Is TSH the Best Test?

Why has Thyroid Stimulating Hormone (TSH) become the Rodney Dangerfield of hormone tests? If I had a nickel for every time I’ve seen a practitioner of some stripe claim that we can’t rely on TSH, I would be drowning in nickels. But why do people defecate on TSH? Is it really as inaccurate a reflection of your thyroid status as many an Alternative Medicine aficionado would have you believe? Does TSH only tell you what your pituitary thinks about your thyroid hormone levels, as opposed to how the rest of your body feels about said levels? Must you discount TSH results in favor of T3 and reverse T3 levels? Do these questions even have clear, unambiguous answers?

A Brief History of TSH

In the mid 1910s, scientists figured out an easier way to measure basal metabolic rate (BMR). Recognizing that a low BMR was associated with hypothyroidism, physicians used the presence of a low BMR and other signs/symptoms of hypothyroidism to make the diagnosis. They also used BMR to titrate the dose of thyroid hormone.

By the 1940s, serum protein-bound iodine (PBI) emerged as both a diagnostic and therapeutic marker; this was the only way to quantitate thyroid hormone status at the time. Unfortunately, T4 monotherapy would often increase PBI above normal, while T3 monotherapy would normalize BMR but not increase PBI. Combination T4/T3 therapy, however, had the advantage of normalizing PBI.

At the time – like today – it was well-recognized that things like cholesterol, deep tendon reflexes, and symptoms were just not sensitive or specific enough to guide thyroid hormone replacement therapy.

In 1971, the first TSH radioimmunoassay was developed. This turned out to be a game changer. When scientists studied patients who had previously been treated to normalize symptoms, BMR, and PBI, they found that most of these patients had a suppressed TSH.

One could argue that a suppressed TSH by itself could not, at this stage of the research, be considered conclusive evidence that patients were being over-treated. After all, perhaps pituitary secretion of TSH just wasn’t a good marker for overall thyroid status, right? Wrong. Studies at the time found that T4-treated hypothyroid patients could be rendered biochemically and clinically indistinguishable from healthy controls, using a T4 dose just high enough to normalize the TSH. These doses turned out to be about 1/4 to 1/2 the doses previously used to normalize BMR and PBI – two markers that were nowhere near as sensitive or specific as TSH.

And thus it became accepted that hypothyroid patients had been overmedicated for decades, standard T4 replacement doses dropped dramatically, and everyone lived happily ever after…

But I Still Don’t Feel Well

As anyone reading this site is well-aware, there is a sizable minority of hypothyroid folks who do not feel normal after normalizing the TSH. So what gives?

In many cases, it’s just not your thyroid. Having access to a diagnostic marker as sensitive as TSH is a double-edged sword. On one hand, people with very subtle perturbations of thyroid function can now be diagnosed and treated early, before they spend years feeling like crap. On the other hand, a large number of people will have mild elevations of TSH in the presence of “hypothyroid symptoms,” but those nonspecific symptoms are often not due to hypothyroidism. Unfortunately, once someone is labeled as hypothyroid, it can be difficult for both patient and clinician to look past that label. This results in constant tinkering with the dose or preparation of thyroid hormone, embarking on a Quixotic quest to find the magical balance of T4, T3, and TSH that will restore the person to “normal.”

In case the preceding paragraph did not make my position clear, let me state this very plainly: if you have been tinkering with your thyroid hormone dose and/or preparation for more than a year, and you feel little to no improvement in your symptoms, your symptoms almost certainly are not caused by your hypothyroidism. In fact, you may not even have hypothyroidism – especially if you were diagnosed by a naturopath, functional medicine doctor, or chiropractor. Let me remind you of an axiom commonly stated or implied throughout this blog: if you enter an Alt Med provider’s office wondering aloud if you have hypothyroidism, you have a better than 95% chance of coming out with that diagnosis. Given that the prevalence of hypothyroidism in the US is about 1 in 300 people, the likelihood of being incorrectly labeled as hypothyroid is exceedingly high.

No, Really – Pretty Sure it’s My Thyroid

But what about folks who have absolutely no other plausible explanation for their symptoms? This is where things start to get as murky as a bayou swamp, and where I hope to provide at least a modicum of clarity. I think the best way to achieve this is to debunk Alt Med’s claims about TSH one by one:

Claim: There are myriad conditions (stress, depression, chronic fatigue syndrome, etc) in which T4 and T3 levels drop, but TSH levels do not rise accordingly. Therefore, TSH cannot be used as a diagnostic or monitoring tool in these settings.

HD: Mostly False. Alt Med loves to dredge up the well-described phenomenon of non-thyroidal illness syndrome (NTIS) and make it the poster child for discrediting the utility of TSH. The problem with this is that NTIS is usually a transient entity seen primarily in severely ill patients. In NTIS, thyroid function studies can be variable and incredibly challenging to interpret, but the relevant pattern for this post would be slightly low/low-normal TSH, T4 and T3.

The literature on this subject is confusing and conflicting. The consensus opinion among experts in the field, however, is that most instances of NTIS do not require treatment with thyroid hormone. It is thought that the lower thyroid hormone levels in periods of critical illness may be a protective response, guarding against excessive tissue catabolism (breakdown). This is plausible, given that a body under that much stress has more important metabolic priorities – like staying alive.

It is also recognized that the lower T4 and T3 may be a maladaptive response in some circumstances, in which case the patient might benefit from treatment. An in-depth discussion of how to make this distinction is outside the scope of this post, but I will tell you that there is no elegant way to make the diagnosis or determine the “right” treatment. It’s really, really, really hard.

What I can say, however, is that most free-living people (non-ICU dwellers) who have stress, depression, or any number of other conditions will not have NTIS. If you walk into my office under your own power, and your thyroid function tests appear fairly normal, you almost certainly do not have clinically meaningful hypothyroidism.

While there are – for example – studies showing that some patients hospitalized for severe depression may have lower T3 levels than controls, these patients with normal TSHs generally do not fulfill any other clinical/biochemical criteria for making a diagnosis of hypothyroidism. In addition, when randomized, double-blind trials have looked at giving T3 to euthyroid, severely depressed patients, there has been no benefit.

The bottom line: equating conditions like fibromyalgia, chronic fatigue syndrome, or PMS with NTIS is a misapplication of our understanding of the hypothalamic-pituitary-thyroid axis. This oft-employed strategy by Alt Med is yet another way they can diagnose absolutely anyone with hypothyroidism, embarking on a treatment journey that ultimately will prove to be fruitless.

Claim: The pituitary is different from all other tissues in the body. In some circumstances, T3 levels in the pituitary may be normal, while T3 levels in the rest of the body are low. Therefore, it is possible to have clinically meaningful hypothyroidism in all the body’s tissues except the pituitary gland. These normal pituitary T3 levels tell the gland that the body’s thyroid hormone levels are fine when they aren’t, leading to a normal TSH.

HD: Partly False. Unfortunately, the part that is false is the most important part. In order to explain, this may get a bit dense. But my readers tend to be pretty smart, so here goes:

Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling, Balazs et al, Endocrine Reviews 2008 Dec; 29(7) 898-938.

Whoa!!! System overload, HD!

Bear with me, y’all; I promise I’ll do my best to not hurt your brains here. Let’s walk through the process of how TSH-producing cells in the pituitary decide whether to make more TSH (thyroid hormone levels aren’t high enough, so the thyroid needs to be encouraged to make more) or less TSH (thyroid hormone levels are too high, so the thyroid doesn’t need any more encouragement).

As you may remember from my post about reverse T3, the body has a few types of deiodinase enzymes that do many things, including conversion of T4 to T3 and local regulation of thyroid hormone bioactivity.

The classic pathways of thyroid hormone metabolism – Scientific Figure on ResearchGate. 

The type 2 deiodinase (D2) is found in multiple tissues throughout the body, including the pituitary. Because our bodies like homeostasis, they are very good at defending T3 production when T4 is a bit low and decreasing T3 production when T4 is a bit high. This means that D2 activity is up-regulated when T4 is a little low and down-regulated when T4 is a little high.

If that was the only mechanism by which T4 to T3 conversion was controlled, then TSH would not be a good thermostat for thyroid function, right? Think about it: let’s say the thyroid is overactive and T4 levels rise, but T3 conversion is kept constant through down-regulation of D2 activity, then the pituitary would think that thyroid hormone levels were just fine, and the TSH would not be suppressed. But that’s not what happens.

It turns out that – in the above example – the down-regulation of D2 activity is more than offset by a rise in reactivation of previously inactivated D2 and an increase in D2 synthesis.

If you want a visual representation of this process, go back to the pretty diagram with the colors. Notice the bidirectional arrows between the yellow (active) D2 and pink (inactive) D2. You see that the inactive D2 can be reactivated by yet another enzyme that we won’t discuss. Also, if the pituitary is making more of the active D2, it will lead to accurate transduction of the high T4 levels, by making more T3 inside the pituitary cell.

Let’s press pause for a moment and put this all into context. Alternative Medicine claims that the pituitary is special. That is correct. Although we don’t fully understand the mechanisms that allow this system to operate, we think that massive D2 synthesis in the pituitary exceeds the maximal rate at which higher T4 levels cause inactivation of D2. Therefore, the net effect is that higher T4 levels in the body will lead to higher T3 levels in the pituitary and lower T4 levels to lower T3 levels. Basically, we’re saying that the feedback system between the thyroid and pituitary is appropriate, and we’ve postulated how it works.

Alternative Medicine also claims that the pituitary will remain in a state of blissful ignorance when the body’s thyroid hormone levels are too low. They claim this is why the TSH is unreliable – it won’t rise in the setting of “tissue hypothyroidism,” because T3 levels in the pituitary are peachy, thanks to the turbocharged conversion of T4 to T3 by D2. Although there is D2 activity in other tissues besides pituitary, D1 does much of the heavy lifting elsewhere, when it comes to converting T4 to T3. Since D1 is not up-regulated to the same extent as D2, then the argument goes that the body can suffer low thyroid hormone levels without an appropriate rise in TSH.

Unfortunately, this logic is based almost entirely on research about NTIS, which I already told you is seen in critically ill, hospitalized patients. You simply can’t apply NTIS data to someone with a common “outpatient” disease like fibromyalgia or depression. To the best of my knowledge, there are no credible data proving that patients with any of these outpatient diseases suffer from some nebulous form of chronic NTIS.

Under normal circumstances – which apply to just about everyone reading this – if the pituitary is making normal amounts of TSH, you should infer that thyroid hormones levels in the rest of the body are adequate.

Claim: Deiodinase enzyme activity and nuclear thyroid hormone receptor/transporter activity vary depending on physiological conditions. These processes contribute to regulation of tissue thyroid hormone levels. Therefore, serum thyroid hormone levels and – by extension – TSH may not adequately predict tissue thyroid hormone levels.

HD: Mostly True. This is a prime example of Alt Med taking science and manipulating it to draw the conclusion they want. It’s true that deiodinase enzymes will have different levels of activity in different tissues depending on the needs of that particular tissue at that particular moment. It is also true that thyroid hormone receptors, as well as the transporters that carry thyroid hormone into the cell, will be up- or down-regulated depending on the needs of the cell at that moment. These are complex processes that cannot be measured in patients.

It is also true – for example – when treating hypothyroidism with levothyroxine, serum T3 levels are often low-normal or even slightly low. As the vast majority of people on levothyroxine with normal TSHs feel fine, the clinical significance of the T3 levels is unknown. It is often assumed that deiodinase and cellular transport activity acts to maintain cellular T3 levels, which would explain why most of these folks feel just fine.

The derailing of this train of thought occurs by asserting that TSH does not adequately predict tissue thyroid hormone levels. I apologize for sounding like a broken record, but it is only in NTIS and other rare circumstances (e.g. central hypothyroidism) that this is true. There are copious data showing that euthyroid people, people with well-treated hypothyroidism, and people with well-controlled hyperthyroidism have normal TSHs. There are also copious data showing that most people with uncontrolled hypo- or hyperthyroidism have abnormal TSHs. I don’t really know how to say it any clearer than that.

Sure, the local regulation of thyroid hormone conversion, transport, and action is a complex process. It is true that we can’t measure tissue thyroid hormone levels in any meaningful way. What you need to remember is that the body is constantly aiming for homeostasis, and it’s generally excellent at achieving that. But Alt Med wants you to believe that humans have evolved a spectacularly dysfunctional thyroid hormone production and signaling system. It is so messed up, in fact, that almost any chronic illness/disease can throw the thyroid system completely out of whack. What’s more, it’s impossible to accurately measure the degree of disarray, so the obvious solution is simply to treat everyone who feels poorly with thyroid hormone. Titrate the dose to resolution of symptoms or atrial fibrillation, whichever comes first. Ridiculous.

Claim: Some people have a genetic mutation that affects the pituitary’s conversion of T4 to T3. Therefore, a hypothyroid patient with this mutation may have a normal TSH, even when they clearly need a higher dose of thyroid hormone.

HD: True. This is the last Claim I’ll address today, as I’m pretty sure I’m burning out your attention span. There are many known single nucleotide polymorphisms (SNPs) in the deiodinase genes. The functional relevance of most of these is unknown, but there is one that has been reasonably well-researched. It’s called Thr92Ala – a SNP in the D2 gene.

The Thr92Ala change in the coding region of D2 does seem to be associated with slower T4 to T3 conversion. Studies in people with the SNP have shown a few interesting things:

  • A correlation between the SNP and TSH in healthy people, but not between the SNP and thyroid hormone levels.
  • A lower TSH in people with one copy of the SNP, when compared to people without the SNP and when compared to people with two copies of the SNP (surprising!).
  • Thyroidectomized people with the SNP may require a higher T4 dose to normalize the TSH.
  • One study showed the SNP was not correlated with general condition, neurocognitive functioning, or response to combination T4/T3 therapy; a second study showed an impairment in well-being that was mildly improved with combination T4/T3 therapy.

So what should we make of this? First, know that if you are euthyroid, you probably have nothing to worry about. Remember that the body is great at achieving homeostasis. If there is slightly sluggish T4 to T3 conversion in tissues that use D2, the body has many available tools to mitigate that. It can inactivate D2 more slowly, reactivate D2 faster, increase thyroid hormone transport into the cell, etc. Bottom line: if you ordered one of those DIY genetic profiles online and it says you have the SNP, relax.

Second, if you’re hypothyroid because your gland doesn’t work great (as opposed to having had surgery to remove it), much of the above will still apply to you. But if you feel poorly on levothyroxine despite a normal TSH, then you may wish to broach the idea of adding in a small dose of liothyronine. Just keep your expectations low, as T3 is not the cure-all as Alt Med portrays it.

Third, if your thyroid has been surgically removed and you still don’t feel well despite having “optimized” your TSH on levothyroxine, there is some credible evidence that you might feel better with the addition of T3 to your T4 therapy.


The regulation of thyroid hormone conversion, transport, and action at the tissue/cellular level is extraordinarily complex. At this time, we do not have accurate ways to measure thyroid hormone levels in individual tissues. We do, however, have the TSH test. When T4/T3 levels drop a tiny bit within the normal range – assuming that’s not normal for your tissues – TSH will shoot way up above the upper limit of normal. When T4/T3 levels rise a tiny bit within the normal range – assuming that’s not normal for your tissues – TSH will drop way below the lower limit of normal.

Is it a leap of faith to assume that TSH reflects the tissues’ thyroid status, as opposed to merely the pituitary’s T3 content? Perhaps. But in my opinion, Alt Med has not offered a more plausible theory. I simply do not believe that there are millions of people with undiagnosed hypothyroidism, for whom replacement therapy will solve their problems.

Questions? Comments? Let me know below! By using this site and interacting with me in the Comments, you agree to abide by my Disclaimer.

Featured Image Credit: Photo by Tiago Felipe Ferreira on Unsplash

67 Replies to “Is TSH the Best Test?”

    1. Ha, thanks for honing in on the important stuff. 😉

      It is acceptable to capitalize the Q since the word can refer to Don Quixote, though you are right that the q is more often lowercase.

      I guess I like to be contrarian.

  1. Saw a cardiologist who said I have an irregular heartbeat, prescribed Cartizem. Can the irregular heartbeat be caused by almost six years of thyroid supplementation for hypothyroidism, a disease I never had. At Mayo Clinic to get answers about celiac disease

    1. While I can’t comment on your situation, I can say that people who are over replaced with thyroid hormone can experience heart arrhythmias.

    2. Yes overmedication for hypothyroidism absolutely causes irregular heartbeat. It was my first symptom. I took almost 8 years of thyroid meds I didn’t need and became very overmedicated. I too went to Mayo and saw an endo but because my blood tests were (barely) in range I was told “don’t know why you have symptoms perhaps it’s chronic fatigue”. In my case by the time the severe overmedication showed in my blood it was too late – damage done. I am now months on NO thyroid med and although I am better I am far from normal. Another specialist who has been really good/caring told me it can take 6 to 12 months to work out the overmedication. Good luck to you.

    3. I think the key here is “over” replacement but not “proper” replacement. I would look elsewhere if the patient was euthyroid. Anyone laying an atrial fibrillation etiology at the foot of a euthyroid patient who is supplementing, is wasting time, money, and health barking up the wrong tree.

  2. Is there a good resource for patients that lists other possible causes of symptoms that have been attributed to hypothyroidism?

    1. I do cover this issue throughout the posts on this blog. It’s tough to cite a single resource for this question, as the symptoms of hypothyroidism are so nonspecific and overlap with so much: stress, poor sleep, sleep apnea, poor nutrition, lack of exercise, anemia, depression, etc.

  3. As a fellow practitioner I can’t overstate the usefulness of your writing in helping materialize my understanding of these concepts in a way I can serve at a “but I READ…” patient that brings us to a mutual understanding. Thank you!

  4. Thank you for this post! This is something I’ve been wondering about for a while, and it’s one more argument against the pseudoscience peddlers.

  5. This blog gives me such a sense of relief. Had partial thyroidectomy 20 years ago and have felt well on Synthroid. Reading thyroid blogs has created anxiety because my numbers are not “optimal.” My free T3 remains low. Alt med
    blames ferritin/iron and cortisol problems. At one point I requested T3 and ended with terrible palpitations and high blood pressure. I also think during some years I was overmedicated on Synthroid and now have Osteoperosis. The confusion about thyroid health is crazy and this blog gives me peace to continue on a more moderate dose of Synthroid and to be content with my normal TSH and low normal free T3. I would love to hear you discuss thyroid medication’s impact on bone health, particularly suppressed TSH and high FT3. Thanks😊

    1. I’m glad this post was able to set your mind at ease. Your story bolsters my oft-repeated claim that thyroid blogs hurt people.

      As for bone health, long-term exposure to high thyroid hormone levels that suppress the TSH to below 0.10 for extended periods of time is what it generally takes to cause harm.

      1. Hi HD,
        What would consider “extended periods of time”? Are we talking years or decades?
        Thanks 🙂

  6. Thank you so much for this, your blog is wonderful! I was one of those people who subscribed to Alt-Med and was on dessicated thyroid for 5+ years with a very suppressed TSH…eventually I got panic attacks, headaches, dizziness, and developed elevated blood sugar (I’m 35, active female and eat ridiculously healthy) and had to stop abruptly and get on levothyroxine (that was not an easy transition). Now my T3 is low on levo and I worry about that, but reading your blog makes me feel at ease. I was wondering if there is a TSH that you have found to be optimal for thyroid patients? Mine has been about 2.9 on levo, yet the endo wants me to continue with it for now. I feel ok, a little tired, but sleeping well. When my TSH was around 0.4 when I was initially finding my right dose of levo, I felt horrible, insomnia, muscle twitches, arm weakness. I guess my question is, do some people feel better with a higher TSH (even when medicated), and is this healthy long-term?

    1. I am also interested into that question but from another standpoint:

      I would like to know what can happen as symptoms in a person with Hashimoto disease who stop any thyroïd medication, namely Synthroïd, for a length of 6 months.


        1. I see. To provide more information, this is for myself and I do intend to ask my primary care doctor about it but here’s the details:

          1-: controlled TSH in the normal range (I don’t have the bloodwork results but there’s been no changes for at least 8 to 10 years).

          2-: 137µg dose of Synthroid daily.

          3-: No other physical health issues (mental: ADD, can be managed by exercise).

          The 6 month pause is because I want to do the required training to be an armed force officer. There is a “no medication” clause enforced during the training period.


          1. I can’t speak to your situation, Alain. But I can say that – if one is truly hypothyroid on a full (or close to full) replacement dose of levothyroxine – stopping it for 6 months would likely lead to feeling lousy at best, serious health issues of all sorts at worst.

          2. If I understand right, 137 µg of Synthroid is a total dose replacement or close to what is naturally produced by a healthy thyroïd gland?


          3. It depends on the person, their weight, and other variables. But for an average male, 137 would be about a full replacement dose.

          4. In my case, I guess it is. weight: 140lbs, height: 6 feet 1. Bloodwork, all in the low range of normal for cholesterol, creatinine, etc… and I used to walk about 100km (62~63 miles) per week. I still manage about 50km of walk per week.


    2. Absolutely, there are people who feel better with a higher TSH. I realize this contradicts the Alt Med credo of “why settle for average when you could be higher,” but it reflects reality. There is no downside to running a low-normal, mid-normal, or high-normal TSH, if that is where one feels best.

      1. Thank you for your reply, HD! Alt-Med blogs have me thinking I’m a ticking-time bomb with a TSH over 1.5 and low-normal T3, but I feel much calmer now on T4 only, less anxious all around, blood sugar is better too. Thank you for all the work you do.

        1. We sound like we are in the same boat. My TSH is 2.5 and FT3 is low normal, but I feel great. I think what happens in these groups is that a small number of “experts” tend to push their agenda. Desperate people looking for answers jump on board. Many probably fall away as they become disenchanted with the advice and the ones who remain continue to push the agenda. I think some people are helped, but I suspect many more are not or feel like failures for not attaining the promised results. Many may feel better by coincidence. I am in complete remission from Myasthenia Gravis. There are many things that may have helped but I will never know exactly what. I could push an agenda or start a group based on the things I have done, but I know most people will not have my experience.

          1. That’s awesome Susan! Years ago when I was trying to increase my dosage of dessicated thyroid to “optimal” levels, I had such a difficult time, yet persisted because that’s what I thought I needed to do according to all the Alt-Med thyroid blogs. I probably should have listened to my body. I felt great for awhile on a high dose, but when I could no longer tolerate it, the “come down” off of the dessicated thyroid was just awful…almost like a drug withdrawal (I suspect from the T3). I feel better now with a higher TSH on levothyroxine (Tirosint) and am glad to know I’m not the only one and that we are not damaging our bodies! Thanks for sharing your experience!

  7. So if TSH is low-normal, and Free T4 is low (below reference range), then does that indicate a pituitary gland issue? I mean, if the TSH is that sensitive…

    I realize that hypopituitarism is rare, so I am wondering if there is another explanation for that combination of results. The follow-up with my endo is next week.

    1. Assuming we are talking about someone who is not taking thyroid hormone, then that could reflect central hypothyroidism, yes.

      There are other possibilities, including assay interference, that could produce numbers like that.

      In people on desiccated thyroid, however, it is common to see a lowing TSH with a low FT4 and elevated FT3.

    2. Allison, I would love to communicate if you are willing. I also have low-normal TSH and low (below range) T4 when taking nothing and when taking low-dose levothyroxine. I can’t find much info on people like me. Endocrinology tells me these numbers are normal and there is nothing wrong, despite the fact that low doses of levo cut my 40 year chronic headaches by 2/3. If you got good info, I’d be so grateful if you shared!
      tryscience at hotmail dot com.

  8. I wonder if it would be worth doing a post on the ‘normal range’ and what it means medically? Several of the questions above might well be answered by understanding that being at a particular place in the normal range may be right for them, after all some number of people are going to be at each place under that curve.

    Thanks again for your posts, they are always informative.

      1. I had to remind several of the GP’s at the last practice I was registered with that the aim of treatment was to get me symptom free, not to a particular place in the range, as every time they checked my TSH level I came in on the lower borderline of normal which made them twitchy. However as I am overweight (and wasn’t losing any except when I tried to) had no palpitations etc etc they did see sense. It was rather irritating though when it happened with every GP in the practice (eight of them) in turn. Thankfully my current GP practice seem to be more clued up abut this, and many other things. Anyway if doctors are getting it wrong they are probably not explaining the concept to their patients at all well.

  9. Only a big pharma/insurance shill would blatantly lie that testing for tsh is good enough while ignoring t3 and excess rt3.

  10. I have seen a lot of people who have had their thyroids removed have issues going by TSH only. They also seem to benefit from a combination of T4 and T3. I did see this concept of combo therapy discussed in official thyroid guidelines.

    I think for the vast amount of thyroid patients on T4 only treatment TSH probably is accurate enough. But I’m not certain with people on combo treatments. Since combo treatments are not often done by endocrinologists, I wonder if more research is needed in that area.

    My current endocrinologist is willing to do T3 in combination (not NDT), and has some people she sees doing it. But I’m a bit nervous to try it unless I never get things going well. She mentioned my anxiety as a reason to avoid it at this point.

  11. Even as a GP in training I saw plenty of people with fatigue and chronic stress coming in; ‘but what about my thyroid, Doc?’ So when I started to get symptoms of fatigue, depession, some weight gain, I put it down to stress for my thesis, work and lack of exercise. It took my some time to realise that I had full blown Hashimoto’s.
    But I do understand why people want it to be their thyroid. Because then they have an explanation for their symptoms and a good treatment. After 12 weeks my TSH levels were back to normal with levo and I felt normal again. With nothing else than a pill every day. A lot easier to do than chaging your lifestyle, eating habits and stressful familiy life.

  12. This paper challenges the use of TSH only:

    For certain on patient run sites, TSH only analysis is not popular. This seems to me like something that requires more study. And because hardly any doctors run FT4 and FT3 tests (or believes in them), there may not be much experience interpreting how all these go together….and seeing patterns which would help the patient get the right treatment.

    1. Yes, I’ve seen this article before. The authors make some valid points, though I wish they had written the paper in a more straightforward manner. At times, they seem so impressed with their ability to use big words that they actually wind up making it difficult to know what they’re talking about.

      1. One of the authors of this paper regularly posts in a popular UK patient thyroid forum. He advocates using free T3 for monitoring hypothyroidism over TSH and regularly makes comments about the ignorance of doctors and their inability to understand biochemistry. I understand that he invented or patented a free T3 blood test (this has made me wonder at times, if there could be some kind of ulterior motive). He often posts papers by his research group in the forum, but I find the language in some of them hard to follow. Is this point of view something you are familiar with? I have found your blogs very helpful, thank you.

        1. I’m familiar with the point of view, though I believe that using T3 levels to gauge the adequacy of TH replacement is misguided and unhelpful. I will plead ignorance regarding whether the author of that paper has the conflict of interest you state. If he does, then that should certainly be taken into account when assessing his argument.

  13. Thanks for your blog, although to be fair, your portrayal of “Alt Med” could probably be a bit more balanced. Conventional medicine has a TON of problems, so the optimal approach for everyone would be to take therapies that work well from both sides, educate each other and use them in their practice. Then your patients will really be better off.

    I stopped seeing my endocrinologist after 20 years – he never explained to me what kind of hypothyroidism I had (I got diagnosed with a TSH of 100 after potentially many years of going un/misdiagnosed). He would always say that I shouldn’t worry since 95% of cases were Hashimoto’s. “And here is your new prescription for the increased dose of Synthroid”. Finally found a doctor who agreed to do the tests – and what do you know? The thyroid antibodies are through the roof, and my dose needs to go up again. So I don’t know about other people, but I am seeing a functional MD for this – I do believe that some diet and lifestyle changes could help me quiet down the immune system. If I can fix my dose of Synthroid and not have it go to infinity within the next few years, it would be great. This is something my endocrinologist cannot help me with. Even if he believed that stopping the progression of an autoimmune condition could be possible, he would never stick his neck out to give me advice that may be unconventional in any way. He scalded me for elevated cholesterol and extra pounds and recommended a whole grain/low fat diet. He had a few choice things to say when I went on Keto instead. And when I lost lots of weight and my cholesterol went down, “well of course it did since you lost so much weight, but your diet is terrible and doesn’t work”. I laughed, of course, and never went back.

    All of this said, I would love to hear your thoughts on autoimmunity and thyroid.

    Thanks a lot and I just subscribed to your emails 🙂


    1. Ksi, you’re right – I do find it difficult to adopt a more balanced approach to Alt Med, but that’s because a significant percentage of what they promote is nonsense. With the cacophony of craziness saturating the internet, my attempts to debunk it need to be fairly strenuous. Unfortunately, most Mainstream Medicine sites do little to address why Alt Med’s suggestions are often so misguided. So patients are reading information from Alt Med that sounds plausible – on the surface – and there is very little out there that directly debunks it.

      If Alt Med would promote “natural” therapies that actually work/have data, then it would be much easier to adopt a balanced approach to fusing Alt Med’s and Mainstream Med’s recommendations. I’d be happy to have patients see their MM PCPs for illness and Alt Med for wellness – if Alt Med’s approach to wellness was to focus on how to get great sleep; eat well; exercise efficiently; and reduce stress; while forgoing the 7 pages of unnecessary labs and the shopping bag of useless supplements. But I don’t see that happening.

      The false dichotomy I want to address is that some people think we should embrace Alt Med because Mainstream Med has so many problems. Just because MM has a hard time giving patients what they want or think they need, that does not lend credibility to Alt Med’s efforts to fill the gap. All it means is that there are MM docs who are unable – for whatever reason – to forge a therapeutic relationship with their patients. FWIW, I think that most cases boil down to insufficient time per visit; if MM docs had 30-90 minutes for every patient, I believe that patient satisfaction would increase exponentially.

      As for autoimmunity and the thyroid, I’ve written about that in various other posts; did you have a specific question? Thanks for your comments!

      1. Dear HD,

        Thanks for your reply. Lots more comments on the Alt Med (i have a feeling you mean something else by it than i do) and questions on autoimmunity, but i have a more pressing issue – appropriate for this thread.

        I asked my 15-year-old daughter’s pediatrician to run a few thyroid tests on her, and her TSH just came back at 5.4. She has been more spacey than usual and complained about being tired, so that fits. The antibodies and free T4 are within the range. The doctor’s recommendation was to take vitamin D, get as much sleep as possible and retest in 3 months. Does this mean anything serious or is this normal for teenagers? Can TSH be more volatile at that age than in older people?


        1. I can’t speak to her situation, but I can say that one high or high-normal TSH with normal FT4 and negative antibodies typically would not worry me. In the setting of symptoms that suggest hypothyroidism, it is something I would usually follow. Occasionally I treat with low-dose thyroid hormone if the patient has a strong preference to do something right away.

          1. Thanks very much – we will watch it for a couple of months, then test again. Keeping my fingers crossed.

  14. So, for someone undiagnosed & untreated (my primary doc insists all values are normal&healthy) with a TSH at 1.54, within the functional range (around 0.4-5.0; depending on the labs normals) and FT3 & FT4 BOTH within the functional ranges (of 3.2 & 1.09 respectively) BUT with fairly significant symptoms pointing to hypothyroidism, what does all of that mean?? Do we ignore all of the symptoms? Treat them all individually never connecting any of them to one underlying cause? I mean I’m aware that not all of the symptoms or issues that happen to correspond with hypo are necessarily connected to it BUT at the same time when I have so many symptoms pointing to a thyroid issue (such as depression {being treated by the now 7th SSRI in the past year}, low basal body temp {I’ve been tracking for almost 6 months as a form of sympto-thermal birth control tracking my cycle and cervical changes}, dry cracked heels, unexplained bumps on my legs and occasionally my arms; dry, soft, flaking, fingernails, constant hangnails, no lunula on my nails; thick, yellow, cracked toenails, ingrown; excessive sweating & significant weight gain {initially blamed on SSRIs & nuvaring so stopped them w no change} with little to no change no matter how I change my diet {Noom;Weight Watchers,low carb, decreased sugar} and exercise {more difficult with my toddler}, and even tried Adipex. I did lose 12-15 lbs overall with this over the first 2 months and plateaued so stopped after 4 months. I have had issues with muscle aches and pains in my back and *neck (*more than 10 years*) and shoulders worsening in the last 6 months. I have had a change in my naturally curly hair texture that is now more frizzy and more coarse. This became an issue 2 years ago after my daughter was born (which I expected and wasn’t too concerned about) but then, as it’s continued, along with issues growing my eyebrows after last waxing them 4-5 years ago… I mean it’s just a LOT of stuff to ignore and call “non-specific” and unrelated simply because lab values fall within “normal” ranges set by the lab. I was told I’m tired because I’m a mom, that I should diet and exercise more and better, and that nothing is wrong with me. I wake tired and oversleep daily, even tho I’m getting 8,9,10 hours of sleep, if my husband is home. Which leaves me feeling I have nowhere to turn. If an endocrinologist is going to look at these labs while ignoring my symptoms same as my primary doctor then it makes me feel I’d rather not waste my time trying but would rather seek treatment with an alt med doctor if they’re going to actually look at and address my symptoms. All of which have pretty much worsened in the past 2 years since my child was born.

  15. (I originally wrote this for the older “T3 or not T3 post”, but thought it was better for this post – both have been very helpful)

    Thanks for such an informative blog post on this topic. I have some questions regarding the genetic variant / polymorphism reason for considering including T3 in the treatment for hypothyroidism, but need to provide some background too.

    My daughter, currently 8 years old, has Down Syndrome / Trisomy 21 (T21). About 18 months ago she tested positive for hypothyroidism. Given the condition of T21, we’ve been on a steep learning curve for how to best care for her overall, including medically. This has led us into many communities, including that of functional medicine and alternative therapies. We stick with evidence based medicine, and manage everything else with diet and exercise, though we always have our eyes open for alternative approaches and new research. Presently she remains on levothyroxine monotherapy and her labs have gotten to normal.

    To this end, this research came to our attention – ( – which pointed to T21 truly being an immune system disorder – meaning that while she has Down Syndrome, the many of the associated effects of this are largely due to the immune system not functioning normally. With an immune system that is always-on so to speak, and being hypothyroid, and now also type-1 diabetic – we are looking for the best ways to combat this reality, and recognize that her thyroid will be under attack for the rest of her life or for as long as the thyroid is able to function.

    We also came across this article ( pointing to a Dio2 polymorphism that, if she has it, could indicate that her body may not be able to convert T4 to T3 as well as those without the polymorphism. Since T21 also results in cognitive delay and impairment, getting T3 into the brain tissue is very important to not cause further disability.

    Given the rapidly declining costs of genetic testing, we did have her tested for the Dio2 polymorphism, and she came back Heterozygous for DIO2(T92A) rs225014, making it unclear but I guess still possible she has a problem).

    I know you are not here to give specific medical advice, but I am curious on a few topics (1) does this fall under the #1 in the list of 5 types of people who might consider T3?, (2) do you see / have suggestions for people with T21 in terms of care for the thyroid that may differ from those without this genetic condition? (3) do you suggest any other reading material in this genetic polymorphism? Also, I’m not a medical professional, so if anything above is misstated, please feel free to point me to the evidence.

    Our endocrinologist is open to using T3, but as I have understood the downsides, we have so far erred on the side of further caution, even though it is extremely important to provide the maximum amount of support for cognitive functioning and growth for people with T21 so that they may have independent lives and be able to contribute actively in the world.

    1. To answer your questions:

      1. Based on the limited data that exist, I think someone with 1 or 2 copies of the polymorphism could consider a trial of T3. In my reading, I was surprised by the fact that people heterozygous for the polymorphism had lower TSHs than people who were homozygous. While this doesn’t prove that it’s “worse” to be heterozygous (which doesn’t seem intuitive anyway), I think it’s interesting.

      2. I don’t know enough about T21 to comment on this.

      3. I think I’ve read and summarized the best of the studies out there, so I’m not sure it’s worth doing that much more reading. We just don’t know enough about the clinical implications of these polymorphisms at this point, so we have to use judgment when considering whether someone with the polymorphism and a normal TSH is truly “euthyroid.”

      1. Thanks for responding.

        “In my reading, I was surprised by the fact that people heterozygous for the polymorphism had lower TSHs than people who were homozygous. While this doesn’t prove that it’s “worse” to be heterozygous (which doesn’t seem intuitive anyway), I think it’s interesting.”

        Yes, I’ve seen this too and was quite surprised. My daughter seems relatively asymptomatic for hypothyroid at this point, but we are trying to be extra vigilant to do everything to help her brain development and IQ.

        She is presently on 25 ug Levothyroxine with Tirosint … the new prescription that we have is for Novothyral with 100 ug of Levothyroxine and 20 ug of Liothyroninum (5:1 ratio vs. what you state above should be 15:1 instead). Any reason why Merck (I think they produce Novothyral) would use a 5:1 ratio when the human body is 15:1 of T4:T3?

        I’m likely going to ask our endocrinologist if we can just get a direct dosage of Liothyroninum at 1/15th of the current Tirosint dosage, which seems to be working OK.

        1. Regarding the 5:1 ratio, I don’t know the history of that decision. If I had to speculate, I’d guess that they were trying to make a pharmaceutical-grade version of desiccated pig thyroid, which was the standard of care before levothyroxine came along.

  16. The advantage of altmed is that their main concern is how the patient feels and for their clinical wellbeing, whereas your interest lies mostly in the results of lab tests. If a patient feels well they have a right to decide on the best treatment for them, whatever the TSH result. Otherwise why bother with a human, just treat a phial of blood! Many patients dislike a dictatorial and paternalistic attitude. Why do you think altmed is so popular?

    1. False dichotomy. We SHOULD consider the lab test result and the way the patient feels, then make a considered recommendation based on the whole picture.

      What we shouldn’t do is ignore test results that show our intended treatment plan would be dangerous or unnecessary. This is what I see Alt med do a lot of.

  17. I’m hoping I can ask you an off-the-record curbside regarding TSH testing.
    I am the PCP for an elderly woman with some mild cognitive impairment and hypothyroidism on levo replacement x years. Her family has moved her close because of age and impairment. She has comorbid depression. We’ve been fighting the fight to ascertain whether cognition will get better after normalizing TSH and treating depression well.
    Her TSH was previously 30 before I met her, due mainly to lack of adherence. After family moved her, it went down to 18 as the granddaughter reminded her to take her pills and checked on her frequently. She lives in apt behind granddaughter, who also is physician.
    We hatched a plan that babysitter will give pills mid-day (to avoid any interfering calcium) and observe her take them. After 8 weeks of this observed dosing, TSH is now 24. No history of any gastric disease or interfering illness. I increased dose, and we are waiting on her 8 week test this week.
    Is it possible that a person can be so hypothyroid that after you replace them, their metabolism revs up, then their requirement goes up, such that their TSH can initially reduce then go back out again? Any other ideas about why she’d initially respond then TSH rise, if we are ensuring adherence? Thanks in advance.

  18. Is the TSH the optimal unique test for patient that had thyroidectomy for cancer?
    I know most of them woukd need the TSH to be suppressed, so how comes that if the TSH is almost 0, FT4 is still in the range (medium/ upper part) and FT3 is really low in the range? From this article I understand that TSH should be suppressed only in a really over medicated situation, right?

    Other question: is there a relationship between suppressed TSH and high prolactin?

    1. In thyroid cancer, we often aim for a TSH that is low, but still detectable. The degree of suppression depends on the risk of recurrence. Very low risk patients don’t need any TSH suppression, whereas very high risk patients may require significant suppression. On levothyroxine alone, the T4 can be anywhere from mid-normal to mildly elevated when the TSH is suppressed. This has to do with the fact that everyone’s set point for T4 is in a fairly narrow portion of the range. So if your T4 likes to live in the lower third of the range (corresponding to a normal TSH), then a high-normal T4 may cause your TSH to be very suppressed. T3 levels, for reasons I have discussed in other posts, will often be low-normal or slightly low in patients on levo alone.

      As for prolactin, high prolactin levels can be found in untreated hypothyroidism (high TSH), but otherwise shouldn’t be an issue.

      1. Thanks for the explanation. I have really low TSH (but not suppressed) and doctors say that now on I don’t need it to be fully suppressed as I’m a low risk of recurrence, so I could reduce my levo.

        I feel all right with this levels, apart from having gastritis (can be related to low TSH?)

        I’m honestly scared of reducing levo, I’m being honest. I saw my body changing so much: first I had hyperthyroidism with all the symptoms and a lot of weight lost, then I went on treatment for hyper and I put on so much weight that I felt like an inflated baloon. Then I was diagnosed with cancer and had TT and RAI and felt I didn’t have enough energy to survive almost.

        Now my energy is fine, my weight is stable even if I can’t lose any, but I can function.

        So my question is: as I can’t know my ideal levels pre-TT and pre-hyper, what should I trust more, my TSH test results or how I feel? I’m scared that I can’t function well by medicine levo and also I don’t want to put on weight, as it fluctuated so much in the last 6-8 years.

        1. It’s all important – TSH and how people feel. A good doctor will take all of it into account, consider judicious use of T3 when the person feels “not optimized” on T4, etc.

  19. My understanding is that high TRab can also interfere with or give a false TSH reading. Is this true? I have been listening to alt med for way too long and have a lot to unlearn. But they often mix good information with bad conclusions and I’m still sorting it out.

    Your blog and comments section has been a tremendous help and I’m slowly reading my way through the entire site. Thank you!

    1. I’m not aware of thyroid hormone receptor antibodies interfering with the TSH assay. There are other kinds of antibodies that can do that – like heterophile Abs – but not TRAb as far as I know.

      1. I just found your response after re reading this post. I think this is the study that led me to that belief. Although they’re calling it TBii and the study is done along with anti-thyroid drugs. So much to learn. This thyroid stuff is a serious rabbit hole. The more I read, the more questions I have.

        I found this info when reading about blocking and stimulating Trab. Perhaps this is the cause of “sub-clinical hyperthyroid”. Which may be a good subject for a future article.

        Btw, I now get notices for responses and new articles. Very interested in reading your next article on T3.

        1. Arthur, I agree that the antibody stuff gets ridiculous and very confusing. What makes it worse is that some of these antibody terms are synonymous with each other. In addition, people with one type of antibody very likely have lots of the others as well. This article on Thyroid Disease Manager is dense, but it gets into the antibody discussion a little more:

  20. I’m wondering about thyroid hormone autoantibodies (anti-T4, anti-T3 antibodies) and how this impacts TSH, and symptoms.

    Does it mean that T4/T3 is present and recognized by the pituitary, but that the antibodies interfere with how these hormones are utilized in the body? Do the antibodies “attack” T4/T3?

    Do these antibodies inhibit the effects of T4/T3 similiar to how anti-growth hormone antibodies decrease the effect of GH treatment?

    I’ve not been able to find much written about the antibodies other than some research articles and textbook. Thank you!

    1. I think anti-T4/T3 antibodies are mainly thought about as something that can interfere with the FT4/FT3 assays. I’d have to do some more digging to see if there are any papers describing a true clinical implication of these Abs, as I haven’t come across this much. Let me put it on my list.

      1. Thank you! I was familiar with the test interference issues but would love to know more about how this impacts physiology and symptoms. I’ve wondered if there isn’t much known/studied about the topic hence, the lack of information.

  21. I have Hashimotos (10+ years). For the majority of that time I was treated with NDT (Armor). Two years ago, I developed extreme hyper symptoms although my labs were on the hypo side (TSH of 5, low free T4 with mid range free T3). Lost LOTS of weight and went off all thyroid med for 5 months which elevated my TSH to 41 but had very few hypo symptoms. While off meds, TSH lowered to 21. Free T3 remained low normal. I continued to lose weight to a low of 94 lbs with muscle weakness, twitching, near syncope, etc. All testing with the exception of thyroid labs came back normal. I am now on Tirosint SOL with additional T3 (NP thyroid) and am finally beginning to feel human again after adding a low dose of estridiol/progesterone. My question is how/why could my symptoms be so hyper when my labs were so hypo? My major complaint now is heart racing/palpitations/heart beat in ears mornings from about 1 hour post Tirosint lasting until 5 hours post Tirosint. My afternoon dose of 15 NP Thyroid does NOT produce this. My TSH is still on the high side (4.8) with free T4 of 1.5 and free T3 of 2.5. I’m befuddled. I see virtually nothing about people with Hashimotos who experience hyper symptoms while under treated or correctly treated on meds unless it is the beginning of the disease where the thyroid “spurts” out hormone while it destroys itself. I’ve had this disease over 10 years so why now? Are there other Hashimotos patients who experience this and better yet, how can it be resolved?

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