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 logarithmic 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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