach an fT3 above the mean even with a fully suppressed TSH.
What this means for you: with weak conversion, a higher dose may mainly raise fT4. The authors therefore consider fT3 a possible additional treatment target.
Midgley JEM et al. Endocr Connect. 2015. DOI: 10.1530/EC-15-0056Why is that? One possible explanation comes from the animal lab. Imagine the thermostat in your apartment hangs right next to the heater in the hallway. It reports: warm enough. The back rooms still stay cool.
A team led by Antonio Bianco studied in rats without a thyroid why TSH becomes normal on T4 while T3 stays low. High amounts of T4 throttled D2 conversion throughout the body, because the enzyme is then increasingly tagged for breakdown. In the hypothalamus, the control center of the feedback loop, D2 on the other hand remained largely active. Only a steady supply of both T4 and T3 brought all T3-dependent metabolic markers in the animals into the normal range.
What this means for you: in the animal model, the control center responds more sensitively to T4 than the rest of the body. Whether the same applies in humans has not been conclusively proven.
Werneck de Castro JP et al. J Clin Invest. 2015. DOI: 10.1172/JCI77588To be fair, not all studies come to the same result. Jacqueline Jonklaas from Georgetown University in Washington measured 50 people before and after removal of their thyroid. On levothyroxine, T3 was on average just as high as before, only fT4 was higher. A study from the Kuma Hospital in Kobe with 135 operated patients, by contrast, found a lower fT3 at normal TSH than before surgery. There, it only reached its previous level with a slightly suppressed TSH.
Please do not increase or decrease your levothyroxine on your own, and do not take T3 without medical supervision. Too much thyroid hormone can promote a racing heart, heart rhythm disorders and, over time, bone loss. Every change takes a few weeks and a follow-up test before a new value is meaningful.
You will find further reasons for fatigue despite the tablet, from how you take it to iron and autoimmunity, in Tired on levothyroxine and Symptoms despite levothyroxine.
If more of the same is not getting you anywhere, that is rarely down to you or your discipline. It may be down to the point where the blank becomes a key. That point can be looked at.
And now you know why a perfect TSH and feeling unwell do not have to be a contradiction.
The five brakes on conversion
Imagine you are driving uphill and wonder why the car has no pull. You step on the gas, meaning more blanks. Yet perhaps the handbrake is simply on. In the conversion of T4 to T3, there are several such brakes. Five of them have been studied well enough to introduce them to you.
Energy shortage
Fasting, crash diets, very few carbohydrates, lots of exercise with little food
Chronic stress
Cortisol, lack of sleep, ongoing strain
Inflammation
Severe illness, infections, messengers such as interleukin-6
Building blocks
Lack of selenium, iron or zinc
Genes
Variants such as DIO2 Thr92Ala
Brake 1: energy shortage, fasting and very few carbohydrates
You want to lose weight, have been eating very little for weeks and still train hard. At some point you are constantly cold, sleep badly and feel empty. Your body might be making a very old decision right now: to save.
A team led by A. G. Vagenakis and L. E. Braverman had overweight volunteers go on a total fast. T3 fell markedly, and reverse T3 rose in the same proportion. The same happened in four participants who had previously received T4 for a month in an amount that suppressed TSH. After five days of normal eating, both values were back in the baseline range.
What this means for you: even when T4 comes from outside as a tablet, your energy state helps decide what becomes of it. So this affects precisely those who take levothyroxine.
Vagenakis AG et al. J Clin Endocrinol Metab. 1975. DOI: 10.1210/jcem-41-1-191S. W. Spaulding and I. J. Chopra had overweight people fast and then gave them, in random order, diets of 800 calories that differed in their carbohydrate content. During total fasting, T3 fell by 53 percent and reverse T3 rose by 58 percent. Without carbohydrates, T3 fell by 47 percent even at 800 calories. With at least 50 grams of carbohydrates a day, it remained stable.
What this means for you: not only the amount counts, but also the composition. This is study knowledge about a very low-calorie diet, not a nutritional recommendation for you.
Spaulding SW et al. J Clin Endocrinol Metab. 1976. DOI: 10.1210/jcem-42-1-197A. B. Loucks and E. M. Heath from Ohio University had 27 untrained women exercise on an ergometer for four days and set precisely how much energy remained after exercise. When this energy fell below about 25 kilocalories per kilogram of fat-free mass, T3 dropped abruptly by 16 percent and fT3 by 9 percent. Below about 19 kilocalories, fT4 also rose by 11 percent and reverse T3 by 22 percent.
What this means for you: conversion apparently responds to a threshold. If you train a lot and eat little, you can drop below it sooner than you might think.
Loucks AB, Heath EM. Am J Physiol. 1994. DOI: 10.1152/ajpregu.1994.266.3.R817Long-term calorie restriction leaves traces too. Luigi Fontana and colleagues from St. Louis compared 28 people who had been deliberately eating little but nutrient-rich food for years with two comparison groups. Their T3 was 73.6 nanograms per deciliter, compared with 91.0 and 94.3 in the comparison groups. T4, reverse T3 and TSH, by contrast, were the same. The authors interpret this as possibly part of a program for a long life. If you feel exhausted and cold, you are more likely to experience the same adaptation as a burden.
A team from Erzurum and Istanbul led by S. Ulupınar summarized studies on fasting periods of at least 24 hours in 2026. Both fT3 and total T3 fell markedly, TSH moderately, and fT4 remained stable. The authors interpret this pattern as altered conversion in the tissues and not as declining production by the thyroid.
What this means for you: fasting shifts exactly the ratio that matters for the conversion question. A lab result taken during or shortly after a fasting phase is therefore hard to interpret.
Ulupınar S et al. Front Endocrinol (Lausanne). 2026. DOI: 10.3389/fendo.2026.1876045Your body does not read your diet plan. It only registers: less energy is coming in. Then it throttles the active hormone to conserve reserves. That is not a failure of your thyroid, but a protective program that can make sense during a famine.
What does this mean for you? If you are exhausted on levothyroxine, an honest look at your energy balance is worthwhile. Long phases of very little food, very few carbohydrates or lots of endurance exercise on a tight diet belong in the conversation with your doctor before the dose goes up. If you would like to fast with Hashimoto's, you will find an assessment in the article Fasting with Hashimoto's. On the subject of weight, feel free to read Thyroid and weight.
Brake 2: chronic stress, cortisol and too little sleep
Maybe you have been carrying too much for months. Work, family, worries, hardly any breaks. You function, but your body pays for it. Part of that bill could end up with your thyroid.
A team led by I. J. Chopra gave the corticosteroid dexamethasone to 15 people, including four with hypothyroidism on T4 tablets. As early as eight hours after the first dose, reverse T3 rose markedly, in the four on T4 tablets from an average of 58 to 87 nanograms per 100 milliliters. T3 fell after about one day and remained low in them for one to two days after the drug was stopped.
What this means for you: glucocorticoids, which include your body's own cortisol, can shift conversion toward reverse T3. However, the dose in this study was high and cannot be transferred directly to everyday stress.
Chopra IJ et al. J Clin Endocrinol Metab. 1975. DOI: 10.1210/jcem-41-5-911A team from a US Army research institute led by K. E. Friedl followed soldiers through the eight-week Ranger course. There, little sleep, hard physical work, temperature stress and a daily energy deficit of 1,000 to 1,200 kilocalories came together. In the group with the larger deficit, T3 fell below the normal range. As soon as more food was eaten again, it recovered quickly, even though lack of sleep and strain continued.
What this means for you: stress and energy shortage often occur together. In this study, food was the stronger lever for T3.
Friedl KE et al. J Appl Physiol. 2000. DOI: 10.1152/jappl.2000.88.5.1820Seen through the KPNI lens, the nervous system connects two axes here. The stress axis of hypothalamus, pituitary gland and adrenal gland releases cortisol. As the dexamethasone study suggests, cortisol can open the path from T4 toward reverse T3. Lack of sleep and rumination keep this axis on alert. Clinically, I observe that fT3 sometimes only starts to move once everyday life calms down noticeably. Studies on this are thin, so this is experience and not proof.
Stress is not just a feeling in your head. It is also a biochemical message to every cell: save energy, things could get tight. If you give your nervous system a sense of safety, you may take one brake off conversion.
Brake 3: inflammation, loud and quiet
After a bad flu, an operation or during a phase with many infections, you often feel slowed down for weeks. This too can have to do with the thyroid, without the thyroid itself being ill.
A team led by Robin Peeters from Rotterdam examined liver and muscle samples taken from 80 intensive care patients immediately after their death. In the liver, the converting enzyme D1 was throttled. In liver and muscle, the degrading enzyme D3 was active, although it is practically absent there in healthy people. The poorer the blood supply to the organs, the more pronounced this pattern was.
What this means for you: in severe illness, the body actively switches conversion away from the active hormone. The low T3 is then part of an overall response and not simply a deficiency.
Peeters RP et al. J Clin Endocrinol Metab. 2003. DOI: 10.1210/jc.2002-022013Simone Wajner and Ana Luiza Maia from Porto Alegre exposed human cell lines to the inflammatory messenger interleukin-6. T3 production by D1 and D2 dropped sharply, while breakdown by D3 increased. The antioxidant N-acetylcysteine, which replenishes the cells' glutathione stores, prevented the inhibition of T3 production.
What this means for you: inflammation and oxidative stress could act directly on the workshop. This has been shown in cells but has not been established in the same way in humans. Nor is it a reason to take N-acetylcysteine on your own.
Wajner SM et al. J Clin Invest. 2011. DOI: 10.1172/JCI44678A review led by Eric Fliers and Anita Boelen from Amsterdam places low T3 syndrome in severe illness as follows: at the beginning, it is a consequence of the inflammatory response and scarce nutrition, and this could even be protective. According to this paper, it remains open whether it makes sense to stimulate the axis from outside in intensive care.
How closely inflammation and energy are linked is shown by a small randomized study from Chicago with 35 ventilated patients. Those who received the full amount rather than 40 percent of the calculated calories had a 54 percent higher ratio of T3 to reverse T3 on the first day. After three more days, however, this advantage had disappeared.
And in everyday life, beyond the intensive care unit? This is where the solid study evidence ends. It is mechanistically plausible that quieter inflammation can also slow the workshops. This includes, for example, active Hashimoto's thyroiditis, recurrent infections, an irritated gut or a lot of inflammatory belly fat. There are hardly any good human studies on whether this measurably lowers fT3 in everyday life. I therefore regard it as a lead and not as a diagnosis. You can find out how autoimmunity can be influenced in Lowering Hashimoto's antibodies.
A low T3 during an illness is not automatically a fault that you need to compensate for immediately. It can be a sign that your body is pooling its strength. You should pay attention if the energy-saving mode keeps running long after the illness is over.
Brake 4: missing building blocks such as selenium, iron and zinc
Have you been eating a very one-sided diet for a long time, do you have heavy periods or a sensitive digestion? Then it is worth asking whether your workshops are short of material.
Selenium sits in the active center of the deiodinases. In a review, Michael Zimmermann from Zurich and Josef Köhrle describe how the thyroid holds on to selenium even when intake is scarce. It needs iron for the enzyme that incorporates iodine into the hormone. If several of these building blocks are lacking at the same time, this can further impair thyroid function.
A team at the University of Verona led by O. Olivieri compared selenium status and thyroid levels in 109 healthy people. With age, selenium and the ratio of T3 to T4 declined, and in the older participants the two were closely linked. In a small double-blind study with 36 nursing home residents, selenium improved selenium status and lowered T4.
What this means for you: a selenium deficiency in old age can go hand in hand with weaker conversion. That is an argument for measuring, not for taking it on suspicion.
Olivieri O et al. Clin Sci (Lond). 1995. DOI: 10.1042/cs0890637Kristian Hillert Winther and Laszlo Hegedüs from Odense gave 491 people aged 60 to 74 in Denmark, where selenium intake tends to be low, either selenium or a placebo for up to five years. TSH and fT4 fell minimally. Neither fT3 nor the ratio of fT3 to fT4 changed, and the authors therefore do not consider selenium indicated when supply is only slightly low.
What this means for you: selenium is no turbo for conversion if there is no actual deficiency. More is not better here, because too much selenium can itself cause harm.
Winther KH et al. Eur J Endocrinol. 2015. DOI: 10.1530/EJE-15-0069J. L. Beard and colleagues at Pennsylvania State University placed women with iron deficiency anemia, women with empty iron stores but no anemia, and healthy women in a water bath at 28 degrees Celsius. The women with anemia cooled down more and had lower T4 and T3 levels. In them, iron improved body temperature and, in part, hormone levels. The women with empty stores but no anemia, by contrast, responded like the healthy women.
What this means for you: in this study, the effect only appeared with genuine anemia. Low stores alone did not stand out here, but they remain relevant to your energy for other reasons.
Beard JL et al. Am J Clin Nutr. 1990. DOI: 10.1093/ajcn/52.5.813For zinc, the data are even thinner. A small study from Kumamoto in Japan found 13 people with low fT3 and normal T4 among 134 people with disabilities. Nine of them had a zinc deficiency. After twelve months of zinc, fT3 and T3 were in the normal range, and reverse T3 had fallen. There was no control group, so the result is a hint and not proof.
What you can take away from this
- Always have ferritin assessed together with an inflammation marker such as CRP, because inflammation can raise ferritin and mask a deficiency.
- Only supplement selenium after measuring it and in agreement with your doctor, because the gap between too little and too much is small.
- Have zinc measured if a deficiency seems likely, for example with a very one-sided diet or bowel diseases.
- Take iron and other minerals at a distance from levothyroxine, because they can interfere with the absorption of the tablet. You will find details in Taking levothyroxine correctly.
You can read in detail how the individual building blocks show up in lab tests and what matters there in Selenium, zinc, iron and vitamin D. On iron stores, Ferritin level: what is normal? is also a good fit.
A building block is only of use where it is missing. If you supplement on suspicion, you sometimes fill a warehouse that has long been full. If you measure, you may find the one gap that can make the difference.
Brake 5: genes that change the workshop
Some people do everything. They eat enough, sleep, have good iron levels, and their fT3 still stays low. Then a question often comes up: is it my genes?
Maria Grazia Castagna and Domenico Salvatore from Siena and Naples compared 140 people before and after removal of the thyroid at a similar TSH. In carriers of the DIO2 variant Thr92Ala, fT3 after surgery was lower than in people without the variant. In the latter, it matched the value before surgery. In cell experiments, the altered enzyme produced less T3.
What this means for you: in people without a thyroid of their own, this variant might help determine whether fT3 is sufficient. This applies to this group and not automatically to everyone.
Castagna MG et al. J Clin Endocrinol Metab. 2017. DOI: 10.1210/jc.2016-2587Vijay Panicker and Colin Dayan from Bristol genetically examined 552 people from a British study on combining T4 and T3. Those who carried the rarer form of the variant on both gene copies, 16 percent of participants, felt worse on T4 alone. This group benefited more from the combination, by 2.3 points on the well-being questionnaire after three months. Blood hormone levels did not differ, and the authors stress that the result needs to be confirmed.
What this means for you: genes could explain why some people respond to the combination and others do not. This has not yet been established.
Panicker V et al. J Clin Endocrinol Metab. 2009. DOI: 10.1210/jc.2008-1301A team led by Sungro Jo and Antonio Bianco also introduced the variant into mice. The altered enzyme caused stress in the cell and produced less T3. In individual brain regions, a kind of local hypothyroidism developed. The animals moved less, slept more and took longer to remember objects, and T3 improved their memory. This is an animal model that describes a possible mechanism, but not a finding in humans.
Hanneke Wouters and Bruce Wolffenbuttel from Groningen studied 12,625 people in the LifeLines study, including 364 on thyroid hormone. The variant was linked neither to hormone levels nor to quality of life or cognitive performance. Regardless of their genes, those treated had more fT4, less fT3 and a lower ratio. Treated women also reported lower quality of life.
What this means for you: genes alone apparently do not explain the gap. But the pattern of high fT4 and low fT3 on treatment shows up here again.
Wouters HJCM et al. Thyroid. 2017. DOI: 10.1089/thy.2016.0199What does this mean for you? A genetic test for DIO2 is exciting, but so far not a routine tool for treatment decisions. The major professional societies call for future studies to be designed specifically so that they also examine such variants. Until then, what counts is how you feel, how your values develop over time and the four brakes that can be influenced.
Genes are not a verdict, more of a tendency. A workshop that works a little more slowly may react more sensitively to every additional brake. All the more reason to keep an eye on the other four.
And now you know why the same tablet can lead to very different well-being in two people with the same TSH.
And what about combining with T3? What studies and guidelines say
Maybe you are thinking now: if conversion is stalling, why not simply add the finished T3? The question is justified. The answer is more complicated than it sounds.
A team from Monterrey and the Mayo Clinic led by René Rodríguez-Gutiérrez summarized 18 studies comparing T4 alone with the combination of T4 and T3. There was no difference in quality of life, mood and fatigue, and the certainty of the evidence was low to moderate. Asked about their preference, 43 percent chose the combination and 23 percent T4-only therapy, while 30 percent had no preference.
What this means for you: on average across all participants, the combination brings no measurable advantage. Even so, there are apparently people who clearly prefer it.
Millan-Alanis JM et al. Thyroid. 2021. DOI: 10.1089/thy.2021.0270Mohamed Shakir and Thanh Hoang from the Walter Reed military medical center gave 75 people with hypothyroidism T4, T4 with T3, and desiccated thyroid extract in turn, double-blind, for 22 weeks each. For the group as a whole, symptoms, quality of life, memory and mood did not differ, and the DIO2 variant played no role. The third with the most severe symptoms on T4, however, clearly preferred the treatments containing T3 and performed better with them on several tests.
What this means for you: averages can hide a subgroup that benefits. This is a hint from a subgroup analysis that needs to be confirmed in larger studies.
Shakir MKM et al. J Clin Endocrinol Metab. 2021. DOI: 10.1210/clinem/dgab478From this body of evidence, the professional societies have derived recommendations that are cautious but not closed. Here are the most important positions at a glance.
Separate rules apply here. The 2026 guideline of the American Thyroid Association recommends that women planning a pregnancy use no preparations other than levothyroxine, meaning neither liothyronine nor thyroid extract. The unborn child's brain makes its T3 mainly by itself from the mother's T4. If you take preparations containing T3 and want to become pregnant, discuss switching with your doctor in good time.
My view as a doctor working in functional medicine: a combination with T3 can be a sensible, medically supervised trial for selected people. For me, though, it comes at the end of a chain and not at the beginning. First come intake, energy, stress, inflammation and building blocks. Not infrequently, this shifts the picture so much that the T3 question looks different. That is clinical experience and not a study finding. You can read what is behind thyroid extracts in Natural thyroid hormones (NDT).
The question is not T4 or T3. It is: why is conversion stalling, and can something be done about it? Only once this question has been answered honestly does the decision about T3 become a good decision.
And now you know why the guidelines word things so cautiously on the combination and still leave a door open.
What you can do now: three levers
Maybe you are feeling relief right now. Finally a name for something you have felt for a long time. Maybe impatience too. Here are three steps you can take starting today, without adjusting your medication yourself.
Have the whole picture measured
Ask your doctor to measure TSH, fT4 and fT3 together, always at the same time of day and at the same interval after your tablet. Depending on the situation, ferritin with CRP, selenium and zinc can be added. Note down whether you are currently fasting, dieting, have been ill or are under particular strain.
Look at the brakes before the dose goes up
Eat enough, especially in phases with a lot of training, and avoid long crash diets. Give your sleep and your nervous system room, for example with regular breaks and calm breathing in the evening. Have sources of inflammation and measured deficiencies assessed by a doctor and addressed in a targeted way.
Raise the topic of conversion openly
Ask your doctor about the ratio of fT3 to fT4 and whether you are taking your tablet in the best possible way. If marked symptoms remain despite everything, you can ask whether a supervised trial according to the criteria of the professional societies might be an option for you. Please do not change anything on your own.
This is about more than a lab value. Energy is not a small thing. It is the freedom to shape your day yourself. When conversion gets going again, some of exactly this freedom can return.
Well established
Fasting and severe energy shortage lower T3 and in part raise reverse T3. On levothyroxine, fT4 is higher on average and fT3 lower than in healthy people. On average across all those treated, combination with T3 brings no measurable advantage.
Plausible, limited human data
A lack of selenium, iron or zinc can slow conversion. Glucocorticoids can shift conversion toward reverse T3. A subgroup with severe symptoms might benefit from treatment containing T3.
Still open
Whether quiet, chronic inflammation measurably lowers fT3 in everyday life. What role DIO2 variants play in individual cases. Whether fT3 should help guide dosing in the future.
And now you know where you can start before it comes to more hormone. If you do not just want to read but want to get started right away: below this article, you will find the option to book an appointment.
Frequently asked questions about impaired conversion
What is a T4 to T3 conversion disorder?
It means that the body does not convert the storage hormone T4 into the active hormone T3 to the expected extent. Typically, free T4 is in the upper and free T3 in the lower part of the normal range, sometimes with an elevated reverse T3. This is not an official diagnostic term in endocrinology. Specialist articles speak of reduced conversion efficiency or a low T3 to T4 ratio. In psychiatry, the term conversion disorder means something entirely different.
How can I recognize impaired conversion in my lab results?
Clues come from comparing free T4 and free T3 from the same blood draw. If fT4 is high in the normal range and fT3 is low, the ratio between the two is shifted. There is no generally accepted cutoff for this ratio so far, and laboratories measure differently. That is why the values should always be assessed together with symptoms, medications, diet and other conditions.
Does an elevated reverse T3 prove impaired conversion?
No. Reverse T3 is formed when T4 loses an iodine atom at a different position, and it is considered largely inactive. It rises in severe illness, during fasting and with some medications such as amiodarone. On levothyroxine, more T4 is also available, from which more reverse T3 can be formed. A review from laboratory medicine notes that the measurement does not yet have a firm place in routine diagnostics.
Why do I feel unwell on levothyroxine despite good levels?
There are several possible reasons, and conversion is one of them. In a study from Catania, 15.2 percent of 1,811 people without a thyroid of their own had a lower free T3 than healthy people despite a normal TSH. In US population data, the ratio of T3 to T4 on levothyroxine was about 15 to 20 percent lower. Iron deficiency, other autoimmune diseases, sleep problems and the way the tablet is taken are also possible factors.
Does a higher levothyroxine dose bring more T3?
Not necessarily. In data from 9,850 treated people, T3 rose markedly with fT4 only up to a turning point, after which the curve flattened, while TSH kept falling steeply. A study from Lüdenscheid and Bochum found the lowest fT3 levels in the poorest converters despite the highest dose. Overdosing can strain the heart and bones, which is why any change in dose belongs in medical hands.
Can diets and fasting slow conversion?
Yes, this has been studied well. During total fasting, T3 fell by 53 percent in one study, and reverse T3 rose by 58 percent. A carbohydrate-free diet of 800 calories lowered T3 by 47 percent, while with at least 50 grams of carbohydrates a day it remained stable. A meta-analysis of 15 studies found a marked drop in fT3 with stable fT4 during fasting. After eating resumed, the values in the studies mostly recovered quickly.
What role does stress play in the conversion of T4 to T3?
High levels of glucocorticoids can shift conversion toward reverse T3. In a classic study, reverse T3 rose as early as eight hours after a dose of dexamethasone, and T3 fell after about one day. In soldiers in Ranger training with lack of sleep, strain and an energy deficit, T3 fell below the normal range and recovered with more food, even though the other stresses remained. Energy shortage seems to be a particularly strong lever here.
Can selenium improve conversion?
This is plausible above all where selenium is lacking. The enzymes of conversion carry selenium in their active center, and in older people a low selenium status was linked to a lower T3 to T4 ratio. In a Danish study with 491 older people, selenium given for up to five years changed neither fT3 nor the ratio of fT3 to fT4. Selenium has a narrow range between too little and too much, so it is worth checking your status first.
Do iron and zinc affect thyroid hormones?
Both are needed in hormone metabolism. Iron is a building block of the enzyme that makes the hormones in the thyroid. In one study, women with iron deficiency anemia had lower T4 and T3 levels, which partly improved with iron. For zinc, a small Japanese study without a control group showed a higher T3 and a lower reverse T3 after twelve months of zinc. Both should be measured and supplemented under medical supervision.
What does the DIO2 gene have to do with conversion?
DIO2 contains the blueprint for type 2 deiodinase, which produces a large share of the T3 in tissue. For the common variant Thr92Ala, studies found lower enzyme activity and, after removal of the thyroid, lower fT3 levels. A Dutch population study with 12,625 people, on the other hand, found no link with hormone levels or quality of life. A genetic test is therefore not yet a routine tool for treatment decisions.
Does a combination of T4 and T3 make sense?
For the group as a whole, studies have so far shown no advantage. A meta-analysis of 18 studies found no difference in quality of life and fatigue, but 43 percent preferred the combination and 23 percent T4-only therapy. In a double-blind study, the third with the most severe symptoms did better on treatment containing T3. European and British professional societies describe a medically supervised trial for selected people with persistent symptoms once other causes have been ruled out.
What applies if you are trying to conceive or are pregnant?
Separate rules apply here. The 2026 ATA guideline recommends not using any preparations other than levothyroxine in women who are planning a pregnancy, meaning neither liothyronine nor thyroid extract. The unborn child's brain makes its T3 mainly by itself from the mother's T4. If you take preparations containing T3 and want to become pregnant, you should discuss switching with your doctor in good time.
Can inflammation disrupt conversion?
In severe illness, this has been studied well. In tissue samples from intensive care patients, the converting enzyme D1 was throttled in the liver and the degrading enzyme D3 was active in liver and muscle. In human cells, the inflammatory messenger interleukin-6 blocked the production of T3 and promoted its breakdown. Whether quiet, chronic inflammation in everyday life has the same effect has not yet been studied sufficiently in humans.
Can I take T3 on my own or change my dose?
Please don't. T3 is a potent prescription hormone, and even small amounts can promote a racing heart, rhythm disorders and, over time, bone loss. Raising levothyroxine on your own carries these risks too. It makes sense to go through fT3, fT4, how you take your tablet and the possible brakes with your doctor and to plan every change together.
Further reading on related topics
Fasting with Hashimoto's
What fasting periods can mean for the thyroid and the immune system.
Why am I not losing weight even though I eat little?
Feedback loops instead of calorie guilt.
Iron deficiency and the thyroid as sleep thieves
Ferritin, TSH and waking up at night.
Ferritin level: what is normal?
Why iron stores belong in the search for causes.
Recognizing overtraining
When training, food and recovery no longer fit together.
Fasting and exhaustion
Stress axis, energy and the limits of fasting.
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