Thyroid Guide · Hormone replacement

Natural thyroid hormones: what is behind NDT

Dried thyroid tissue from pigs. More than a hundred years old, not licensed in Germany, disputed for decades. Here is what is documented, what is open, and where the risks are.

SJ
Shukri Jarmoukli · Physician, Integrative Medicine · ViveCura Berlin
Hormone replacement Guidelines quoted in full Safety and dosing 25 sources with DOI
Why I am writing this

In German, natural thyroid hormones are usually written about in only two registers. As a quiet promise that is finally supposed to bring relief. Or as a footnote that gets cleared away in two sentences. Both cut the evidence short. I am trying a third way here: writing all of it down, including the uncomfortable parts, and doing so for both sides.

There is one sentence I hear often in my consulting room. It comes quietly, and it comes at the end of the conversation.

I read something on the internet. About natural thyroid hormones.

Then comes a small pause. Inside that pause sits a question that few people ask out loud: do you now think I am being difficult?

No. Anyone who still cannot get out of bed in the morning after two years of stable laboratory values has good reason to keep asking. And this topic is not an invention of the internet. It is the oldest treatment for hypothyroidism there is.

It is just that the matter is more complicated than either camp would like. Many people know the feeling of standing between two very confident opinions and having none of their own.

What awaits you here

  • What an NDT tablet actually contains, with numbers
  • The history and the reason for the switch to levothyroxine
  • The two randomised trials, reported in full
  • The preference paradox and possible explanations
  • Why this debate is fought so emotionally
  • The four guideline arguments from ATA and ETA, each with a number
  • TSH suppression: fractures, atrial fibrillation, warning signs
  • Section 73 of the German Medicines Act and the supply situation
  • For whom the question comes up, and for whom explicitly not
Clinical Randomised trials and guidelines Observation Cohorts, meta-analyses, reviews Animal model Studies in mice Cell culture In vitro data
Important before we start

Natural thyroid hormones are prescription only medicines. This text puts the evidence into perspective. It is not a recommendation for or against any product and not a reason to change anything about ongoing treatment.

An existing thyroid therapy is never changed, reduced, switched or stopped on your own. Every change belongs in medical hands, with a prescription, laboratory checks and scheduled follow up appointments. That applies to levothyroxine just as much as to any T3 containing product.

What an NDT tablet actually contains

Natural. That word carries a lot. It sounds like origin, like something that was around long before anyone rebuilt it in a laboratory. There is something to the word. Just not what most people take it to mean.

Natural thyroid hormones are dried, ground thyroid tissue from pigs, standardised to a hormone content and pressed into tablets. Internationally the group is called NDT or DTE, that is desiccated thyroid extract. Well known products are Armour Thyroid, NP Thyroid, Erfa Thyroid and Thyroid-S. I name these as factual information, because you will read them in forums, not as a recommendation.

The two numbers this really turns on

That tissue contains both thyroid hormones. T4, the storage hormone, and T3, the active form. They sit in there in a ratio that the pig's body set, not yours.

Review The hardest numbers on the content

In 2020, Tania Idrees and Antonio Bianco collected in the journal Thyroid what is known about liothyronine and desiccated thyroid extract. Bianco counts among the researchers most open to T3 containing therapies, which makes his critical sentences on NDT particularly robust.

Two figures stand out. NDT has a T4 to T3 ratio of roughly 4 to 1. And the mean daily dose that brings TSH into the reference range contains about 11 micrograms of T3. Alongside that stands the sentence that the consistency of the hormone content is monitored solely by the manufacturers.

For you that means: the amount of T3 is not freely selectable. It is built into the product. Anyone who raises the total dose raises both, always in the same ratio.

Idrees T, Palmer S, Maciel RMB, Bianco AC. Thyroid. 2020;30(10):1399-1413. PMID: 32279609 · DOI: 10.1089/thy.2020.0153 [Review]

This set ratio is the quiet lead character of this article. Keep it in mind: roughly 4 to 1.

And what about T2, T1 and thyroglobulin?

You will hear one argument almost every time. NDT contains more than T4 and T3, namely T2, T1 and thyroglobulin, and that is where the difference lies. The first part is correct. The second is open.

Cell culture In vivo, mouse What we know about the small metabolites

A group around Josef Köhrle from the Institute of Experimental Endocrinology at the Charité in Berlin and from Greifswald summarised in 2020 what is known about 3,5-T2, about thyronamines and about thyroacetic acids.

The data come from cell culture, cell lines and mouse models after pharmacological doses, not from controlled human studies. And whether these substances can be measured analytically in human blood is still disputed, because classical immunoassay and mass spectrometry diverge.

For you that means: anyone arguing for NDT with T2 and T1 is arguing with cell culture and mouse. Mechanistically interesting, but based on current data not strong enough as proof of benefit in humans.

Homuth G, Lietzow J, Schanze N, Golchert J, Köhrle J. Exp Clin Endocrinol Diabetes. 2020;128(6-07):401-413. PMID: 32450582 · DOI: 10.1055/a-1139-9200 [Mechanism Review]

Mechanistically plausible, human data thin: that is exactly how this point should be described, not as an argument that settles the question.

The reframe

Natural describes the origin, not the fit. A substance from a pig is not more suitable for a human simply because it comes from a living creature.

The useful question is not: is it natural. It is: in what ratio does it arrive, how evenly, and can it be adjusted to your need.

Why the immune system attacks its own thyroid in the most common cause of an underactive gland is covered in the guide Hashimoto and the immune system.

And now you know why the number 4 to 1 will appear several more times in this text.

More than a hundred years old: the history and the switch

If someone tells you that natural thyroid hormones are an internet fashion, the opposite is true. Animal thyroid preparations were the first pharmacological treatment for hypothyroidism at all and dominated the market for most of the twentieth century. In this story, levothyroxine is the newcomer.

A note on honesty about the year. In forums you almost always read 1892. The scientific reviews are more careful and speak of more than a century, or of the last roughly 130 years. I therefore write end of the nineteenth century, because I do not hold a clean source for the exact year.

The arc in four stations
  1. End of the nineteenth centuryAnimal thyroid tissue becomes the first pharmacological treatment for hypothyroidism. It is the only option there is.
  2. First half of the twentieth centuryNatural preparations dominate the market. Dosing follows symptoms, basal metabolic rate and protein bound iodine. A TSH value does not yet exist.
  3. 1970s, first developmentThe serum TSH radioimmunoassay arrives. It makes visible that many treated people are overdosed. The usual replacement doses are cut drastically.
  4. 1970s, second developmentThe deiodinase mediated conversion of T4 into T3 is described. That gives a physiological rationale for monotherapy.
Review The sentence that gets in the way of romanticising

In 2016, Elizabeth McAninch and Antonio Bianco traced the history of hypothyroidism treatment in the Annals of Internal Medicine, from the first animal preparations to today's standard therapy.

They describe how, in the era before the TSH test, dosing followed symptoms, basal metabolic rate and protein bound iodine. And then it says, without any dramatisation: thyrotoxic side effects were not uncommon in the process.

For you that means: the good old days were not good old days for the thyroid. They were a time without a measuring instrument. Anyone defending NDT by saying it was the standard for decades is defending a practice in which overdosing was normal, because nobody could see it.

McAninch EA, Bianco AC. Ann Intern Med. 2016;164(1):50-56. PMID: 26747302 · DOI: 10.7326/M15-1799 [Review]

A second, independent research group arrives at the same picture. James Hennessey traced how levothyroxine came to prevail, and describes that the use of animal preparations has been scientifically documented for around 130 years and that refinements in manufacturing and regulation continue to this day.

Hennessey JV. Endocrine. 2017;55(1):6-18. PMID: 27981511 · DOI: 10.1007/s12020-016-1199-8 [Review]

Why the switch was a good decision

Something matters to me here: the move to levothyroxine was not a conspiracy against nature but, with the data available at the time, a good medical decision. A synthetic single active substance can be set to a defined amount, while a biological material varies. T4 stays in the blood for about a week and can smooth out fluctuations that way, T3 is shorter lived. And if the body converts T4 into T3 anyway, the storage hormone is theoretically enough.

The last point is the only one where something has moved since. The conversion is not an automatic machine that runs the same way in everyone. It depends on enzymes that are themselves regulated. How that works is covered in the guide From T4 to T3: the conversion. That is the mechanism the entire debate revolves around.

The reframe

There was no villain in this story. There was a new measuring instrument that made an old problem visible, and a new insight that allowed a simpler solution.

The interesting question is not whether the switch was right. It is: for whom was the simpler solution never quite enough, and how do you recognise those people?

And now you know why I do not set up a battle line on this topic. Endocrinology did clean work here. It just left a remainder group behind.

The decisive question: is NDT better than levothyroxine?

This is the question you came here for. You get it answered in full, including the numbers that do not fit the picture.

What surprises many people: there are exactly two randomised double blind trials of NDT against levothyroxine, both from the same research group.

2randomised double blind trials of NDT worldwide
6,394hits a 2024 meta-analysis screened to find those two
22weeks was the longest randomised observation per arm

These three numbers tell you how much weight any statement here can carry.

RCT, n=70 The most cited and most abbreviated study

Thanh Hoang and colleagues at the Walter Reed National Military Medical Center randomised 70 people with hypothyroidism who had been stable on levothyroxine for at least six months. Sixteen weeks on one product, then a switch, then sixteen weeks on the other. Double blind, crossover.

The result has two halves. First: no differences in symptoms and neurocognitive measures, with weight around 1.4 kilograms lower on NDT, p less than 0.001. Second the preference: 48.6 percent for NDT, 18.6 percent for levothyroxine, 32.9 percent with no preference.

For you that means: anyone quoting only the preference is cutting it short. Anyone quoting only the null result is cutting it short just as much. The authors themselves write that NDT did not lead to a significant improvement in quality of life, but that it could be relevant for some of those affected.

Hoang TD, Olsen CH, Mai VQ, Clyde PW, Shakir MKM. J Clin Endocrinol Metab. 2013;98(5):1982-1990. PMID: 23539727 · DOI: 10.1210/jc.2012-4107 [RCT, n=70]
RCT, n=75 Three arms, 22 weeks, one important secondary finding

Mohamed Shakir and colleagues randomised 75 people to three treatments: levothyroxine alone, levothyroxine plus liothyronine, and NDT. Twenty two weeks each, double blind, crossover, measured with four instruments.

TSH stayed within the reference range in all three arms. No differences in the primary and secondary endpoints, with one exception: a slightly higher heart rate on NDT. Preference did not differ in the overall group either. Then the subgroup analysis: in the third who were most burdened on levothyroxine, a clear preference for T3 containing therapy showed up, with better values across all four instruments.

For you that means: across the board no difference. In the group of the heavily burdened a marked one. That is the cleanest available answer to the question of who this topic could be relevant for.

Shakir MKM, Brooks DI, McAninch EA et al. J Clin Endocrinol Metab. 2021;106(11):e4400-e4413. PMID: 34185829 · DOI: 10.1210/clinem/dgab478 [RCT, n=75]
RCT, n=143 The finding that points in both directions

The same authors analysed both randomised trials together in 2025, 143 participants in total, split by symptom burden on levothyroxine into few, moderate and many symptoms. All measurements taken at normal TSH.

Those with many symptoms did significantly better on NDT, in cohort two with p less than 0.01. The middle group as well, with p equal to 0.02. And then the direction that is rarely quoted: those who had only few symptoms on levothyroxine did significantly better on levothyroxine than on NDT, p equal to 0.03, and better than on the combination, p equal to 0.02.

For you that means: it is not about better or worse, but about your starting point. Those who felt well on levothyroxine did on average worse on NDT in these trials. That is a strong argument against the idea that NDT is fundamentally the more suitable product.

Hoang TD, Patel AA, Spiro AJ, Watson NL, Shakir MKM. Endocr Pract. 2026;32(1):53-59. PMID: 40947017 · DOI: 10.1016/j.eprac.2025.09.007 [RCT, n=143]
Meta-analysis, k=16 The laboratory values shift, the questionnaires do not

Mahmoud Nassar and colleagues searched Embase, Medline and Web of Science up to the end of November 2023. Out of 6,394 hits, 16 randomised trials qualified, exactly two of them on NDT.

For NDT against levothyroxine alone, total T3 was clearly higher, mean difference 50.90. Total T4 and free T4 were lower, TSH moderately higher at 0.49. No significant difference, by contrast, in heart rate, SHBG, lipid profile and the three questionnaires on symptoms, general well being and depressive mood. Heterogeneity was low.

For you that means: NDT shifts the blood values measurably and in the expected direction. In this synthesis it does not shift the measured quality of life.

Nassar M, Hassan A, Ramadan S et al. BMC Endocr Disord. 2024;24(1):90. PMID: 38877429 · DOI: 10.1186/s12902-024-01612-6 [Meta-analysis, k=16]
Cohort, n=1,260,000 Hard endpoints for the first time, but retrospective

A group around Bianco compared 1.26 million people with hypothyroidism against 3.32 million controls in 2026 using registry data, over up to 20 years, with propensity score matching and Cox models.

People with hypothyroidism had an around 1.4 fold higher dementia risk and a more than twofold higher mortality risk, most pronounced when TSH was outside the target range. Comparing monotherapy against T3 containing therapy, there was a 27 percent lower dementia risk and a 31 percent lower mortality risk on the combination. In the adjusted model these figures shrank to 16 and 25 percent.

For you that means: interesting, but not proof yet. These are claims data, and the gap between 27 and 16 percent shows exactly that. The authors themselves call for further studies.

Beltrão FEL, Carvalhal G, Meneghini V et al. J Clin Endocrinol Metab. 2026;111(2):561-571. PMID: 40579157 · DOI: 10.1210/clinem/dgaf367 [Cohort, n=1,260,000]

Why complaints can persist on levothyroxine at all has far more facets than the choice of product. That is covered in the guide Levothyroxine and persisting symptoms.

The reframe

No difference in the mean does not mean no difference in you. A mean can contain two opposing movements and still look quiet.

That is exactly what the 2025 analysis shows. One group does better, another does worse, and the sum is a zero. That zero is not a result. It is a question.

One note that belongs here: subgroup findings like these are a reason for a medical conversation, not for a switch on your own. Whether someone belongs to one of these subgroups cannot be read off any text, only from history, findings and course under medical supervision. And anyone already taking a thyroid medicine changes nothing about it without a medical prescription.

And now you know why both camps can quote the same studies and still arrive at opposite conclusions.

The preference paradox

Picture two rooms. In the first sit statisticians looking at questionnaire scores. They say: no difference. In the second sit the participants of the same study, asked which product they would like to keep. About half of them say: the other one.

Both rooms are right. That is exactly what makes this topic so hard to grasp.

Meta-analysis, k=11, n=1,135 The preference is robust, not anecdotal

A Brazilian and American group around Fabyan Esberard de Lima Beltrão carried out a systematic review with meta-analysis, meta-regression and network meta-analysis. Eleven randomised trials with 1,135 participants were included, eight of them with a crossover design.

The distribution of preference: 52 percent for a combination or NDT, 24 percent for levothyroxine alone, 24 percent with no preference, relative risk 2.20. After excluding four trials, heterogeneity fell from 81 to 24 percent without changing the result: 1.97, p less than 0.00001.

For you that means: this preference is not a collection of forum opinions. It shows up in controlled trials and stays stable under statistical correction. The authors conclude from it that patient preferences belong in shared decision making.

de Lima Beltrão FE, Carvalhal G, de Almeida Beltrão DC et al. J Clin Endocrinol Metab. 2025;110(3):887-900. PMID: 39290156 · DOI: 10.1210/clinem/dgae651 [Meta-analysis, k=11, n=1,135]
Survey, n=12,146 Large number, weak design, important message

A group around Bianco and Jonklaas published an online survey in 2018, hosted on the website of the American Thyroid Association. 12,146 people answered in full.

Satisfaction overall sat at a median of 5 on a scale up to 10. In the subgroup without accompanying conditions, 3,670 people, the median was 7 on NDT, 6 on levothyroxine plus liothyronine and 5 on levothyroxine alone.

For you that means: these numbers are self selected. Anyone who has already switched and stayed with it is by construction more satisfied, and the size of the sample does not change that. The real message is not the comparison of products but the median of 5 across all respondents.

Peterson SJ, Cappola AR, Castro MR et al. Thyroid. 2018;28(6):707-721. PMID: 29620972 · DOI: 10.1089/thy.2017.0681 [Survey, n=12,146]
Case Series, n=673 How people actually arrive at NDT

A Mayo Clinic group around Freddy Toloza analysed posts from three large hypothyroidism forums, from 673 people who were currently taking NDT.

In 46 percent, a medical professional had sparked the interest in NDT, not the internet. Reasons for switching: absent improvement in 58 percent, side effects that had appeared in 22 percent. And: one fifth described side effects on NDT as well. The recurring themes of the analysis were a lack of individualised treatment and the feeling of not being heard.

For you that means two things. The image of the person experimenting on their own does not hold up. And the number on side effects appears on none of the German websites I read for this article.

Toloza FJK, Espinoza Suarez NR, El Kawkgi O et al. Medicina (Kaunas). 2020;56(4):161. PMID: 32260044 · DOI: 10.3390/medicina56040161 [Case Series, n=673]

The genetic attempt at an explanation, and why it does not hold

There is a hypothesis that could explain this paradox, and it is mechanistically elegant. Perhaps some people convert T4 into T3 less well for genetic reasons.

RCT secondary analysis, n=552 A signal that did not find its confirmation

In 2009, Vijay Panicker and colleagues examined in 552 people from a British trial whether variants in the deiodinase genes are linked to psychological well being and to the response to T4 plus T3.

The rarer CC genotype in the deiodinase 2 gene was present in 16 percent. This group had worse baseline values on T4, 14.1 against 12.8 points, and improved by 2.3 points more on the combination. The decisive subordinate clause: the polymorphism had no effect whatsoever on circulating hormone levels. The authors themselves called for replication.

For you that means: the replication came and turned out negative. The randomised trial of 2021 measured precisely this polymorphism prospectively and found no influence. A DIO2 test is therefore not suitable as a basis for a decision, neither for nor against.

Panicker V, Saravanan P, Vaidya B et al. J Clin Endocrinol Metab. 2009;94(5):1623-1629. PMID: 19190113 · DOI: 10.1210/jc.2008-1301 [RCT secondary analysis, n=552]

I write this with regret. That finding would have been an elegant explanation.

Three possible explanations, without committing to one

First the study design. In a crossover trial, every person experiences both products one after the other. Expressing a preference is then easy, and order effects cannot be fully calculated out.

Second the measuring instrument. The questionnaires capture symptom lists, general well being and depressive mood. Perhaps they do not capture what people mean when they say that on one product they felt more like themselves. From the perspective of clinical psychoneuroimmunology that is not an odd idea: drive, sense of warmth and resilience arise from the interplay of nervous system, immune system and metabolism, and they are hard to press into 36 points.

Third a genuine subgroup. Perhaps a portion really does benefit, and this effect disappears in the mean because another portion gets worse. That is exactly what the subgroup analyses of 2021 and 2025 point to.

The reframe

Preference and quality of life score are not the same measure. One asks: which one do you want to keep. The other asks: how many points on a scale.

Both answers are valid. They only contradict each other if you take them for the same question.

And now you know why this debate so often ends with one side accused of ignoring the studies and the other of ignoring the people. Both accusations miss at the same spot.

Why this debate is fought so emotionally

Hardly any medical topic generates this much heat. Not blood pressure, not cholesterol. Why is that? I believe it comes down to four things that apply at the same time.

First, this is about a remainder group that is not small. The most recent high ranking seminar on hypothyroidism in the Lancet writes that levothyroxine is safe and inexpensive, brings values into the reference range and improves symptoms in the majority. And in the same paragraph, that around 10 percent have persisting complaints despite unremarkable values. For statistics that is a fringe group. For the individual person it is their whole life.

Taylor PN, Medici MM, Hubalewska-Dydejczyk A, Boelaert K. Lancet. 2024;404(10460):1347-1364. PMID: 39368843 · DOI: 10.1016/S0140-6736(24)01614-3 [Systematic Review]

Second, the asymmetry between population and person. A guideline asks what is on average the best decision for the population. That is its job, and it does it well. A person in the consulting room asks something else: what is right for me, with my starting point, in this year of my life. These two questions do not always have the same answer.

The mean is not a person. It is a summary of people, and sometimes it summarises two opposing movements into a zero.

The core sentence of this section

Third, the feeling of not being heard. The Mayo analysis of 673 people had exactly this as its core theme, not the product. Anyone who is told for years that the values are fine, and still does not function in the morning, develops mistrust towards the sentence that everything is fine. And then that person finds a website that describes exactly their complaints and offers a solution.

Fourth, there are interests on both sides. Suppliers of NDT products earn money from this topic, manufacturers of levothyroxine do too. That is not an argument against either side, but it is a reason to check texts against their sources, mine included. That is why every study here carries a PMID and a DOI.

Clinical tradition and anthroposophical perspective, explicitly not a study finding: in anthroposophic medicine the thyroid is described as an organ at a border, where thinking passes into the voice and the will passes into the warmth of metabolism. That is a way of looking, not a measurement, and it stands beside physiology, not in its place. What I like about it is a question it raises: why does this organ of all organs so often affect people who endure a lot and say little? I have no evidence based answer to that and I simply observe it. More on the term natural in medicine is covered in the guide Anthroposophic medicine.

The reframe

This debate runs so hot because both sides are defending something that is right. One defends carefulness, the other defends experience.

Anyone who plays carefulness off against experience always loses one of the two. And you need both.

And now you know why I do not take their arguments away from either side in this text.

What ATA and ETA say, and why they say it

The professional societies do not reject NDT on principle, but as routine therapy, and they give four reasons for it. Each can be backed with a number. You get all four, then the other side just as fully, and at the end, where I weight things differently.

Reason one: the ratio that does not fit

The numerical argument of the guideline

T4 to T3, placed side by side

NDT, dried thyroid tissue from pigs
roughly 4 to 1
Lower limit of the corridor recommended by the ETA
13 to 1
Upper limit of the corridor recommended by the ETA
20 to 1
Share of T4 Share of T3

The T3 share in NDT is therefore many times higher than what the European guideline describes as sensible for combinations. That is the factual core of the objection, and it is not an opinion but a ratio.

Guideline The sentence that is almost never quoted in Germany

A task force of the European Thyroid Association around Wilmar Wiersinga published a guideline in 2012 on the use of L-T4 plus L-T3 in hypothyroidism.

It records: in 5 to 10 percent of treated people with normal TSH, complaints persist. As possible explanations it names, among others, accompanying autoimmune conditions and the inability of levothyroxine treatment to restore physiological T4 and T3 concentrations in serum and tissues. The combination counts as an experimental approach, only through accredited specialists, with discontinuation after three months without improvement. And then the decisive sentence: a T4 to T3 ratio between 13 to 1 and 20 to 1 by weight is recommended, and all currently available combination products fall below that and are therefore not recommended.

For you that means: the main objection is not a prejudice against animal derived products. And the same text explicitly names the inadequacy of standard therapy as a possible reason for persisting complaints. That stands in the guideline, not in a blog.

Wiersinga WM, Duntas L, Fadeyev V, Nygaard B, Vanderpump MPJ. Eur Thyroid J. 2012;1(2):55-71. PMID: 24782999 · DOI: 10.1159/000339444 [Guideline]

Reason two: batch variability and recalls

Standardising a biological material to a hormone content is difficult. This is not a theoretical objection: it happened twice within eleven months.

13lots of NP Thyroid the FDA recalled in 2020 for super potency
115 %of the declared T3 those lots could contain
under 90 %T3 or T4 was in the lots recalled in 2021

In its 2020 recall notice the FDA names the possible consequences explicitly: signs of an overactive thyroid up to chest pain and cardiac arrhythmia, and for pregnant women miscarriage and impaired fetal development. Fairness requires adding: that these recalls happened also shows that oversight exists and takes effect. Both have since been closed.

Reason three: missing long term data on hard endpoints

Guideline The ATA names the gap itself

A task force of the American Thyroid Association around Jacqueline Jonklaas assessed the literature on 24 questions of hypothyroidism treatment in 2014, explicitly including thyroid extracts, combination therapy, T3 therapy and compounded preparations.

The result: levothyroxine should remain the treatment standard, because no consistently strong evidence was found for the superiority of alternative products with respect to improving health outcomes. And then the guideline names its own research needs: better biomarkers for euthyroidism in addition to TSH, mechanistic research on serum T3 levels, and long term endpoint studies on combination therapy or thyroid extracts including subgroup effects.

For you that means: this guideline does not say that this is nonsense. It says the data are not enough to change the standard, and here is the list of the data that are missing.

Jonklaas J, Bianco AC, Bauer AJ et al. Thyroid. 2014;24(12):1670-1751. PMID: 25266247 · DOI: 10.1089/thy.2014.0028 [Guideline]

Reason four: the risk of a suppressed TSH

This is the point that actually protects people, and it gets its own section in a moment. In short: because NDT contains a proportionally large amount of T3, and T3 can push TSH down more strongly, it is easier to end up in a range with a very low TSH on this product. And that range is not harmless.

And now the other side, just as fully

Guideline Three professional societies declare the question open

The American Thyroid Association, the British Thyroid Association and the European Thyroid Association held a joint conference on 3 November 2019 with twelve experts, live streamed between Chicago and London. A consensus document emerged from it in 2021.

The starting observation: 14 clinical trials have shown no consistent advantage of combination therapy, and at the same time it is widely used. What matters is the shared conclusion that equipoise exists for a new clinical trial. Equipoise is the technical term for a question being considered open. Of 34 statements put to a vote, 28 reached at least 75 percent agreement, 13 of them even 100 percent.

For you that means: three large professional societies say together that we do not know it with enough certainty, and that we consider the question open enough to investigate it anew. Anyone presenting NDT as refuted is as far off as anyone presenting it as secretly endorsed.

Jonklaas J, Bianco AC, Cappola AR et al. Thyroid. 2021;31(2):156-182. PMID: 33276704 · DOI: 10.1089/thy.2020.0720 · published simultaneously in Eur Thyroid J. 2021;10(1):10-38, PMID: 33777817 [Guideline]
BodyYearStatement on NDT and combination
ATA2014Levothyroxine remains the standard. No consistently strong evidence for alternatives. Long term endpoint studies are missing.
ETA2012Combination only as an experiment, only through specialists, discontinuation after three months. Recommended ratio 13 to 1 up to 20 to 1, available products fall below that.
ATA, BTA and ETA2021Fourteen trials without a consistent advantage. At the same time consensus: equipoise exists.
ATA pregnancy2017Its own framework, its own target values, T4 centred.
My reasoned position, clearly marked as such

Where I weight things differently, and why

I share the four objections of the guidelines. All four. The ratio of roughly 4 to 1 is a genuine pharmacological problem, the batch variability is documented, the long term data are missing, and a suppressed TSH is a risk.

I weight things differently in a single place: in how the remainder group is handled. A guideline has to look at the population and, in case of doubt, defend the standard. In a consulting room there is no mean sitting in front of you. When someone has had well adjusted values for years, all the building blocks have been checked and the complaints remain, then I find the question about a different product a legitimate medical conversation. Not as a first step, but as one of the last.

I base that on three things from the sources: the ETA itself names the inadequacy of standard therapy as a possible reason for persisting complaints, the three professional societies have established equipoise, and the subgroup signals point consistently in the same direction. In my clinical experience, the open conversation alone changes something, regardless of what is prescribed in the end. That is an observation, not a study result.

The reframe

The guideline does not say: this is nonsense. It says: the data are not enough for that, and here is the list of the data that are missing.

That is something other than rejection, and something other than agreement. It is an open question named as an open question. That is good science.

And now you know why I go into this section in such detail. It is the part of the topic that most German websites skip.

Safety: the point is not the product, it is the dose

If you keep only one section from this article, please make it this one.

The safety question does not turn on whether the raw material comes from a pig. It turns on one number: your TSH. It is the signal with which the pituitary addresses the thyroid. If the hormone level rises, TSH falls. If it is very low, a lot of thyroid hormone is on the move. And that low range is well studied.

Cohort, n=17,684 The most differentiated work on the safety question

Robert Flynn and colleagues analysed everyone in Tayside, Scotland who received thyroid hormone replacement therapy between 1993 and 2001. 17,684 people, linked with regional data sets.

Against a TSH within the reference range, a suppressed TSH came with a hazard ratio of 1.37 for cardiovascular disease, 1.6 for arrhythmias and 2.02 for fractures. An elevated TSH was similarly risky at 1.95, 1.80 and 1.83. The most important finding: a low but not suppressed TSH came with no increased risk.

For you that means: this work is uncomfortable for both camps. It shows that anxious underdosing can be similarly risky to overdosing. And it shows that a truly suppressed TSH doubled the fracture risk in this cohort.

Flynn RW, Bonellie SR, Jung RT et al. J Clin Endocrinol Metab. 2010;95(1):186-193. PMID: 19906785 · DOI: 10.1210/jc.2009-1625 [Cohort, n=17,684]
Meta-analysis, k=13, n=70,298 The strongest number in the whole topic

Manuel Blum and colleagues pooled participant data from 13 prospective cohorts in the United States, Europe, Australia and Japan in JAMA. 70,298 people, 762,401 person years.

In subclinical hyperthyroidism the hazard ratio for hip fractures was 1.36, for all fractures 1.28. Below a TSH of 0.10 the figures rose markedly: hip fracture 1.61, all fractures 1.98, vertebral fractures 3.57 with a confidence interval from 1.88 to 6.78. For subclinical hypothyroidism, by contrast, no link with fracture risk was found.

For you that means: below a TSH of 0.10, the risk of vertebral fractures in this analysis was more than three and a half times higher. That number belongs on the table without softening, whichever product is involved.

Blum MR, Bauer DC, Collet TH et al. JAMA. 2015;313(20):2055-2065. PMID: 26010634 · DOI: 10.1001/jama.2015.5161 [Meta-analysis, k=13, n=70,298]
Meta-analysis, k=10, n=52,674 The heart, and why lower is not better

Tinh-Hai Collet and colleagues pooled individual data from 52,674 people out of ten prospective cohorts. Coronary events were recorded in 22,437 people, newly occurring atrial fibrillation in 8,711.

4.2 percent had subclinical hyperthyroidism. After adjustment, the hazard ratio for all cause mortality was 1.24, for coronary mortality 1.29 and for atrial fibrillation 1.68. What matters is the trend: below a TSH of 0.10 the risks were higher than between 0.10 and 0.44.

For you that means: a very low TSH came with a 68 percent higher risk of atrial fibrillation, and the lower it went, the more pronounced it became. For context: people on thyroid medication were excluded here, so this is about an overactive gland arising in the body itself. The mechanism is the same.

Collet TH, Gussekloo J, Bauer DC et al. Arch Intern Med. 2012;172(10):799-809. PMID: 22529182 · DOI: 10.1001/archinternmed.2012.402 [Meta-analysis, k=10, n=52,674]

A claim I would like to correct, kindly but clearly

On several German language websites it says that a TSH below 0.1 is normal and harmless on NDT, because TSH simply behaves differently on T3 containing therapy. The first part is correct: T3 can push TSH down more strongly. The second part is not supported by the data. The three works above together cover more than 140,000 people and point consistently in the same direction below 0.10.

I do not assume bad intent from anyone. This sentence probably arises from an understandable observation: people often feel better with a low TSH, at least in the short term. It is just that bones and heart rhythm say nothing as long as they are still keeping up. That is precisely why we measure.

Warning signs that belong in medical hands

Signs that can point to too much thyroid hormone: a racing heart, palpitations or an irregular pulse. Marked inner restlessness or tremor. Unexplained weight loss. Heat intolerance and increased sweating. Newly appearing insomnia. Muscle weakness, especially in the thighs.

Signs that can point to too little: increasing sensitivity to cold, marked slowing, a very slow pulse, constipation, weight gain without a change in diet, puffy swelling in the face, strong lack of drive. The Scottish cohort above shows that a TSH that is too high came with risks similar to a suppressed one. Anxious underdosing is therefore not the safe side.

Seek medical care immediately, if in doubt via the emergency number 112: a high fever together with a very fast pulse, vomiting, agitation and confusion can point to a thyroid storm. Increasing drowsiness up to clouded consciousness with hypothermia and very slow breathing can point to a myxoedema coma. Both are rare and both are emergencies.

Independent of the hormone dose: a new or rapidly growing swelling on the neck, a palpable nodule, difficulty swallowing, hoarseness or a feeling of tightness need to be examined, regardless of what the laboratory values look like. How such a workup proceeds is covered in the guide Nodules and goiter: the workup.

Particular caution applies with known heart disease, in older age, with atrial fibrillation in the history and with osteoporosis or an increased fracture risk. In these situations the distance between enough and too much is smaller, and monitoring belongs correspondingly closer.

Please read this box, even if you skip the rest

Prescription only. Medically supervised. Not a self experiment.

  • Natural thyroid hormones are prescription only medicines. They belong exclusively in a medical prescription and through a pharmacy.
  • No sourcing from the internet, from abroad without a prescription or via acquaintances. There, neither origin nor content nor legal framework is secured.
  • No self experiment and no self dosing. The distance between enough and too much is small with this product, and too much is not harmless.
  • An existing thyroid therapy is never changed, reduced or stopped on your own. Every change happens under medical supervision only, with laboratory checks and scheduled follow up appointments.
  • With heart disease, in older age, with osteoporosis and during pregnancy, additional precautions apply.

This article puts the evidence into perspective. It is not a recommendation for or against any product and does not replace a medical conversation.

Pregnancy: its own framework with its own target values

In pregnancy, different target values and a different care setting apply. There is a dedicated guideline from the American Thyroid Association from 2017 for this, reaching from the preconception phase into the breastfeeding period. The physiological reason is simple: in the first trimester the fetus depends on maternal T4, and T4 is the form that crosses the placenta to a relevant degree. That is why a T3 heavy replacement is not the standard route here. Everything concerning thyroid therapy in pregnancy belongs in medical hands without exception.

Alexander EK, Pearce EN, Brent GA et al. Thyroid. 2017;27(3):315-389. PMID: 28056690 · DOI: 10.1089/thy.2016.0457 [Guideline]

When a T3 containing product is discussed, a TSH value alone is not enough. What makes sense is the combination of TSH, free T4 and free T3, at a defined time interval from intake, because T3 levels fluctuate over the course of the day. Which values say what is covered in the guide Thyroid values: which ones really count.

The reframe

The question is not: is NDT dangerous. The question is: at which dose and which TSH does the risk rise, and who checks regularly.

A product without close monitoring is riskier than the same product with monitoring. That applies to levothyroxine just the same.

And now you know why the sentence about the supposedly harmless TSH below 0.1 is the sentence I find most uncomfortable in this field.

The legal and supply situation in Germany

Suppose you now think: fine, that would be worth a conversation. Then in Germany you run into a hurdle that hardly anyone writes about.

No NDT product is licensed as a finished medicinal product in Germany. So there is nothing here that could simply be prescribed and collected at a pharmacy.

The legal route is called single patient import and is set out in section 73 paragraph 3 of the German Medicines Act. This provision allows finished medicines that are not licensed in Germany to be brought in under narrow conditions.

The conditions of single patient import, in the sense of the wording

  • On an existing order from individual people and in small quantity. No stock, no trade.
  • Dispensing through a pharmacy within the scope of its existing pharmacy operating licence.
  • Lawful marketability in the country of origin. The product has to be licensed where it comes from.
  • No comparable licensed medicine available. There must be no medicine with an identical active substance and comparable strength available for the indication. With thyroid hormones that is a question a physician has to justify.
  • A medical or dental prescription is required for medicines from non EU countries.

German Medicines Act, section 73 paragraph 3. Federal Ministry of Justice, gesetze-im-internet.de [Agency Document]

The second option is compounded preparations through specialised pharmacies. That too is prescription only and no way around a medical prescription.

It is not a grey area and not a loophole, but a clearly regulated route with high requirements. Anyone ordering NDT online without a prescription is moving outside this framework, with no certainty about origin and content. As a rule it is not covered by statutory insurance and runs on a private prescription.

A look across the Atlantic that surprises people

Many assume that NDT is normally licensed in the United States. That is not the case.

0NDT finished medicinal products licensed in Germany
notFDA approved are the US products from animal tissue either
1.5 mpeople are prescribed them in the US regardless, estimated

The FDA itself records that these products derived from animal tissue are not FDA approved. It applies a risk based enforcement approach and has announced to manufacturers that it will issue guidance on developing these products towards marketing applications.

This tension between regulatory status and lived practice is perhaps the most honest frame for the topic. Not a fringe phenomenon, and still nowhere a regularly licensed medicine.

The reframe

Not licensed does not mean forbidden. It means: the responsibility lies entirely with the prescribing person, and monitoring has to be closer than with a licensed product.

A change of batch is therefore not an administrative act but an occasion for a new laboratory check.

And now you know why a serious conversation about this topic starts with the legal framework and not with the product.

For whom the question comes up, and what a responsible framework looks like

That leaves the question from the beginning: who is this actually relevant for?

For whom it comes up: for the roughly 10 percent who have persisting complaints despite well adjusted values. This group is a topic of its own, and it has many possible causes beyond the product. Both are covered in detail in Normal values and still symptoms and in Functional hypothyroidism.

For whom explicitly not: for everyone who feels well on levothyroxine. That is the most important sentence of this section, and it does not come from me but from the post hoc analysis of 143 participants. In the group with few symptoms, the values on levothyroxine were significantly better than on NDT. A switch there would, based on this evidence, not be a gain but a step backwards.

What belongs on the table first

From the perspective of functional medicine the order is decisive: first the building blocks and the context, then the product.

Questions that come before the question of the product

  • Intake and absorption. The interval to meals, coffee, calcium, iron, acid blockers. Surprisingly often the explanation sits here.
  • Iron and ferritin. A deficiency can create tiredness that looks like an underactive thyroid. See Iron deficiency, thyroid and sleep.
  • Selenium, zinc and vitamin D. The cofactors without which conversion and immune regulation can run harder. See Selenium, zinc, iron and vitamin D.
  • Accompanying autoimmune conditions and coeliac disease. The ETA names this explicitly as a point that can be clarified before a combination is discussed. See also Nutrition in Hashimoto.
  • Sleep and cortisol rhythm. Exhaustion rarely has only one source.
  • Menopause and cycle. Oestrogen can change the transport proteins and with them the arithmetic. See Thyroid and female hormones.

What a responsible framework looks like

If the question remains after all of that, then it belongs in a conversation with clear rules. And these are the rules.

A medical prescription, no going it alone. Monitoring intervals with laboratory checks agreed in advance. What is monitored is TSH, free T4 and free T3, not one value alone. Stopping criteria set in advance and an agreed point in time for an honest interim assessment. For the combination the ETA names three months as the period after which treatment is discontinued if there is no improvement. I consider that clarity one of the strongest points of the guideline.

What this text cannot and should not deliver: a recommendation for or against NDT in your case. That takes a history, an examination and a conversation, and none of it fits into a blog article.

What I would like to leave you with

Natural thyroid hormones are neither the suppressed remedy nor malpractice. They are a group of products more than a hundred years old, hard to standardise, with a built in, unchanging ratio of T4 to T3 that cannot be adjusted to the need of the individual person.

For the small group who continue to feel unwell on levothyroxine despite good values, the topic is worth discussing with a physician. Precisely for that reason it belongs in medical care with close monitoring and not in your own hands.

The reframe

The most interesting question in this field is not: which product is better. It is: how burdened are you on what you are taking right now, and what has not been checked yet.

Anyone who answers those two questions honestly often does not need to ask the question about the product at all.

And now you know why I do not consider anyone difficult for raising this topic. It is a good question. It just has a more complicated answer than either side on the internet claims.

Frequently asked questions about natural thyroid hormones

These are the questions that come my way most often on this topic, in the consulting room as well as by email.

What exactly are natural thyroid hormones?

It is dried, ground thyroid tissue from pigs, standardised to a hormone content. Internationally the group is called NDT or DTE, that is desiccated thyroid extract. Well known products are Armour Thyroid, NP Thyroid, Erfa Thyroid and Thyroid-S. They contain T4 and T3 in a largely set ratio of roughly 4 to 1, plus T2, T1 and thyroglobulin. These products are prescription only and not licensed as finished medicinal products in Germany.

Is NDT more natural than levothyroxine, and is more natural better?

Natural describes the origin here, not the fit. The mixing ratio in a pig thyroid is different from what a human body turns over each day. The European professional society recommends a T4 to T3 ratio between 13 to 1 and 20 to 1 for combinations, while NDT sits at roughly 4 to 1. Natural and fitting are two different questions.

What is the T4 to T3 ratio in NDT, and why does it matter?

The ratio is roughly 4 to 1. A 2020 review states that the mean daily dose that brings TSH into the reference range contains about 11 micrograms of T3. It matters because the 2012 ETA guideline recommends a ratio between 13 to 1 and 20 to 1 and writes that all available combination products fall below that and are therefore not recommended.

What do T2, T1 and thyroglobulin contribute in NDT?

That they are present is correct. What they do in humans is open. A 2020 review from Berlin and Greifswald collected what is known about 3,5-T2: the data come from cell culture and from mouse models after pharmacological doses. In humans, whether these substances can be measured reliably in blood is still disputed. Based on current data, no human study on a therapeutic benefit of the T2 fraction is known.

Is NDT better than levothyroxine in studies?

Based on the available evidence, no. There are exactly two randomised double blind trials, both from the same research group. Hoang 2013 with 70 participants found no differences in symptoms and neurocognitive tests, but around 1.4 kilograms lower weight on NDT. Shakir 2021 with 75 participants found no difference at group level, apart from a slightly higher heart rate. The 2024 meta-analysis confirms this.

If studies show no difference, why do so many people prefer NDT?

This tension is real and unexplained. A network meta-analysis of 11 randomised trials with 1,135 people found 52 percent preference for NDT or a combination against 24 percent for levothyroxine alone, relative risk 1.97. At the same time the questionnaire scores show no difference. It is possible that crossover designs favour preference judgements, that the questionnaires do not capture what matters, or that an effect in one subgroup disappears in the mean.

Why do the professional societies not recommend NDT as standard therapy?

They name four reasons, each backed by a number. First the ratio of roughly 4 to 1 against the recommended 13 to 1 up to 20 to 1. Second batch variability: in 2020 the FDA recalled thirteen lots for super potency of up to 115 percent of the declared T3, and further lots in 2021 for sub potency. Third the missing long term data, since the longest randomised observation ran 22 weeks per arm. Fourth the risk of a suppressed TSH.

Is NDT licensed in Germany, and how would anyone obtain it?

No, no NDT product is licensed as a finished medicinal product in Germany. The legal route is single patient import under section 73 paragraph 3 of the German Medicines Act: on a medical prescription, through a pharmacy, in small quantity, and only if no licensed medicine with an identical active substance and comparable strength is available. Compounded preparations are an alternative. In the United States these products are not FDA approved either, although an estimated 1.5 million people are prescribed them there.

Does statutory health insurance cover natural thyroid hormones?

As a rule, no. A single patient import under section 73 paragraph 3 of the German Medicines Act concerns a medicine that is not licensed in Germany, and there is no regular entitlement to reimbursement for it. In practice this runs on a private prescription, plus the cost of the close laboratory monitoring. For compounded preparations the situation is similar. Coverage in an individual case is a question for the respective insurer.

What are the risks of NDT, and how do you notice that the dose is too high?

The biggest risk is a dose that is too high with a suppressed TSH, independent of the product. In a Scottish cohort of 17,684 treated people, a suppressed TSH was associated with a fracture risk of hazard ratio 2.02. A meta-analysis with 70,298 people found a more than three and a half fold increased risk of vertebral fractures below a TSH of 0.10. Warning signs are a racing heart, inner restlessness, unexplained weight loss, heat intolerance and tremor.

Is a TSH below 0.1 normal on NDT?

This claim appears on several German websites, but it is not supported by the data. A pooled analysis of 52,674 people found a 68 percent higher risk of atrial fibrillation at low TSH, rising below 0.10. A meta-analysis with 70,298 people found a vertebral fracture risk there of hazard ratio 3.57. A low but not suppressed TSH, by contrast, was not associated with increased risks.

Can I simply switch from levothyroxine to NDT?

No. An existing thyroid therapy is never changed, reduced or stopped on your own. Every change happens under medical supervision only, with a prescription, defined monitoring intervals and laboratory checks. There is no validated conversion: the tables circulating online have not been tested in studies. On top of that comes the finding from the post hoc analysis of 143 participants, that people with few complaints on levothyroxine did measurably worse on NDT.

What applies during pregnancy?

Pregnancy is its own care setting with its own target values, and there is a dedicated guideline from 2017 for it. In the first trimester the fetus depends on maternal T4, and T4 is the form that crosses the placenta to a relevant degree. That is the reason why a T3 heavy replacement is not the standard route here. In its 2020 recall notice the FDA explicitly names miscarriage and impaired fetal development. Changes here happen under medical supervision without exception.

Does a genetic test for the DIO2 variant help with the decision?

Based on current data, no. A secondary analysis of 552 people found in 2009 that carriers of the rarer CC genotype in the deiodinase 2 gene, around 16 percent, had worse baseline values and gained more from T4 plus T3, with no difference in hormone levels. The authors themselves called for replication. The randomised trial of 2021 measured the polymorphism prospectively and found no influence.

The thyroid and the rest of the body

A thyroid hormone is never on the road alone. It hangs on cofactors, on the stress axis and on the energy balance. From here several paths lead onwards.

SJ

Shukri Jarmoukli

Physician, Integrative Medicine · ViveCura Berlin

I work in my private practice at the intersection of conventional medicine, functional medicine and clinical psychoneuroimmunology. In thyroid topics I am less interested in the question of which product is the right one than in which questions before it are still unanswered.

This article does not replace medical advice and is not a recommendation for or against any product. It is meant to help you ask better questions in your next conversation.

ViveCura, Privatpraxis Shukri Jarmoukli, Skalitzer Straße 137, 10999 Berlin

Scientific sources

  1. Hoang TD, Olsen CH, Mai VQ, Clyde PW, Shakir MKM. Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: a randomized, double-blind, crossover study. J Clin Endocrinol Metab. 2013;98(5):1982-1990. PMID: 23539727 · DOI: 10.1210/jc.2012-4107 [RCT, n=70]
  2. Shakir MKM, Brooks DI, McAninch EA, Fonseca TL, Mai VQ et al. Comparative Effectiveness of Levothyroxine, Desiccated Thyroid Extract, and Levothyroxine+Liothyronine in Hypothyroidism. J Clin Endocrinol Metab. 2021;106(11):e4400-e4413. PMID: 34185829 · DOI: 10.1210/clinem/dgab478 [RCT, n=75]
  3. Hoang TD, Patel AA, Spiro AJ, Watson NL, Shakir MKM. Use of the 36-Point Thyroid Symptom Questionnaire to Potentially Guide Optimal Thyroid Hormone Replacement Therapy. Endocr Pract. 2026;32(1):53-59. PMID: 40947017 · DOI: 10.1016/j.eprac.2025.09.007 [RCT, n=143]
  4. Nassar M, Hassan A, Ramadan S, Desouki MT, Hassan MA et al. Evaluating the effectiveness of combined T4 and T3 therapy or desiccated thyroid versus T4 monotherapy in hypothyroidism. BMC Endocr Disord. 2024;24(1):90. PMID: 38877429 · DOI: 10.1186/s12902-024-01612-6 [Meta-analysis, k=16]
  5. de Lima Beltrão FE, Carvalhal G, de Almeida Beltrão DC, Ribeiro MO, Ettleson MD et al. Treatment Preferences in Patients With Hypothyroidism. J Clin Endocrinol Metab. 2025;110(3):887-900. PMID: 39290156 · DOI: 10.1210/clinem/dgae651 [Meta-analysis, k=11, n=1,135]
  6. Beltrão FEL, Carvalhal G, Meneghini V, Matos DAR, Golovko G et al. Treatment of Hypothyroidism That Contains Liothyronine is Associated With Reduced Risk of Dementia and Mortality. J Clin Endocrinol Metab. 2026;111(2):561-571. PMID: 40579157 · DOI: 10.1210/clinem/dgaf367 [Cohort, n=1,260,000]
  7. Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR et al. Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014;24(12):1670-1751. PMID: 25266247 · DOI: 10.1089/thy.2014.0028 [Guideline]
  8. Wiersinga WM, Duntas L, Fadeyev V, Nygaard B, Vanderpump MPJ. 2012 ETA Guidelines: The Use of L-T4 + L-T3 in the Treatment of Hypothyroidism. Eur Thyroid J. 2012;1(2):55-71. PMID: 24782999 · DOI: 10.1159/000339444 [Guideline]
  9. Jonklaas J, Bianco AC, Cappola AR, Celi FS, Fliers E et al. Evidence-Based Use of Levothyroxine/Liothyronine Combinations in Treating Hypothyroidism: A Consensus Document. Thyroid. 2021;31(2):156-182. PMID: 33276704 · DOI: 10.1089/thy.2020.0720 · published simultaneously in Eur Thyroid J. 2021;10(1):10-38, PMID: 33777817, DOI: 10.1159/000512970 [Guideline]
  10. Alexander EK, Pearce EN, Brent GA, Brown RS, Chen H et al. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum. Thyroid. 2017;27(3):315-389. PMID: 28056690 · DOI: 10.1089/thy.2016.0457 [Guideline]
  11. Idrees T, Palmer S, Maciel RMB, Bianco AC. Liothyronine and Desiccated Thyroid Extract in the Treatment of Hypothyroidism. Thyroid. 2020;30(10):1399-1413. PMID: 32279609 · DOI: 10.1089/thy.2020.0153 [Review]
  12. McAninch EA, Bianco AC. The History and Future of Treatment of Hypothyroidism. Ann Intern Med. 2016;164(1):50-56. PMID: 26747302 · DOI: 10.7326/M15-1799 [Review]
  13. Hennessey JV. The emergence of levothyroxine as a treatment for hypothyroidism. Endocrine. 2017;55(1):6-18. PMID: 27981511 · DOI: 10.1007/s12020-016-1199-8 [Review]
  14. Taylor PN, Medici MM, Hubalewska-Dydejczyk A, Boelaert K. Hypothyroidism. Lancet. 2024;404(10460):1347-1364. PMID: 39368843 · DOI: 10.1016/S0140-6736(24)01614-3 [Systematic Review]
  15. Flynn RW, Bonellie SR, Jung RT, MacDonald TM, Morris AD, Leese GP. Serum thyroid-stimulating hormone concentration and morbidity from cardiovascular disease and fractures in patients on long-term thyroxine therapy. J Clin Endocrinol Metab. 2010;95(1):186-193. PMID: 19906785 · DOI: 10.1210/jc.2009-1625 [Cohort, n=17,684]
  16. Collet TH, Gussekloo J, Bauer DC, den Elzen WPJ, Cappola AR et al. Subclinical hyperthyroidism and the risk of coronary heart disease and mortality. Arch Intern Med. 2012;172(10):799-809. PMID: 22529182 · DOI: 10.1001/archinternmed.2012.402 [Meta-analysis, k=10, n=52,674]
  17. Blum MR, Bauer DC, Collet TH, Fink HA, Cappola AR et al. Subclinical thyroid dysfunction and fracture risk: a meta-analysis. JAMA. 2015;313(20):2055-2065. PMID: 26010634 · DOI: 10.1001/jama.2015.5161 [Meta-analysis, k=13, n=70,298]
  18. Peterson SJ, Cappola AR, Castro MR, Dayan CM, Farwell AP et al. An Online Survey of Hypothyroid Patients Demonstrates Prominent Dissatisfaction. Thyroid. 2018;28(6):707-721. PMID: 29620972 · DOI: 10.1089/thy.2017.0681 [Survey, n=12,146]
  19. Toloza FJK, Espinoza Suarez NR, El Kawkgi O, Golembiewski EH, Ponce OJ et al. Patient Experiences and Perceptions Associated with the Use of Desiccated Thyroid Extract. Medicina (Kaunas). 2020;56(4):161. PMID: 32260044 · DOI: 10.3390/medicina56040161 [Case Series, n=673]
  20. Panicker V, Saravanan P, Vaidya B, Evans J, Hattersley AT et al. Common variation in the DIO2 gene predicts baseline psychological well-being and response to combination thyroxine plus triiodothyronine therapy in hypothyroid patients. J Clin Endocrinol Metab. 2009;94(5):1623-1629. PMID: 19190113 · DOI: 10.1210/jc.2008-1301 [RCT secondary analysis, n=552]
  21. Homuth G, Lietzow J, Schanze N, Golchert J, Köhrle J. Endocrine, Metabolic and Pharmacological Effects of Thyronamines, Thyroacetic Acids and Thyroid Hormone Metabolites. Exp Clin Endocrinol Diabetes. 2020;128(6-07):401-413. PMID: 32450582 · DOI: 10.1055/a-1139-9200 [Mechanism Review]
  22. German Medicines Act (AMG), section 73 paragraph 3: prohibition on bringing in medicines and exemptions for single patient import. Federal Ministry of Justice. gesetze-im-internet.de [Agency Document]
  23. U.S. Food and Drug Administration. Acella Pharmaceuticals, LLC Issues Voluntary Nationwide Recall of Certain Lots of NP Thyroid (Thyroid Tablets, USP) Due to Super Potency. FDA Recalls, Market Withdrawals and Safety Alerts, 2020. fda.gov [Agency Document]
  24. U.S. Food and Drug Administration. Acella Pharmaceuticals, LLC Issues Voluntary Nationwide Recall of Certain Lots of NP Thyroid (Thyroid Tablets, USP) Due to Sub Potency. FDA Recalls, Market Withdrawals and Safety Alerts, April 2021. fda.gov [Agency Document]
  25. U.S. Food and Drug Administration. FDA Actions to Address Unapproved Thyroid Medications. FDA Enforcement Activities, Drugs. fda.gov [Agency Document]
Transparency on the evidence On NDT against levothyroxine there are exactly two randomised double blind trials worldwide, with 70 and 75 participants, both from the same research group and with partly the same authors. The 2024 meta-analysis was able to include exactly these two out of 6,394 hits. That is a narrow and not very independent basis for a topic that has been disputed for decades. The longest randomised observation period is 22 weeks per arm, so there are no long term data on heart and bone. The registry analysis of 2026 is retrospective and not randomised. What T2, T1 and thyroglobulin do in humans is unclear, the data come from cell culture and mouse, and whether these substances can be measured in blood is disputed. None of the products named is licensed in Germany, and in the United States they are not FDA approved either. Preference and quality of life data appear to contradict each other, both are methodologically sound, and nobody knows with certainty why that is. The DIO2 polymorphism is a plausible but unconfirmed attempt at an explanation. The satisfaction data from online surveys and forum analyses are self selected. For children, pregnant women and people with heart disease there are practically no controlled data on NDT, since the randomised trials enrolled adults between 18 and 65 without relevant accompanying conditions. What I describe from my consulting room is marked as an observation and is not a study result.

Have questions or want to book an appointment?

We'd be happy to advise you personally at our practice.

Book appointment