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I want the full thyroid panel.
This common statement is second only to “I want the natural thyroid hormone” as the most misguided request I receive. The U.S. medical establishment has unintentionally cultivated a “more is better” expectation from our patients. With the proliferation of evidence-based clinical practice guidelines in the Kingdom of Endocrinology, sage physicians have tried to rein in profligate ordering of unnecessary tests. These doctors understand that more information does not always equal better outcomes. Instead, more information often results in false positives – abnormal results that do not indicate a real clinical problem. This leads to sending patients and their providers off on wild goose chases at best, and it leads to patient harm at worst.
Sadly, the horse has already exploded out of the barn with respect to thyroid testing, and that horse is still galloping across the plains of Nebraska*. The thyroid is ripe for this sort of nonsense, because there are so many darn tests on the menu. I’m here to emphatically state that you don’t need 90% of the stuff on that menu.
But I’m special.
No, you’re not.
But my naturopath told me I’m a non-converter.
No, you’re not a non-converter. And I hate double negatives.
But I have inflammation, so we need to check all the thyroid antibody levels.
I don’t even know what you mean by “inflammation.” And no.
With that preamble, I present to you: Thyroid Function Tests Demystified: Hypothyroidism Edition.
The competence of your health care provider is inversely proportional to the number of thyroid tests she orders for you.
Said another way, your HCP probably has quacky tendencies if she orders more than 1-2 TFTs for you on a recurring basis.
When hypothyroidism is suspected, TSH (thyroid stimulating hormone) should be the initial screening test, period.
There are uncommon situations which probably don’t apply to you – remember, you are not special – in which the TSH is not an adequate screen for hypothyroidism (e.g. hypopituitarism and critical illness). In the vast majority of situations, however, TSH is the best indicator of even the most subtle thyroid hormone abnormalities.
Remember Jeff Foxworthy’s You Might be a Redneck… routine? Your thyroid provider might be a quack if…
The Laboratory she uses has redefined the upper limit of normal for TSH as 2.5 mIU/L. Your provider is almost certainly a quack if she has crossed out the Lab’s standard upper limit of 4.0 – 5.5 and written in a value from 2.0 – 2.5. While I agree that, as theTSH climbs into the upper half of the normal range, it could indicate early/mild hypothyroidism, I strongly reject the idea that we should automatically and thoughtlessly label hundreds of thousands more people as having a disease that they almost certainly do not have. How the heck is that responsible practice of medicine?
Now, using TSH for monitoring thyroid hormone replacement therapy is a bit different. I still maintain that the Lab’s reported upper limit of normal should be left unmolested at around 4.0. Most patients will feel the same regardless of where their TSH is within the normal range. However, there are many people on thyroid replacement who feel best with a TSH in the lower half of the normal range, and it is perfectly acceptable to aim for that, on a case-by-case basis. It is not ok to claim that every hypothyroid person can only be considered adequately replaced once the TSH is in the lower half of the range. In my experience, there are plenty of hypothyroid patients who feel better with a high-normal TSH; these patients would clearly be harmed by inappropriately lowering the upper limit of normal for TSH.
If the screening TSH is in the upper half of the normal range, in the presence of symptoms suggestive of hypothyroidism, then repeat the TSH and check a free T4 (FT4) and thyroperoxidase antibodies (TPO Abs).
One reason why the alt-thyroid cult – oops…uh…I mean – community has gained so much traction is because of click-baity headlines like “Why Your Normal Thyroid Numbers Don’t Tell the Whole Story.” As a lot of quackery does, this starts with a kernel of truth, and then it devolves into histrionic idiocy.
It is true that a patient can have clinically meaningful hypothyroidism with a normal screening TSH. However, when I see someone with a screening TSH value of 1.0 and a normal FT4, who has been started on thyroid hormone because of “symptoms,” I know that the train has gone off the rails. Remember, for a small, linear drop in FT4, the TSH will increase exponentially. Therefore, the TSH is an ultra-sensitive indicator of subtle thyroid hormone abnormalities. If it is high-normal, with a normal FT4, then TPO Abs may be a useful tool in figuring out whether the symptoms are actually due to a thyroid problem.
TPO Abs are produced by the immune system, and they attack the thyroid, causing a destruction of its ability to make thyroid hormone. The presence of TPO Abs in the blood does not mean that one has hypothyroidism; it does mean that one is at risk of developing hypothyroidism. In the setting of a high-normal TSH, an elevated concentration of TPO Abs could indicate early hypothyroidism, and a trial of levothyroxine is reasonable. While a negative TPO Ab test does not make it impossible to have hypothyroidism, it makes it less likely.
Other thyroid antibodies have no role in the diagnosis and management of hypothyroidism.
You may have seen the following tests on your lab reports in the past: thyroglobulin (anti-thyroid) antibodies, TSH receptor antibodies, or thyroid stimulating immunoglobulins. While each of these tests has utility in the management of a thyroid disease, hypothyroidism is not that disease.
TPO Abs, once found to be elevated, never need to be checked again.
If I had a dollar for every patient I’ve seen who obsesses over the direction in which her TPO Abs are trending, I could buy a few rounds of $20 craft cocktails for all the patrons in one of those secret speak-easy joints in Manhattan – on a Saturday night. Do you know how hard it is to reeducate someone whose naturopath has been insisting for years that their Hashimoto’s is still uncontrolled, because the TPO Abs are still elevated? Very. Very. Hard.
TPO Abs are a diagnostic tool, usually used to help determine whether someone with a borderline high TSH (as above) has clinically meaningful hypothyroidism. Because the thyroid continues to be present in the body after starting thyroid hormone replacement therapy, the immune system will continue to react against it. That’s just the nature of an immune reaction – if something is in the body that the immune system doesn’t like, it will generate antibodies against that thing. If you remove the offending antigen (the target of the immune reaction), then the immune system will stop reacting against it. You want to see your TPO Abs drop to zero? Go to a surgeon and have your thyroid removed. I can’t imagine why in the world you would want to do that, but it’ll work to make your lab test look prettier.
But how else can I lower my TPO Ab level?
To be unambiguously clear, I do not care what your antibody level is. Let’s focus on getting you on a thyroid replacement regimen that gets your TSH normal and stable, and gets you feeling better.
But my antibodies are still high! You’re just treating the symptoms and not the disease! Shouldn’t I avoid gluten and all cruciferous vegetables, take selenium, and get started on low-dose naltrexone?
You see what I’m dealing with? It is often near-impossible to redirect someone once they become invested in that TPO Ab number. Because I’ve built up a significant callous on my forehead from repeatedly banging it into my exam room wall over the years, I will try to redirect an insistent patient two or three times. After that, I just have to change the subject and move on, or risk concussion.
T3 levels have no role in the management of hypothyroidism…
Unless you’re a doctor trying to prove to a patient that her heroic dose of pig thyroid is, indeed, resulting in abnormally high blood levels of T3. As I’ve explained in a prior post, T3 levels in the blood do not necessarily reflect what’s happening in your tissues, with respect to the conversion of T4 to T3 by deiodinase enzymes.
But my T3 level is low! That means I have Wilson’s Syndrome and I need to be put on T3…now!
This is the kind of logic that, in my experience, leads to naturopaths titrating the T3 dose to atrial fibrillation. Once again, please read my prior post about this issue, then get back to me if you still have questions.
Forget you ever read about reverse T3, T0, T1, and T2. End of story.
If you’re reading this site, it’s probably because you like to understand things – believe me, I get that. I don’t ask for many favors, but I’m asking you to trust me this once…the above tests will add absolutely nothing to your medical care. It is totally unnecessary to invest your ATP in figuring out how to use or interpret these tests.
Update 11/2018: If you really, really want to know more about reverse T3, check out my post, Everything You Never Needed to Know About Reverse T3.
TSH is the only test needed to guide thyroid hormone replacement therapy.
Remember the exponential change in TSH for a small, linear change in the T4 level? For this reason, TSH is the only useful blood test for monitoring thyroid status on levothyroxine (+/- liothyronine). If your TSH is high or low, but anywhere within spitting distance of the normal range, your FT4 level is almost guaranteed to be within the normal range – therefore, the FT4 adds nothing useful to your management.
In the unlikely event that you are special, and you have a pituitary problem, TSH cannot be used to diagnose hypothyroidism or guide thyroid hormone replacement therapy.
In hypothyroidism resulting from pituitary disease, the screening TSH will be low or normal. Once treated with thyroid hormone replacement, the TSH will usually be low. This is actually incredibly important, but for just a small number of people. Unfortunately, while many primary care providers know that TSH can’t be used in this situation, it is common for them to forget that the patient has secondary (also known as central) hypothyroidism – not surprising, given that the majority of their patients have garden-variety primary hypothyroidism. This often results in the patient having her dose of levothyroxine lowered, because the low TSH is thought to indicate over-replacement with thyroid hormone. While this would be correct management of primary hypothyroidism, it is incorrect in secondary hypothyroidism.
If you have this condition (please don’t ask me if you have it – if you have to ask, you probably don’t), I would recommend making sure that your doctor always monitors your FT4. While some doctors also like to see the TSH, as it should be low if on a therapeutic dose of levothyroxine, the FT4 is the more helpful test. Nonetheless, I sometimes find it challenging to optimize the levothyroxine dose, as different people seem to feel best with their FT4 in different portions of the normal range. I have to rely more on symptoms to guide replacement therapy, which is even more problematic in patients with central – as opposed to primary – hypothyroidism. Patients with central hypothyroidism are often on other hormone replacement therapies (hydrocortisone, testosterone/estrogen, growth hormone) as well, and these other therapies have equally poor (or worse) biomarkers, with respect to helping me determine the proper dose of the hormone. As a result, it’s fairly easy to confuse the symptoms of one inadequately replaced hormone deficiency with another.
If I could send you off with a simple, take-home message, it’s that hypothyroidism just isn’t as complicated or esoteric as many of those ridiculous thyroid blogs would have you believe. While I intend this post to be the “ultimate guide” to thyroid function testing in hypothyroidism, I suspect there are things I haven’t covered in which you’re interested. Let me know in the comments below!
* Why Nebraska? Seriously, have you guys every driven across that state? It is flat in every direction, as far as the eye can see; I bet a horse could gallop in any given direction until dropping from dehydration and malnutrition. If I had fallen asleep due to boredom, I probably could have woken an hour later to find myself still in my lane, pointed due west.
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65 Replies to “The Ultimate Guide to Thyroid Function Testing – Hypothyroidism Edition”
I’m surprised you would suggest that it doesn’t matter if your antibody levels are trending up or down. Isn’t it true that elevated TPO antibodies increase the risk of miscarriage, goiter, nodules, developing a secondary autoimmune disease, and thyroid (and possibly other) cancer? Wouldn’t reducing the risk of the development of other diseases be a good reason to supplement with selenium? Please accept this as an honest question– my endocrinologist advises selenium supplementation, and my antibody levels have declined substantially over time, which seemed to coincide with the end of some of my weirder symptoms, such as Raynaud’s. It is my sincere wish to avoid any head-banging. 🙂
Referencing these two articles:
Fröhlich, E., Wahl, R. “Thyroid Autoimmunity: Role of Anti-thyroid Antibodies in Thyroid and Extra-Thyroidal Diseases.” Frontiers in Immunology. 2017; 8: 521. Published online 2017 May 9.
Kent, Athol. “Thyroid Antibodies Associated With Miscarriage and Preterm Birth.” Reviews in Obstetrics and Gynecology 4.3-4 (2011): 128–129. 2011.
Fair question. However, the antibody levels themselves are merely a marker for thyroid autoimmunity. The antibodies are not known to directly cause anything other than destruction of the thyroid’s ability to make thyroid hormone. While one would think that lowering the TPO Abs would slow down the destruction of the thyroid, that is not the case (I will write a post about selenium, as this is where selenium comes in).
Reducing the TPO Abs does not lower one’s risk of developing any other disease or condition, because that does not change the underlying fact that the person has an autoimmune predisposition. In addition, while there is evidence that taking levothyroxine reduces the risk of miscarriage in women with + TPO Abs, there is not evidence that lowering those Ab levels with selenium reduces the risk of miscarriage (though it may reduce the risk of postpartum thyroiditis – more to come in a post).
I would love to know more about why lower antibody levels do not mean less destruction of the thyroid tissue, so I will look forward to your selenium post.
I’d like to state again that I’m asking honestly here, but I am confused by this:
>the antibody levels themselves are merely a marker for thyroid autoimmunity. The antibodies are not known to directly cause anything other than destruction of the thyroid’s ability to make thyroid hormone.
You seem to be saying that antibodies are merely a marker, and then go on to point (correctly) out that they are the actual cause of the disease’s tissue damage. What does “merely” mean here? You seem to be saying that having autoimmune disease is the meaningful risk, and the quantity of antibodies is irrelevant. But since the cause of autoimmunity is essentially unknown, to me, personally, it seems reasonable to assume that if something is bringing down the level of anti-self antibodies, that is probably, at least, not a bad sign, and maybe means something good? Obviously, with this level of evidence, not a goal worth chasing with steroids or anything with serious side effects, but I mean, selenium, 200mcg a day? Why the hell not?
I’m also feeling a need for a “citation needed” on this statement:
>Reducing the TPO Abs does not lower one’s risk of developing any other disease or condition
Has this actually been proven? I’m a layperson with access (through my spouse, who is a research scientist) to a lot of medical journals, and I have never been able to come up with anything that specifically analyzed the symptoms or outcomes of those with high antibody levels vs. low antibody levels. It’s one thing to say, “we don’t know if this occurs,” and another to say, “this doesn’t occur.”
Similarly, when you say
>there is not evidence that lowering those Ab levels with selenium reduces the risk of miscarriage
I’m pretty confident that is because there haven’t been any studies on the effects of lowering TPO-antibody levels via selenium on pregnancy outcomes. There have only been a handful of studies on the effect of selenium on antibody levels, and the largest one had a treatment group of only what, 42? How many of those 42 could possibly have been pregnant?
I can understand why, as a doctor, you would say, “Since I have no evidence that this helps, I’m not going to recommend it to my patients,” but I can also understand why a doctor would say, “I don’t know whether lowering antibody levels helps, but since the antibodies are the cause of tissue damage, and selenium has no meaningful side effects at the right dose, I will recommend this to my patients.” After all, doctors still prescribe cholesterol-lowering drugs to people with high cholesterol, even though it’s unclear whether lowering cholesterol by those means actually leads to better outcomes or not.
And I want to present a patient’s point of view on this. When I was a kid, I read an article about cancer patients who were asked to imagine that their immune systems were attacking the cancer cells in a cowboys-and-Indians type scenario. When I learned that I had autoimmune disease, I had this picture in my mind of my T-cells attacking my own tissue in this way, and there is a kind of horror in that thought. And because of my unusual symptoms, I was already being sent through several specialists who were checking me for more anti-self antibodies. Thinking about getting those antibodies down was important to me because it bothered me that my body was being attacked. That’s a fairly natural and normal response, I think– wanting to minimize an attack on one’s body. No one wants to think about being gnawed upon by, or “encrusted with” lymphocytes.
… Immediately after hitting reply, I remembered that I did once see a study that specifically analyzed the symptoms or outcomes of those with high antibody levels vs. low antibody levels– “Symptoms in Euthyroid Hashimoto’s Thyroiditis: Is There a Role for Autoimmunity Itself?” Angela Dardano, Laura Bazzzichi, Stefano Bombardieri, and Fabio Monzani (Thyroid, Volume 22, Number 3, 2012). But it seems to have the opposite conclusion to yours, that high antibody levels do correlate to a high symptom load. I get that this doesn’t prove that reducing antibody levels also reduces symptoms, though.
Yes, I remember reading at least one or two articles in the past that suggested people with TPO Abs and a normal TSH may feel worse than people with negative TPO Abs and a normal TSH. However, the general impression of the Endo community is that the most likely of the possible explanations is: people with TPO Abs may have other – as yet undiagnosed – autoimmune disorders. If they have another autoimmune disorder that is brewing, but “subclinical,” this could account for why they feel worse. While this is just one potential explanation for the finding, it seems more plausible to me than that TPO Abs have some kind of direct effect on how people feel, independent of their effect on the thyroid. I believe that the “other autoimmune disorder” hypothesis would also explain why lowering the TPO Ab level makes no difference in how people feel, as long as we’ve gotten the thyroid hormone replacement regimen correct. But honestly, we just don’t know the answer.
There have been studies showing that, although selenium decreases TPO Ab titers (which intuitively should make Hashimoto’s “better”), it does not decrease the thyroid hormone dose requirement in patients taking it. Unexpected result? Absolutely. It should work to decrease the need for thyroid hormone, but it just doesn’t. Maybe this is where low-dose naltrexone will ultimately prove its worth – who knows?
As far as reducing TPO Abs, that has never been shown to affect the development of thyroid nodules, thyroid cancer, or autoimmune diseases of some other kind. That’s really my point in calling them a marker. Yes, they destroy the thyroid. Yes, there may be an increased risk of a thyroid nodule being cancerous if TPO Abs are positive. But there is no study I know of (and no pathophysiologic mechanism that really makes sense) that would clearly link the TPO Abs to these other conditions as a clear cause and effect. So lowering the Abs doesn’t change the association between TPO Abs and other conditions; it just makes the Ab number look better on paper.
This is analogous to certain cardiovascular risk markers, which we can measure in the blood. Some of these markers, when elevated, are associated with an increased risk of heart attack. We can lower these markers with drugs. But lowering these markers has no impact on heart attack risk.
I get that the concept of one’s body being attacked is disconcerting. All I’m saying is that, so far, lowering TPO Ab levels with selenium hasn’t seemed to do much good (with a few exceptions I’ll talk about in a post).
Thanks so much for your thorough replies. This is really helpful.
I really enjoy reading your blog and your unique style of writing.
As a person with Hashimoto’s, I’ve been specifically waiting for this topic to come up.
Here in Australia, naturopaths and alternative therapies are widely popular and accepted as legitimate. I too was influenced, and believed that sugar, gluten and supplements played a huge role in the management of my disease. Thanks for taking the time to put the information out there. I use it to re-educate myself after years of spending money on quackery.
Interesting. I wonder if you plan to expand on this topic for hyperthyroidism/Graves Disease. I’ve been led to believe that autoimmune antibodies will keep TSH suppressed even after T3 and T4 levels have stabilized on medication (methimazole.) It would be interesting to see your take. Thanks!
Yes, I do plan to do a “hyperthyroidism edition.”
Thank you for such a great post!
I recently inherited a number of patients from a doctor who had left practice. Every single one of her patients with hypothyroidism was getting a TSH, free T4, TPO antibodies, T3 and reverse T3 every 6 months. Unbelievable.
I don’t even think she was a quack- I just think she had no damn clue what she was doing.
I want to point out that if this post is from a “Primary Care Doc” should we assume he/she is not a naturopath? Therefore, if Primary Care Doc inherited some patients from a doctor that left practice, should we assume that this doctor is also not a naturopath?
I say this because quacks can be ANY type of doctor, not just naturopaths. In my experience, MDs, DOs, OBGYNs and ENDOs have all equally made these same errors. We all take a risk seeing ANY TYPE of health care practitioner.
Yes, we can assume that PCD and the doc PCD took over for are not naturopaths. But your statement about all these types of docs having an equal chance of being quacks is overreaching.
Thank you for this explanation. I moved and therefore changed GP’s, the old GP’s tested for TSH and T4, the new just test for TSH and I had wondered about that. However as I have more trust in the new GP’s for other reasons, and appointment lengths limit what one can discuss, I have never asked them about why. Your explanation confirms my impression that this practice is rather more ‘on the ball’ than the previous one.
I was diagnosed with low-level Hashimoto’s in 2009-10 – your article makes me wonder if I even have it or need levothyroxine.
I told my family doctor I was feeling fuzzy-headed, couldn’t think well and had a hard time getting the energy to get myself out of the house. That was because of allergies, but I didn’t know it at the time.
So she did a lot of tests. She found my thyroid peroxidase antibodies were high – 134 IU/mL. My TSH was 2.6 mIU/L. Then she found my free T4 was low at 0.73 ng/dL, my free T3 was 2.11 pg/dL.
So I’ve been taking levothyroxine since then – recently, 67mcg /day.
Since then, my TSH has been as high as 4.51 and my thyroid peroxidase AB have been as high as 141 IU/mL.
But my initial symptoms weren’t actually due to hypothyroidism, and starting levothyroxine didn’t help.
So I’m wondering if I even have Hashimoto’s. I thought the TPO antibodies were diagnostic. But maybe I should try reducing my levothyroxine dose (with a doctor’s help) and see if I feel worse.
Laura raises a good point, in that lots of people will have some borderline or mildly abnormal thyroid numbers, some symptoms that sound like hypothyroid symptoms, but the symptoms might not actually be due to hypothyroidism. This can even happen when people have positive antibodies, as the mere presence of antibodies does not necessarily mean that hypothyroidism has developed yet.
part of the problem – its this crap that keeps thyroid medicine 20+ years behind on any given day
5 years ago it was discussed in media that the average ENDO was then 17 years behind their own field – AVERAGE. its one of few medical interests where a literate patient is almost guaranteed to know more than the doctor, endo incl. my 21 yr old daughter had thyroid cancer except that according to early lab tests, ultrasounds, late stage biopsies etc she didnt… she had every symptom under the sun. thank the gods i persisted and her invasive cancer was dealt to before it was too late – after 20+ yrs of this gig and experiencing some of the most ignorant medical care possible in various countries around the world i knew better than to listen to a ‘specialist’
that patients lived better off ndt prior to the advent of levo is apparently of little use to most modern medical “professionals”. you couldnt make it up
anonymous – no kidding
I’m not really sure where to start to try to turn this into a constructive exchange. I reject the premise of the comment about the average Endocrinologist being 17 years behind, though I’d be interested how that number was calculated. Perhaps you can cite your reference?
Think was the lancet (or sim accredited medical journal) – you were prob hoping for fox news but no
After the latest episode of replacing with levo against my wishes, and the subsequent 55lb myexedema gain in 2 months, new specialist agreed I need to remain on ndt and bumped it up 25%. I am now slowly feeling better but undergoing testing for new heart condition issues from last round. What doc in their right mind would look at a patient that swollen, that fast, and hold to their own stupidity? Several years ago I had heart testing for insurance and results were I was well ahead of my peers – now i struggle to climb stairs and its incredibly upsetting. Most levo patients think their specialist useless so its not just we ‘ndt quacks’
The Lancet claims that the average endocrinologist is 17 years behind? OK, sure. I’d love to see that reference.
Thanks for the great summary. I have been in those thyroid cult groups on Facebook and every one told me to stop eating gluten. I refuse to believe this is necessary. I have post partum thyroiditis, diagnosed with a TSH of 88. I was subclinical before getting pregnant with a TSH of 8 and lots of fatigue. Does post partum Thyroiditis require T4 to manage meds once the normal range of TSH is met?
It will be important to work with your doc on this one, as postpartum thyroiditis can result in temporary or permanent hypothyroidism after the thyrotoxic phase has resolved. Whether the hypothyroidism is temporary or permanent depends on several factors, including presence of TPO Abs, presence of hypothyroidism pre-pregnancy, and degree of hypothyroidism achieved (magnitude of TSH elevation). If one develops permanent hypothyroidism, then yes, thyroid hormone replacement therapy is needed.
Can you comment on TSH ranges over 4 but less than 10 (in both symptomatic and asx)?
Traditionally I was taught (and I think the last AACE guidelines also include) that this range is considered “subclinical,” and there’s lack of benefit in treating, unless patients are symptomatic or have abnormal lipids, although anti-TPO can be helpful in interpreting prognosis. Thus, in patients without symptoms, I’ve been observing levels up to about 6-7, if FT4 in normal range. Still good?
This confuses me in regards to your statement that some folks have hypothyroidism when TSH is in normal range (albeit more towards 4) and FT4 in lower range of normal. Presumably, you’re always talking about symptomatic people here. Guess I’m just wondering if “subclinical” exists at all anymore?
You’re not missing anything – everything you said is spot-on. My only point is that, for patients with positive TPO Abs, it is possible they may be symptomatic with a high-normal TSH and FT4 in the lower third of the normal range. Over the years, I’ve found it interesting that some people feel awful with a TSH of 3 and get better with a TSH of 1, whereas some people feel no different with a TSH of 20 or 2.
If a patient has a TSH of 6-7 and no symptoms, even in the presence of antibodies, it is quite reasonable to watch them, as you are doing.
Thanks. I like your reasonable approach. I’ve read the thyroid boards and have been told by friends to take their literature to my doctor to prove my potentially undiagnosed hypothyroidism, and I can’t imagine any doctor taking such hysteria seriously. I do still wonder if it is my thyroid, despite just reading “it’s not your thyroid” 🙂 My TSH is 3.90, Free T4 0.98 and my TPO Ab 322, yet the endocrinologist says not to worry. I have the symptoms of hypothyroidism (yes, I know they are common to many disorders) but I feel like even when there is a possibility that there may be a thyroid issue, many doctors are unwilling to use medication as a test to see if that is the problem. I don’t really understand this. I guess I need to wait and see if my TSH gets higher. But I respect doctors over quacks any day.
I appreciate your willingness to consider that it’s not your thyroid. And I’m glad you’re not taking any of the thyroid forum literature to your docs – you would see an immediate negative shift in their posture. As I have written, though, I think it is often reasonable to do a trial of levothyroxine in those with a high-normal TSH, low-normal FT4, and positive TPO Abs. Some folks in this zone will, indeed, have symptoms due to mild hypothyroidism (although many people will try medication for 3-6 months and feel no better, typically suggesting that the thyroid was not the answer).
May you briefly explain why rT3 level is irrelevant … or why the notion of rT3, if too high, will block the T3 receptor is wrong?
would love to get an explaination 🙂
The reverse T3 level does not correlate with any clinically useful parameter. In other words, the number you get from the blood test does not give you any actionable information. It was once thought that rT3 levels could be helpful for figuring out why the usual thyroid function tests (TSH, FT4, FT3) might look weird in the setting of chronic starvation or critical illness, but the assay for rT3 really hasn’t proven to be all that helpful in those instances either.
The notion that high rT3 levels “block” the T3 receptor is, as best I can tell, something that has been conjured out of thin air by the alt med community and plastered all over alt-y websites. I have no idea where this idea came from, as to the best of my knowledge, there is no evidence that this happens. Since I can’t prove a negative, that’s the best I can tell you.
Can you comment on so-called “conversion problems”? It’s a commonly cited reason for the need to be on T3 meds, but I can’t find any legitimate info on it. Sometimes it’s claimed rT3 has a role in it, other times the alleged cause is more vague. It serves as a convenient catch-all for the alt thyroid hucksters who want healthy people to believe they can still have thyroid disease, and want thyroid patients to believe they are inadequately treated. Are “conversion problems” in the same bin of “conjured out of thin air” as high rT3 levels having any effect? If someone really couldn’t convert T4, wouldn’t they be critically ill?
All great questions/points, Anne. I think I’ll have to do a couple of posts that cover the myths surrounding failure to convert T4 to T3 and the copious misinformation out there about reverse T3. The bottom line is that complete failure to convert T4 to T3 is not compatible with normal development as a child, and partial failure/reduced conversion is much rarer than the alt med practitioners would have you believe. Of course they claim that someone with hypothyroid “symptoms” is not “converting,” because it allows them to continue tinkering with T3 supplements and other generally unhelpful remedies until the cows come home.
Thanks! I would really appreciate it. It’s one of the newer claims I’ve had a hard time finding detailed information about. I’ve had Hashimoto’s for 40 years, and I read the alt-med thyroid stuff in the 80s and 90s. Fortunately, I never bought into it, even though I dabbled in some other alt-med stuff back then. I recently got sucked back into it when a friend was diagnosed, and I was surprised by how much more bs they’ve added. While most legitimate sites say that routine T3 supplementation is not required, few explain why. There are very few like yours that delve into the quack-mire to try to debunk all the fringe thyroid-related claims in detail.
My friend was panicking about conversion problems. I told her that if someone had a congenital inability to convert T4, they’d probably be mentally and physically stunted, or long dead, if they hadn’t been treated promptly. I developed Hashimoto’s around age 9, but wasn’t diagnosed until almost 14. I had basically stopped growing, and I had other symptoms like the start of precocious puberty at 9, then no puberty. I was 5’2” when I should have been closer to 5’11”. There was nothing vague or mild about it, though it was overlooked as normal late puberty, and my TSH was never tested until I developed a noticeable goiter.
If the alt people are suggesting that inability to convert develops as part of Hashimoto’s for some patients, or it’s its own form of disease, you’d think they’d also be significantly ill in some measurable way, even if it was just partial failure. I’m not even sure exactly what they’re claiming. No surprise that I’ve never gotten clear answers from them. I’ve also read that rT3 is no more than a weak agonist, at best, and the genetic link doesn’t seem to be a big deal. Those who claim they can’t convert should try tripling their dose, and see how they feel then. Ha ha! I seldom notice a change when my TSH gets a little too high, but I definitely feel it when I’m even a little hyper. It feels really good, and really unpleasant at the same time.
I have another question. Does the thyroid shrivel up and die completely over time in some, or all, people with Hashimoto’s? I’ve assumed my thyroid is completely kaput at this point, never had an ultrasound. My levo dose was around 1.00 for about 25 years, then it slowly increased to around 1.75. On average, I’ve been no more than 15 lbs heavier than I was in my 20s, so I don’t think it’s related to my mass. Could the dose increase reflect the destruction of my thyroid? I know some other things can affect dosing. When I quit smoking, I had to increase it, because apparently nicotine has an effect on metabolization of T4, or something like that.
I’m asking partly because T3/NDT is often pushed on people who have had total thyroidectomy, and can’t produce any residual T3 at all. Assuming I have little to no residual production, I am doing remarkably well on just T4, given the alleged horror stories. I was finally able to grow and develop normally, and I’m still basically fine at 50. I’ve had other health issues, including some common ones that can also occur in hypothyroidism, but after 40 years of experience with real thyroid disease, and fluctuations in levels, I know when it’s something else. Hashimoto’s is not that complicated, or debilitating, in almost all cases. Most of the patient claims in the forums don’t reflect rare cases at all. They reflect ignorance, misattribution, or mismanagement, but almost never a true anomaly.
It makes me incredibly angry that they are taking advantage of thyroid patients, and those who don’t even have it. It makes me completely exasperated, and sad for humanity, that anyone still falls for snake oil at all. It seems to have gotten even worse with the internet, and I really appreciate your thoughtful explanations, and your sense of humor. Your site should be in the first page of hits, not buried under all that garbage. It must be incredibly frustrating to deal with it as a doctor. I also survived multiple bilateral PE recently, and no one in those forums is insisting that ct scans are worthless, or pushing homeopathic heparin, or other absurdities. Unfortunately, thyroid disease can be vague enough that it’s ripe for the picking by con artists. 🙁
I agree, thanks!
As for the natural progression of hypothyroidism due to Hashimoto’s, most of these thyroids will atrophy over time, withering down to a small nubbin of mostly nonfunctional tissue. Because this can play out over a long period of time, it is possible to see one’s dose requirement increase, if there is progressive thyroid failure over time. Eventually, when enough of the gland has failed, a person will arrive at a full replacement dose. After that, the dose tends to not change much, as long as one is taking the thyroid hormone the same way all the time.
There are exceptions to that rule, like around the time of menopause, when we sometimes see the dose requirement go down, due to a decrease in estrogen levels, which leads to a decrease in thyroxine binding globulin levels, which leads to more free thyroid hormone in the bloodstream, which leads to a need for less thyroid hormone.
Yeah, I’ll see how menopause changes things. I can’t take any replacement if I need it because of clot risk.
Is there any evidence that not having calcitonin causes any negative effects? I’ve been told that I will suffer some day, or that I’m suffering now but I just don’t know it, because I’m not getting “all the hormones.” Conveniently, all of the so-called symptoms of taking the poison levo for decades are the same as common problems that come with age, and life. A great example is the 70+% of Americans who are overweight or obese. They don’t all have thyroid problems, and not all with Hashimoto’s are overweight. I wouldn’t have grown to be a healthy adult if it didn’t work well in most cases. I know you know that. It just drives me nuts.
To the best of my knowledge, no one has ever shown that calcitonin deficiency is associated with any kind of clinical problem or constellation of symptoms.
I just wanted to stop and say that I was dx’d with Hashimoto’s a few months ago and this blog is a breath of fresh air. With all the nonsense floating around online I’d exiled myself to pubmed to learn about this Illness. While that strategy worked well enough, you’re a whole lot more fun to read!
Thanks for so selflessly kreb’ing(?) your atp on this blog so that we can all save a little.
I really appreciate you taking the time to leave this comment, Buddy. Best of health to you.
If I have not “heard it all” since my Hashimoto’s diagnosis, I’ve almost done. And “it” is nuts! It’s contradictory at best and speculative at worst, or the other way around.
I’ve been so indoctrinated by these blogs and forums that I marched into my diagnosing medical professional (who was, btw, assisting me in the management of my newly diagnosed Type 1 diabetes [onset:age 48] beautifully) suspicious of her intentions and knowledge, demanding T3. She obliged. And we were off to the races!…the ‘downhill’ races, as in: it’s been an overmedicated nightmare in which I dismissed her, found a kindly naturopath who was inclined to let me do my own thing, and my own thing has led me around in circles for nearly two years.
I could never get my head around the idea that conventional medicine was being administered by persons totally devoid of compassion, who are as ignorant about thyroid health as they are unbendingly stuck in “treating by the TSH” (which is touted as the primary evil of unsympathetic endocrinologists everywhere.)
I read mefical journal articles and some ideas began to form, vaguely.
Yours is the most informed, pragmatic, and therefore, best site I have read or seen on this consuming and frustrating dilemma in which I find myself.
I am super grateful it amuses you to expend the energy to pen what is a collection of invaluable writings on the subjects that have preoccupied countless moments of the past two years of my life. Thank you.
Over the months of September and October, I weaned myself off replacement hormones. If nothing else, just for a do over.
Is it your opinion that, in terms of Hashimoto’s, general practitioners and endocrinologists are interchangeable?
Or do you think endocrinologists offer significant advantages?
Again, thank you, thank you, thank you!
Thanks so much for sharing your experience; yours is the exact perspective from which I’d like others to learn. To answer your question, for someone with stable hypothyroidism due to Hashimoto’s, there is usually no advantage to having an Endo involved. For someone with fluctuating levels/symptoms, a good GP can often (but not always) handle it. However, one might get more nuanced advice from an Endo, or at least a more nuanced explanation of the pathophysiology and the interpretation of the blood work. I think there are many patients I follow chronically who could probably have stopped seeing me after 2-3 visits, as I’m not sure how much ongoing value I provide once they’re stable. But I think they become accustomed to having a “specialist” handle the thyroid replacement, so they keep coming back.
After having seen many articles on pubmed relating to ft3/rt3 ratio being a useful tool to diagnose conversion/absorption issues, I necessarily began to believe them due to the source. You have much experience and a certainly believe what you are saying regarding your doubt of their usefulness. Poor medication compliance aside, what in your estimation is a main source of persistent/ worsening symptoms? I have to believe that at least a small portion of your patients can be believed to be fully compliant to the medication/lifestyle you recommend but still have symptoms?
I’d need to see the references you mention, but regardless, check out Everything You Never Needed to Know About Reverse T3 if you haven’t already. It should thoroughly refute the idea that rT3 is useful in clinical practice.
I address your excellent question about persistent symptoms despite good compliance in a number of other posts. I’d recommend reading everything in the “Thyroid” category.
I just got my bloodwork back and rather than TPO antibodies, I was tested for thyroglobulin antibodies. My result was 50, I was told to see a GP doctor and have my thyroid levels and medication checked (I take levothyroxin and liothyronine). The GP said I was fine, but did not test or even see a THS number. I do not really understand thyroglobulin, but I thought I should go see an endocrinologist. I have another disease, achalasia, that is very rare and is believed to be auto-immune/genetic. Then I am told to see a functional medicine doctor, which sounds a little out there when I read about what they do. Also very expensive and not covered by insurance. Arghhh.
I really enjoy reading your articles. I have so many questions by endocrinologist simply doesnt have an answer to. I was diagnosed with hypothyroidism during my first pregnancy. My TSH was low.35, T4 low 9, T3 low 3.3. I was started on levothyroxine, currently 75mcg po od. Now my tsh is .98, t4 15 normal and t3 3.1 still low. I still feel tired, brittle nails, hair falling out, foggy and started on antidepressants. I had an mri brain and it was normal. I dont know why my levels are low. I never had high TSH.
Thank you for your time.
When I ask why I have hypothyroidism I was told by my doctor that he did not know. My antibody test was negative.
Thanks for reading, Tamara. It is my policy to avoid giving individual medical advice. Thank you for understanding.
I understand people who have had their thyroid taken out often have trouble using TSH for dosing. I also understand these folks tend to do better on combination therapy and their TSH will be near 0 (I believe they try to keep their TSH .1-.5 in T4 only replacement also). I’ve seen a lot of studies talking to the issues of folks in this situation. It’s a special case, but it’s one where TSH doesn’t appear to be as useful. I feel for those folks completely without a thyroid.
Let me make it clear that Mike’s statements are his opinions – not facts. I have talked about how some folks with postsurgical hypothyroidism may benefit from combination therapy with a small dose of liothyronine added in, but aggressive TSH suppression is usually reserved for those with a history of thyroid cancer who have some residual risk of recurrence.
Would love a hyperthyroid edition of this topic!
One thing I’m curious about. If a person has had Graves’ disease and then takes RAI, would that change what the treatment would be when they become hypothyroid? I know you’ve mentioned that sometimes combination treatment might be beneficial for those with post surgical hypothyroidism. Would they possibly need t3 supplementation because much or all of their thyroid gland is gone? Should t3 tests be done in this case? I’m hoping you’ll do a hypothyroidism after RAI for Graves disease at some point.
In my experience, most people with postablative hypothyroidism will do fine on levothyroxine alone. However, there is the occasional person who does better with a small dose of liothyronine added in. Whether this is related to one person having more total destruction of thyroid tissue than another person who has less complete destruction is unclear.
Unfortunately, testing T3 levels isn’t helpful to determine who needs T3.
Thanks for your response HD. It’s also good to know that t3 testing won’t help to find out who might find it helpful.
I also wonder if the health of the gut microbiome might affect thyroid health. Could it affect absorption of thyroid medication or conversion of t4-t3? I’m finding the research into the microbiome very interesting and looking forward to reading more.
The gut microbiome is a very interesting field of study, I agree. We have much yet to learn about it, though that has not prevented purveyors of Alt Med from claiming they can test your bacteria levels and help you establish “optimal” levels, whatever that means!
Already? Not surprising I guess. I love the book “Dirt is Good” by Jack Gilbert and Rob Knight. There seems to be a link between autoimmune diseases and microbiome health. It seems like really, just eating lots of veggies and less or no processed foods would be a good start in having a healthy microbiome. Not necessary to pay an Alt Med person to tell you that. :). The science is very interesting. As a person with no medical background, I find the medical studies published online very helpful in learning more. I’m just not always sure which ones are reputable.
Thank you for the information. I appreciate your writing…and it does make me chuckle a little. My question is: Why would my TSH by 3.82 one day, then when tested less than two weeks later, be 6.6? What could account for such a drastic shift? At neither of these test dates was I on any thyroid medication. I saw my doctor for menorrhagia, and was diagnosed with severe anemia. That is what prompted the tests. Thank you.
Reading article after article on your blog. Diagnosed Hashimoto’s with TSH and TPO antibodies. However, all numbers were just over normal ranges. I ate close to AIP (understand the stance on that) didn’t restrict beans mainly no dairy or gluten for about a month or 2 (lost 25lbs from everywhere, weirdly, noticably slimmer ankles and wrists), reduced all relevant labs to within normal range. However, still having symptoms which brought me to the doctor’s in the first place albeit reduced. Tired, low heart rate, moody, not feeling well, achy joints. Never started levo, as I want to avoid a daily medicine I might not be able to procure/afford and the control the hope that diet can cure gives back to you. Wouldn’t taking levo cause you to make less thyroid hormone? Meaning you can never stop taking it? Does reducing all my lab numbers with diet indicate I don’t actually have Hashimoto’s? Should I take the Levo and see if my symptoms improve? Get a referral to an endocrinologist? I’d rather not eat restrictively, I like cheese.
While it’s my policy to not give individual medical advice, I can say that taking a small amount of thyroid hormone when one’s thyroid is functioning will simply result in the thyroid making a little less hormone. That is not a permanent change; if the thyroid hormone is stopped, a healthy thyroid will resume producing hormone regularly.
Now I am rethinking everything I have known . I was diagnosed with hashis due to high thyroglobulin but everything else was normal. My numbers were better back then and have gotten worse since. I’m told I’m severely hypo at a tsh of 4.70. Now I’m even more confused wondering if something else was the problem. I just stopped t3 on my own due to side affects which brought my tsh back up. I’m more confused. Even the new endocrinologist didn’t educate me on any of this.
Thank you for your time💞Had a toxic goiter at age 20, then Rai of course. My levels would fluctuate every lab. Nothing huge every lab just little high little low….20 years or so of this. Had hysterectomy kept ovary in 2019, 2 hernias relate fixed in 2020 and a 3rd with mesh implanted 1 year ago. This year my levels and symptoms have been chaotic. Endo says thyroid has not and does not regrow new cells and no need for surgery. My ENT did a sono and says cells have reproduced/regrown have 2 nodules and lymph nodes are sore. He’s who ran my trab and tpo levels and diagnosed me with hashimotos. Who do I follow as far as the recommendation. Ent and remove again so my levels are easier to manage also riding me of nodules? Or endos advice and keep it. She also doesn’t touch my kneck, is this a good sign ok sign or see another endo? So Sorry for all that but thank you if your able to find time. I should also mention my aunt had hers removed with rai twice so I’m really 😕 confused
So happy to find your site after navigating a lot of garbage. To try to make sure I’m understanding correctly: is the presence of TPO and/or Tg antibodies actually diagnostic of something?
Hi Jessica, I think what you are asking is, “Can we say that a person with elevated TPO Abs has the diagnosis of Hashimoto’s thyroiditis?” Yes, you could say that, but the problem is that it may be meaningless to say that in someone with totally normal thyroid function tests who is trying to figure out what’s going on with them (i.e. why do they have whatever symptoms they have). The Tg Abs are even less helpful, as positive Tg Abs do not make any kind of diagnosis (i.e. I would not label someone with + Tg Abs as having Hashimoto’s). Tg Abs generally should not be checked as part of a workup for vague symptoms.
So, while + TPO Abs could lead to a diagnosis of Hashimoto’s, really what we care about is if the person has thyroid function tests that are either close to abnormal or frankly abnormal, so that we can then consider whether a trial of thyroid hormone is indicated, to see if we can improve their symptoms. If we give thyroid hormone to someone with + TPO Abs, a high-normal TSH, and a low-normal FT4, but they feel no better (despite pushing the TSH low-normal), it becomes increasingly unlikely that the thyroid is what is causing the symptoms. Sure, there are some caveats to that statement, but it mostly holds.
Thank you so much for this quick and thorough reply! That makes so much sense. That brings up a follow-up question – what qualifies as “elevated” TPO Abs? I’ve seen everything from above .5 to above 34 IU/ml. Thanks!
I would use the reference range provided by the Laboratory that runs the test, as there are different reference ranges depending on the actual assay used. Different assays will use very different ranges, but an elevated result is an elevated result. I find it helpful when someone’s TPO Abs are undetectable (below the lower limit of detection of the assay), as I can tell them that it’s highly unlikely they are brewing hypothyroidism. If the Abs are high-normal, it might be worth following that over time, assuming that there are some symptoms, in the context of borderline abnormal TSH/FT4 numbers.
Hope that helps.
Pretty grateful to have found your blog site. Recently dx with hypothyroidism after some blood work revealed my TSH was 32.26. Started to overload with the internet jumbo, ordered a few books that all seemed quite overwhelming…. A few hours later had an entire list of supplements and questions for my endo. Listened to two episodes of docs who lift…. Threw that list right out. Starting with your first posts I shall continue the education process. Now my question is levothyroxine, getting the right dosage… is that the answer to it all? The symptoms, the normalcy,,,,
I sure hope that turns out to be the answer for you. Best of luck Clare.