TSH and T4: Useful or Useless?


It’s unfortunate that in the traditional medical community, physicians believe and typically only use TSH, sometimes with T4 thrown in, as a measure of “thyroid health”.  On the other hand, directly opposing this belief, there are some in the alternative/holistic health community that will say that TSH is totally useless as an indication of thyroid health status, with Total T4 not far behind.  So which is it?

The answer is, of course:  both.  How can this be?

If you are unfamiliar with what TSH (Thyroid Stimulating Hormone) is, look it up to learn more about it.  For my purposes here, the two things to know about TSH are that 1) TSH is like a “signal” that stimulates the thyroid cells to produce more thyroid hormones, and 2) it has a very short half life.  Remember when I talked about half-lives  here (Half Lives of T3/T4)?  Well, TSH has a half life of about 30-60 minutes.  This means it’s a rather rapid acting hormone, and it’s in and out of your circulation pretty quickly.  This means that if you measured your blood TSH every hour for a day, you could conceivably get different numbers with every measurement.  In fact, TSH can increase and decrease quite dramatically, quite quickly.  So why do physicians use TSH as a measure of thyroid health if these wild fluctuations can occur?

Before going any farther, let’s take a detour.  I’d like to use a rather simple analogy that I always think of when trying to describe how the thyroid axis works.  Most people have a thermostat in their home, and are somewhat familiar with how it works.  Let’s say I have the thermostat in my house set to 70° F, and then set this to an “automatic” function.  This means that if my house gets colder than 70°, the heat will automatically turn on.  On the other hand, if my house warms up to 70° or warmer, the heat will automatically shut off.  By using the automatic function on my thermostat, I don’t have to constantly worry about the house getting too cold or too warm.  I don’t have to do any manual adjustments or turn the heat on and off every time there’s a temperature change; the automatic function on the thermostat takes care of that for me.  For the most part, it should stay around 70° at all times in my house, without me doing anything.  In other words, the thermostat is like a “signal switch”, helping to provide temperature stability or “homeostasis” in my house, regardless of the weather outside.

The thermostat has to react fairly quickly to temperature changes in the house.  For example, if the temperature suddenly plummets to below zero outside due to a sudden winter storm, my house will start getting colder than 70° pretty quickly.  I want my automatic thermostat to pick up on that right away, and start turning on the heat.  I don’t want my thermostat to react two weeks from now (by then I’d be frozen to death).  So there’s got to be some kind of programmed response such as “If the temperature goes below 70° for ½ hour or more, turn on the heat”.  And once the temperature increases to 70° or above, I want the thermostat to turn off the heat pretty quickly too, so my house doesn’t end up at 120° –which actually happened to me once.  It was below zero outside, the thermostat broke, and the heater kept running and never shut off, and we were roasting in the house on the coldest day of the year.

This is a lot like what happens in our bodies when it comes to thyroid hormone homeostasis. TSH is like the “signal switch” (thermostat) to “turn on” the thyroid gland (the heat).  Too little heat, you’re going to get cold (hypothyroid), and too much heat, you’re going to get too hot (hyperthyroid).  Your body wants and needs to stay at the same internal temperature no matter what the weather is outside, and TSH is part of the “thermostat” to help maintain that.  TSH needs to have a short half life, because it is like the “signal switch” on our thermostat.  It has to react right away, and then stop reacting, or dissipate from the bloodstream, pretty quickly after that.  You want the right amount of TSH around just long enough to provide the thyroid hormones you need when you need them – and not any longer.  This is why TSH has a short half life.  If too much TSH stayed in the blood stream for too long, your thyroid gland cells would keep on producing thyroid hormones, and you might become hyperthyroid.  On the other hand, if TSH didn’t respond right away once thyroid hormones started getting low, you wouldn’t get the thyroid hormone you need when you need it.

TSH is the “signal” or stimulus to thyroid cells to produce more thyroid hormones.  But the level of thyroid hormones in your body influence TSH production.  This is called a “negative feedback system”.  The thermostat in your house works the same way. The thermostat provides the signal to turn on the heat.  And the temperature in your house (the heat) determines if and when the thermostat turns on and off.   This is why when you are low on thyroid hormones, TSH starts increasing, to increase the signal to the thyroid gland to start producing more hormones.  And if you are too high on thyroid hormones, then TSH decreases, to lower the signal, because you don’t need the gland to produce any more thyroid hormone.  When a person goes to the doctor and finds out that their TSH is really high – like 68, or 120 (and yes, it can get that high and higher), this means that their thyroid gland is really struggling and needs a stronger and stronger “signal” (TSH) to attempt to produce the hormone that’s needed.  It’s like the thermostat keeps clicking on, trying to get a failing furnace to work harder to put out the heat that’s needed to maintain the temperature in your house at 70 degrees.

So, let’s get back to the basic question of:  When is TSH a useful and valid measurement, and when is it not?

TSH is actually responsive to a number of different things, not just thyroid hormones.  With its very short half life, TSH is very sensitive and has the capability of fluctuating rapidly and dramatically.  Yet, for the most part, in people with healthy thyroid axes, TSH remains fairly stable, usually changing only 1-2 units or less throughout the day in a gentle diurnal rhythm.  Why is this?

Enter T4 hormone, more specifically, Total T4.  TSH is influenced by T3 and a number of other factors, but T4 in the blood stream is one of the biggest influences of all on TSH production.  T4 is the great “stabilizer”, or “buffer” of TSH.   Having a steady level of T4 in your bloodstream really helps to keep a steady level of TSH . . . and this steady level of TSH helps keep the steady level of T4.   Having enough T4 in your bloodstream is kind of like living on the equator, where the temperature pretty much stays around 70° all the time . .  and your thermostat doesn’t have to turn and off very often either.  This “negative feedback loop” occurs not only with thyroid hormones, but with other hormones and some neurotransmitters and even some receptors.  At any rate, it is T4 that has one of the biggest influences on TSH.  Why is this?  Again, it’s all about half-lives.  If you remember, T4 has a very long half life – about 7-10 days in most people.  It takes a “long time” for T4 to decrease – or increase – in the body.  Remember, if your thyroid gland 100% stopped working today, for most of us, it would be 7-10 days before we’d notice the change in T4, and this change wouldn’t become dire until about 3-6 weeks post.  And as T4 slowly decreased, TSH would correspondingly slowly increase in an attempt to correct the problem.  There are a lot of mechanisms contributing to the long half life of T4, which are beyond the scope of this document.  But the point is, this longer half life of T4 is part of the “homeostasis” mechanism the body uses to make sure that we always have a supply of thyroid hormone (T4) in the body, and that drastic fluctuations or changes don’t occur.  This is part of the reason T4 is often called the “storage thyroid hormone”.   By making TSH more dependent on T4 levels than anything else, nature made sure that wild fluctuations in TSH wouldn’t be occurring.  The TSH-T4 negative feedback loop is actually a beautifully efficient way to help ensure that T4 (which is the source of most T3 as well as the other iodothyronines and free iodine) is available to us at all times and won’t experience extreme fluctuations in thyroid hormones.

What about T3?  Does T3 also influence TSH?  The answer is:  yes.  Not as much as T4, but it will also influence TSH in its own negative feedback loop with it.  Remember, the half life of T3 is fairly short – 4-6 hours for most people.  So, for example, for people who are ONLY taking T3 medication – and NO T4 – TSH will fluctuate a lot more because it will essentially be dependent on T3 serum levels in this case.  This is because of that “T3 wobble” I talked about earlier.  When the person first takes T3, TSH will be driven down pretty quickly.  As T3 metabolizes off starting at about 4-6 hours, TSH will increase accordingly.  By the end of 24 hours, if the person doesn’t take any more T3 medication, AND there’s NO T4 in the bloodstream, TSH could be quite high.  This is something to be aware of for people who take T3-only.  This is an excellent example of when lab testing of TSH will NOT be useful at all for monitoring thyroid hormone status.  TSH will be fluctuating all day long, increasing and decreasing fairly rapidly and dramatically, with each dose of T3 medication taken.  It will all depend on when the person took their last dose, along with how they metabolize T3, as to what the TSH lab measurement may be.  A good website describing a T3-only protocol is Paul Robinson’s “Recovering with T3“.     The author of this website published several of his lab values while on T3-only, showing the wide variety of TSH values one can get while on T3-only medication.

What about iodine?  Does iodine also influence TSH?  The answer is:  yes.  It’s been a while since I reviewed the mechanisms of iodine metabolism, so I may be mistaken about this, but, to the best of my memory, there is no “negative feedback loop” mechanism between iodine and TSH.  So higher iodine does not mean lower TSH, and vice versa.  However, for many people, taking iodine will increase TSH.  This is because iodine is a necessary “ingredient” in the production of thyroid hormones, and when this “precursor ingredient” increases in the bloodstream, TSH will then increase, to tell the thyroid gland that “it’s time to start producing more thyroid hormone because we’ve got more iodine coming in”.  This is particularly true for people who were low on iodine to begin with, and their thyroid gland needed to “replenish the storehouse” so to speak.  So in general, increasing iodine will increase TSH in some people, if not all people.  So here is another example of when TSH might not be the best indicator of overall thyroid status, since fluctuating levels of iodine alone can influence it.

What else can influence TSH?  Well, it turns out a really big factor can be anti-thyroid antibodiesAnyone who has any of these antibodies potentially has a TSH that is fluctuating due to these antibodies, either directly or indirectly.  In some people (like me), these antibodies are acting antagonistically, and it’s all out war for “control of TSH”.  For example, the TSI (Thyroid Stimulating Immunoglobulin) antibodies mimic TSH, causing the thyroid gland to produced more thyroid hormone, and in extreme cases, hyperthyroidism.  On the other hand, the TBII (Thyrotropin Binding Inhibitory Immunoglobulin), or “blocking antibodies” cause the opposite to occur (tell the thyroid gland to produce less thyroid hormone), and in extreme cases, hypothyroidism.  TPO (Thyroid Peroxidase) and TG (Thyroglobulin) antibodies prevent thyroid hormone formation from occurring, which means less thyroid hormone being produced (thereby driving TSH up).  On the other hand, these two antibodies actually attack the thyroid gland itself, destroying the follicular structure and spewing out the T4/T3 contents into the bloodstream as long as the attack occurs, increasing the levels of these hormones dramatically during “flares” (thereby driving TSH down).  Are you confused yet?  Well so is your TSH, if you’ve got these antibodies.  It’s being pulled every which way, with no consistency.    Anti-Na+/I− symporter antibodies are a more recent discovery of possible thyroid autoantibodies.  It’s not clear what their role is yet, but it’s a pretty good guess they are playing a role in all this as well, if for no other reason than probably influencing iodine metabolism.  In addition, I suspect there are probably any number of other autoantibodies when it comes to the thyroid system, that have yet to be discovered.  TSH, as sensitive a “thermostat” as it is to all of this, can be swinging wildly depending on the type and severity of the onslaught occurring.  Instead of the nice, slow steady homeostasis that should be occurring due to a steady level of T4 in the blood stream, TSH is all over the place, due to T3 flaring and antibodies – regardless of steady serum levels of T4.

This includes TSH being in the “normal” range as it swings from one extreme to the other.   In other words, if you get a “normal” TSH value, is it because your thyroid axis really is working perfectly?   Or is it because at that one moment in time you just happened to have tested while TSH is “on the way down” or “on the way up”?  Indeed, it was this “swinging” in TSH values that were my first clue that something was amiss.   My TSH was swinging in and out of range, going as high as 12 and then back down to in the 3’s again.   Although these values aren’t considered that extreme by most traditional physicians, I had to question them for myself, which is what prompted me to test for the antibodies.

All this internal turmoil with fluctuating thyroid hormones, in particular, T3, can create an emotional roller coaster of unbelievable proportions as well.  Never underestimate the emotional ramifications of AITD.  The whole negative feedback system of TSH and thyroid hormones is designed to create a very controlled steady state of thyroid hormones throughout every cell of the body, including the CNS.  When this homeostasis is disrupted, all hell can break loose.  There are peer reviewed traditional research studies associating AITD with Bipolar Disorder, Schizoprenia, Parkinson’s, and with severe symptoms such as mania, catatonia, depersonalization, depression, hallucinations, paranoia, suicidal and homicidal ideation, seizures, and just about any other mental illness condition you can think of.  In my own case, I could always tell when antibody flaring was going on for a number of reasons, one of them being that I could feel my emotions being buffeted around instantaneously along with all my other CNS symptoms.  For some reason, I always pictured antibodies dive bombing my thyroid gland, or popping on and off receptors like ball valves, flooding my cells and mitochondria with T3 or depriving them of it instantaneously, on top of their effect on the pituitary gland and TSH.  I strongly suspected that these antibodies, or ones as yet unidentified or discovered, were playing some kinds of roles beyond that just of affecting TSH, literally affecting individual non-thyroidal cellular homeostasis as well – especially within the CNS.  An example of this is Hashimoto’s Encephalopathy (HE), an extreme encephalopathy that occurs in correlation with high TPO antibody titers.  The symptoms, along with these high antibody titers, are considered diagnostic for HE, although it’s not known what role, if any, these antibodies actually play in causing these extreme symptoms.  There is a relapsing nature to HE, and symptoms can be as extreme as (from WIKI):  personality changes, aggression, delusional behavior, concentration and memory problems, coma, disorientation, headaches, jerks in the muscles (myoclonus – 65% cases), lack of coordination (ataxia – 65% cases), partial paralysis on the right side, psychosis, seizures (60% cases), sleep abnormalities (55% cases), speech problems (transient aphasia – 80% cases), status epilepticus (20% cases), and tremors (80% cases).  HE is another one of those conditions considered very rare, but is being diagnosed with increasing frequency now that physicians are thinking to look for it.  I don’t have the extremely high antibody titers required for a diagnosis for HE, but I have a fairly elevated antibody titer none the less, and I suspect these were contributing greatly to my CNS and other systemic symptoms.  My right side was more affected than my left with my “head symptoms”, and I’ve always suspected that what I’ve been experiencing is a “milder” form of HE (which is hell despite being a “mild” case).

The antibodies for Grave’s disease can be every bit as damaging as the Hashi’s antibodies to one’s psychological state.  In addition to the typical symptoms of insomnia, hand and muscle tremors, hyperactivity, hair loss, excessive sweating, shaking hands, itching, heat intolerance, weight loss despite increased appetite, diarrhea, frequent defecation, palpitations, muscle weakness, skin warmth and moistness, cardiac arrythmias such as sinus tachycardia, atrial fibrillation, and premature ventricular contractions, hypertension and more, people with hyperthyroidism may experience behavioral and personality changes including: psychosis, mania, anxiety, hallucinations, paranoia, nymphomania, agitation, depression, and more.  Grave’s disease is also associated with painful bulging eyes; whenever I see these homicidal mass gun shooters on the news any more, with their wide eyes bugging out, I always wonder now if hyperthyroidism is one of their many problems and something that should be on the differential list of things to check out. Please note that I’m not trying to say that anyone with Grave’s Disease will become a homicidal mass shooter – it’s highly unlikely — just that autoimmune hyperthyroidism should be on the long list of additional things to look for in this population on top of their most likely many other mental health problems.  One of the mechanisms of action of Lithium medication, by the way, is to decrease T3 levels.

This is why, in my opinion, everyone who is having their “thyroid tested”, whether they are on thyroid hormone replacement medication or not should have the antibody tests done along with a TSH.  Indeed, I think the antibody tests are essentially more important than TSH, because if any of these antibodies exist, then TSH cannot be used as a reliable screen for “thyroid health”.  For people with the anti-thyroid antibodies, 95% of the time, this will be indicated with a simple blood test.  Those are pretty good odds for finding out if you’ve got some kind of abnormal thyroid pathology going on.  There is a small chance, about 5%, that a person can have antibodies destroying the thyroid gland, but it doesn’t show up in typical blood work.  I remember my endocrinologist telling me about doing a thyroidectomy on a patient, and the thyroid gland was completely infiltrated with non-functional immune cells, even though the patient was sero-negative for all antibodies (no antibodies in the blood stream).  So it does happen.  However, a simple blood test that will catch this type of autoimmunity 95% of the time seems like pretty good odds to me, and well worth the testing.  And again, because of the antagonistic mechanisms of the TSI and TBII antibodies (sometimes called TrAb), they are every bit as important as the anti-TPO/TG tests.   I think this is important to test for during the acute phase of being floxed, because I think there might be “hyperthyroid flaring” going on during the acute phase in some people who are floxed (such as myself).  These flares can eventually burn themselves out into hypothyroidism, or simply correct themselves over time with good supportive care if the thyroid gland and axis aren’t too damaged to begin with.  So I think it’s worth testing and monitoring for a couple of years after being floxed, just to get an internal picture of what’s happening over time.  I think it’s also important to continually monitor antibody status once on thyroid hormone replacement medication too – something virtually all physicians, alternative or traditional, don’t do.   Contrary to popular belief, I found my own antibody status to fluctuate consistently and predictively (when I used the same lab for measurements), and I think there’s more to be gained by longer term monitoring than is currently recognized or acknowledged.

I’ve given a number of scenarios when TSH isn’t a reliable screen of “thyroid health”.  So when is it a valid test?  Well, if a person does not have any of the currently known and clinically recognized antibodies, and there’s no “flaring” going on as a result, then presumably TSH is a good indicator of thyroid hormone levels, most notably, T4.  Without flaring, serum T3 tends to be more stable as well.  But traditional physicians still don’t like to use T3 as an indicator of anything simply because of its short half life, and there’s no doubt that it can fluctuate quite a bit throughout the day compared to T4.

However, having said the above, there are still yet even more reasons to question using single point TSH tests as any kind of reliable screen of “thyroid health”.   The following information was taken from the updated Screening for Thyroid Dysfunction: U.S. Preventive Services Task Force Clinical Guidelines.   Note that this information is coming from the US Government and the traditional medical establishment (about as mainstream as you can get), and not the alternative or holistic faction:

“When used to confirm clinically suspected thyroid disease in patients referred to an endocrinologist, the serum TSH test has a sensitivity of about 98% and a specificity of about 92% .  However, its accuracy is more challenging to ascertain when it is used to screen asymptomatic persons for thyroid dysfunction, for several reasons. First, there is no consensus on the appropriate TSH cutoff for a diagnosis of subclinical hypothyroidism or hyperthyroidism . . .  Second, TSH secretion varies among different subpopulations, such as those defined by race/ethnicity, sex, and age . . . Third, TSH secretion is highly sensitive to factors other than thyroid disorders. For example, serum TSH is frequently suppressed during phases of acute illness.  Levels of TSH may also be affected by the administration of drugs or substances, such as iodine, dopamine, glucocorticoids, octreotide, or bexarotene. Adrenal insufficiency, pregnancy (particularly during the first trimester), anorexia nervosa, certain autoimmune diseases, and pituitary adenomas can also interfere with normal circulating levels of TSH . . . Fourth, serum TSH levels can vary by as much as 50% of mean values on a day-to-day basis, with up to 40% variation of values obtained from serial TSH measurements performed at the same time of day . . . All of this confirms the importance of not relying on a single TSH value to establish a diagnosis of thyroid dysfunction. Serial TSH measurements are an essential step in establishing that a thyroid disorder is real and persistent.”

I think the whole point here is that even the US government is saying that doing one TSH test a year isn’t going to catch much of anything.  They are using this information to argue against screening in asymptomatic healthy adults.  Unfortunately, one TSH test is usually all you’re going to get if you are highly symptomatic, and that will be used as a definitive diagnosis of “thyroid health” as a result.    If you’re going to use TSH alone as a screening or monitoring tool in symptomatic patients, then the least that needs to happen is multiple serial TSH measurements over time.


To summarize when TSH is not a valid screen of “thyroid health”:

  1. Any thyroid hormone flaring will cause T4, and especially T3 to fluctuate – thereby causing TSH to fluctuate as a result. Flaring can be the result of autoimmune flares, as described above. It can also be the result of some thyroid nodule cells, or thyroid cancer cells – these cells tend to spit out thyroid hormone randomly, whenever they want, however much they want. These cells don’t “listen” to TSH or respond to the negative feedback system. However, TSH does respond to the fluctuating levels of T4/T3 these cells produce. Flaring can be longer term, over weeks or months – or literally occur multiple times daily.
  1. All the clinically known and tested for antibodies, such as TPO, TgAb, TSI, TrAb, and TBII can cause both longer and shorter term fluctuations in TSH.
  1. The amount of iodine ingestion can affect TSH. Increasing iodine in general will increase TSH.    Increasing amounts of iodine may also increase TPO antibodies in people with Hashi’s, which may then influence TSH.
  1. I haven’t discussed this above, but TSH is actually produced by the pituitary gland in the brain. If the pituitary gland is not working well, then TSH production might suffer – regardless of thyroid hormone status. Having a chronically low TSH along with low T3/T4 may be an indication of this – or, it could be anti-thyroid antibodies as well.


To summarize when TSH is a reliable screen for “thyroid health”:

  1. When you are asymptomatic, there are no anti-thyroid antibodies, no autonomously functioning nodules or thyroid cancer, and the overall HPT axis is working well or you are on stable dose of thyroid hormone replacement medication. TSH can then be used as a monitoring tool. However, you won’t know this unless or until you check your antibody status first, along with a full thyroid panel for TSH, T4, and T3.




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