TSHR Antibodies can distort TSH secretion

TSHR-ANTOBIDOESThere’s an underestimated, under-studied TSH feedback loop that almost nobody talks about.

By means of acting on this feedback loop, a thyroid antibody may have a direct effect on TSH secretion as well as our T4 and T3 levels. This antibody is far more prevalent and clinically relevant than many endocrinologists and our health care systems desire to admit.

In Graves’ disease and its lesser-known hypothyroid variant of atrophic thyroiditis (AT), TSH secretion can come under direct interference from two TSH-receptor antibody variants.

I’m not talking about “anti-TSH” antibodies that can interfere with TSH test results in the laboratory. I am talking about the kind of TSH-Receptor (TSHR) antibodies that can interfere with TSH secretion from the pituitary gland itself.

It is possible for Graves’ disease and atrophic thyroiditis antibodies to directly manipulate TSH secretion by interfering with the “ultrashort feedback loop” at the pituitary. Hashimoto’s patients can also have these TSHR antibodies flowing through their veins, as proven in research I cite here.

Scientific research articles and my personal thyroid therapy experience prove that TSHR antibodies can potentially make TSH test results unreasonably discordant with T4 levels.

TSHR antibodies can make TSH misleading when determining the correct dosage and modality of thyroid therapy, whether a patient is on anti-thyroid therapy for hyperthyroidism or thyroid hormone therapy for hypothyroidism.

A person under the influence of these antibodies can be overdosed on anti-thyroid medications, and be either underdosed or overdosed on thyroid hormones, if a doctor trusts their TSH to tell the full story.

Lack of research-based knowledge of the TSHR blocking antibody has led doctors to blame the discordant TSH on rare thyroid conditions. It has even led doctors to blame patients for being noncompliant.

In this mult-section post, I explain to a thyroid doctor and a thyroid patient what these antibodies are, how they can distort TSH in both directions, how prevalent and unpredictable they are, and how they can cause serious failures in diagnosis and therapy.

I bring knowledge from my extensive reviews of research in the area.

I add data from my own thyroid therapy experience and share some lab test results.

I’ll insert various sections of the long post into several Facebook posts over time for those who don’t want to read it all at once.


2Almost everyone who understands the basics of autoimmune thyroid disease knows that Graves’ disease is caused by the dominance of “TSH receptor-stimulating antibodies.”

Basically, the usual sort of Graves antibodies will continue to overstimulate the thyroid gland even after TSH has been fully suppressed by T4, causing very high levels of T4 and T3 hormone oversecretion from the thyroid gland.

However, few people today understand atrophic thyroiditis, which has been occasionally called “hypothyroid Graves’ disease,” “primary myxedema,” or “non-goitrous thyroiditis” or “Ord’s disease.”

In Atrophic thyroiditis, severe hypothyroidism is caused by a variant of Graves’ disease antibodies.

The three types of Graves’ disease TSH-receptor antibodies are

1. Stimulating,

2. Blocking,

3. Cleavage.

TSH receptor-blocking antibodies block TSH action on the thyroid gland, causing hypothyroidism to the degree that they block.

TSH-receptor cleavage antibodies (formerly called neutral antibodies) can cause thyroid cell apoptosis (cell death).

The end result of the blocking and cleavage antibody variants can be an abnormally tiny thyroid gland that is completely fibrosed (replaced by inactive fibrous tissue).

This is the case with my own atrophied thyroid gland, which I like to call my “fibrosed flap of flesh.”

My thyroid gland, first measured at the age of 46, has an approximate 0.5 ml volume, as calculated by two thyroid volume formulas.

According to Carle et al’s study of thyroid volume within autoimmune thyroid disease and in healthy controls, fewer than 1% of all autoimmune thyroid disease patients have a gland this small.

I am virtually thyroidless without a thyroidectomy because of my TSHR antibodies.

When I look back on my lifetime of thyroid symptoms and various health outcomes, I believe I likely had both stimulating and blocking TSHR antibodies fluctuating over time.

But here, I want to focus on the effects of the TSHR antibody on TSH secretion in Graves’ disease and Hashimoto’s, not just on the shrinking, flattening and fibrosis of the thyroid gland in atrophic thyroiditis.



TSH receptors located in the thyroid gland stimulate it to synthesize thyroid hormones.

However, TSH receptors are located all over the human body, not just in thyroid tissue. The biological role of non-thyroidal TSH receptors has not been fully determined.

The pituitary gland has TSH receptors on it as well.

Thyroid scientists have proven the presence of a pituitary TSH-TSH feedback loop called the “ultrashort feedback loop” (see references).

How does this feedback loop work?

Just as we use our sense of hearing to regulate the volume level of our own voices, the pituitary uses its local level of TSH­-receptor activation or inactivation to regulate its level of TSH secretion.

The activity of this ultrashort feedback loop has been most often studied in Graves’ disease patients. After a hyperthyroid person has a thyroidectomy or their gland is permanently damaged by radioiodine treatment, their TSH can remain mysteriously suppressed despite low T3 and T4, which would cause TSH to rise in a normal person.

Cause 1: The pituitary senses TSH receptor stimulation from antibodies and is tricked into thinking that it’s secreting too much TSH in response to thyroid hormone.

Effect 1: The TSH-receptor-overstimulated pituitary reduces or stops its TSH secretion.

By the same mechanism but opposite cause and effect, blocking antibodies can amplify the pituitary “voice” of TSH secretion to unnecessarily high levels given normal or high-normal T3 and/or T4 levels.

Cause 2: The pituitary can’t sense enough TSH receptor stimulation because antibodies are blocking its “ears” (TSH receptors) to its own TSH secretion. The pituitary is tricked into thinking it’s not secreting enough TSH.

Effect 2: The TSH-receptor-blocked pituitary secretes extra TSH.


The three variants of the Graves’ disease antibody (stimulating, blocking, and cleavage) can coexist in the same patient.

One or another variant can dominate over the others over many years or months.

As these antibodies play a game of tug of war, thyroid gland secretion and pituitary TSH secretion are both victims.

Research has shown that TSH levels are often exceedingly high in patients with atrophic thyroiditis at the time of diagnosis. Over time, TSH-receptor antibodies can continue to fluctuate in Graves’ and atrophic thyroiditis, even after the thyroid gland is removed, destroyed, or fully atrophied.

In a person with this type of autoimmune thyroid disease, there is no such thing as an “antibody-ectomy.” Getting rid of the gland does not get rid of the antibodies to the TSH receptor.

For example, I am a case of Atrophic thyroiditis, and my TSH was over 150 at diagnosis. In some patients, TSH can be inflated much higher than that.

During my final three years and 9 lab tests on T4 monotherapy, My TSH fluctuated unreasonably in relation to Free T4 and small dose changes:

2013/08/11 — 112 mcg Synthroid T4
TSH 0.08* (0.20-4.00 mU/L)
Free T4 25.5* (10.0-25.0 pmol/L) *highest FT4

2013/11/25 — 100 mcg Synthroid T4
TSH 18.08* (0.20-4.00 mU/L)
Free T4 17.7 (10.0-25.0 pmol/L) *lowest FT4 at 51% of reference

2014/02/21 — 112 mcg Synthroid T4 * same dose as test 1 when TSH at 0.08
TSH 5.02* (0.20-4.00 mU/L)
Free T4 23.9 (10.0-25.0 pmol/L)

2015/05/20 — 112/125 mcg Synthroid T4 alternate days
TSH 4.66* (0.20-4.00 mU/L)
Free T4 20.9 (10.0-25.0 pmol/L)

2015/11/05 — 112/125 mcg Synthroid T4 alternate days
TSH 3.33 (0.20-4.00 mU/L) – no other tests performed

2015/12/15 — 112/125 mcg Synthroid T4 alternate days (40 days after previous test)
TSH 8.05* (0.20-4.00 mU/L)
Free T4 21.5 (10.0-25.0 pmol/L)

2016/01/29 — 125 mcg Synthroid T4 (dose raised from 112/125 to 125 on January 20)
TSH 3.72 (0.20-4.00 mU/L)
Free T4 21.6 (10.0-25.0 pmol/L)

2016/02/18 — 125 mcg Synthroid T4 (20 days after previous test. Feb 1-4 increased to 137mcg, but chest pains began Feb 1, so lowered back to 125mcg by Feb 5)
TSH 6.17* (0.20-4.00 mU/L)
Free T4 22 (10.0-25.0 pmol/L)

2016/03/21 — 100-112 mcg Synthroid T4. Dose lowered from 125 to 100-112 Feb 20 to March 3 due to day and night random cardiovascular spasms.
TSH 10.27* (0.20-4.00 mU/L)
Free T4 18.3 (10.0-25.0 pmol/L)

TSH ranged between 0.08 and 18.8, even while Free T4 was in the upper half of reference. At the same T4 dose and only -1.6 lower FT4 level about six months apart, my TSH was first suppressed at 0.8 and later elevated at 5.02. With the exception of the single suppressed TSH, I had an abnormally high TSH for this T4 result.

The quick TSH fluctuations are especially illustrated in 2016, when two tests were 20 days apart. TSH increased from 3.72 to 6.17 without a change in dose and a small +0.4 pmol/L increase in Free T4.

Meanwhile, my T3 level was extremely steady at a level just below reference, so TSH was not responding to changes in Free T3. To be specific, in the first four tests, my Total T3 was between 0.9 and 1.0 (1.1-2.8 nmol/L), and in the final four tests, my Free T3 varied between 2.9 and 3.4 (3.5-6.5 pmol/L). (My poor T4-T3 conversion is a subject for another post.)

It is only reasonable to believe, in light of the research, that my TSH level was responding erratically to fluctuating TSH receptor antibody levels, which were not measured, rather than responding in a logical fashion in relation to changes in Free T4 and/or Free T3.



To complicate matters for people with atrophic thyroiditis, it is often incorrectly assumed that they have the usual variety of Hashimoto’s thyroiditis when they become hypothyroid without a thyroidectomy.

However, Atrophic thyroiditis and Graves’ disease antibodies can coexist with elevated Hashimoto’s antibodies (1. thyroid peroxidase antibody, TPOAb, and 2. thyroglobulin antibody, TGAb).

It is possible for a patient to have both Graves’ disease antibodies and Hashimoto’s antibodies at the same time, but of course it is not possible to be clinically hyper- and hypothyroid at the same time.

Within autoimmune thyroid disease, whether a person is hypo, hyper, or euthyroid depends on which antibodies have been dominant over time and how quickly these antibodies can fluctuate and have their effects.

TSHR antibodies in Graves and AT can fluctuate a lot over time. Sometimes the antibodies can disappear and then reappear.

In my own case, I have measurable Hashimoto’s antibodies of both types, but not inflated above reference.

Therefore, I may have Hashimoto’s as well as a variant of Graves’ disease.

My TSH-receptor antibodies were measured only once, after T3 therapy was commenced, and at that time, only the stimulating antibody was selectively measured (it was the TSAb test – the stimulating antibody test is the only TSHR test offered in my region). TSH receptor stimulating antibody was found to be absent (negative).

I have never been measured for TSH-receptor blocking antibodies, but their effect and outcome should be evident to any knowledgeable thyroidologist given the data from my thyroid ultrasound and final three years’ lab test history.


Graves’ disease and atrophic thyroiditis have been misunderstood because of the variability of TSHR autoimmunity.

As the antibody distorts TSH, T3 and T4 levels over time, it can distort medical diagnosis over time.

When TSHR antibodies are present, a remission of hypothyroidism or hyperthyroidism can occur if one of these antibodies temporarily or permanently disappears.

A remission may even be due to a change in diet or supplementation that affects the underlying autoimmune process.

A supposed remission in thyroid disease can also be caused by one or both of these antibodies increasing levels. For example, an imagined remission of either Graves or Hashimoto’s can occur if blocking and stimulating antibodies are relatively equal in effect and cancel each other out, and if there is enough TSH and/or antibody stimulation to enable a healthy level of thyroid secretion.

As long as enough living thyroid tissue is present and can be variably stimulated, blocked, or permanently killed by these TSHR antibodies, a patient’s thyroid hormone status can change unexpectedly.

Even a damaged thyroid with a fragment of active thyroid tissue can begin to hypersecrete under a flare of TSH-stimulating antibodies, and this can lead to euthyroid balance or hyperthyroidism.

The only certainty is that a completely and permanently fibrosed and/or atrophied gland like mine will be incapable of secreting excess thyroid hormone, as Takasu and Matsushita discovered in their 10-year study of patients with TSHR antibodies.

It used to be thought that long term Graves disease merely “burnt out” the thyroid over time by means of continual overstimulation and led to remission or a reduction in anti-thyroid medication. A better explanation is that the blocking and cleavage antibodies have had their effect on thyroid tissue over time.


In the medical literature, a common interpretation of a discordantly high TSH and high-normal Free T4 is resistance to thyroid hormone (RTH).

RTH is a condition in which a certain variant of thyroid hormone receptor is not as sensitive to T3 and requires more T3 than normal to stimulate it.

However, thyroid hormone resistance is relatively rare. It is usually caused by a genetic flaw in the TRAB gene for thyroid hormone receptor beta.

Thyroid hormone resistance does not present with a TSH that can fluctuate significantly with little change in thyroid therapy dose and only a tiny change in FT4 levels. Yet this kind of fluctuation occurred in my case and in a few of my atrophic thyroiditis acquaintances online.

Genetic polymorphisms on receptors are likely to have their effects from birth and are not likely to cause shifting TSH secretion and T4 secretion patterns later in life.



Some thyroid therapy guidelines have offered an easy way out of explaining discordantly high TSH in the presence of normal or high-normal T4: non-compliance with T4 therapy.

This strategy defends the accuracy of the TSH test by blaming the thyroid patient.

The theory goes like this. The patient was likely not taking her T4 medication regularly, which caused the T4 level to reduce and TSH to increase over many weeks. Then, this patient felt guilty about not taking her meds and worried about what her test results would reveal, so she dosed (or overdosed) T4 medication again in the week or few days before the thyroid lab test, which inflated her T4 before her TSH could begin to fall (TSH takes a while to equilibrate to changing T4 levels).

For example, Biondi and Wartofsky’s 2014 guideline document “Treatment with thyroid hormone” has a section VI. B. entirely devoted to this topic.

They suggest that patients may skip doses because they feel dissatisfaction with side effects or the cost of the medication. They also blame psychiatric disorders.

This article calls noncompliance “pseudomalabsorption,” because the only explanation that they can think of for a high TSH and high T4, besides the patient outright lying about compliance, is that the patient is not absorbing their medication.

They say, “Patients who falsely insist that they are being compliant but have thyroid function tests indicating otherwise (pseudomalabsorption) may be investigated further with parenteral infusion of L-T4 (280).”

The “parenteral infusion” they recommend to prove the patient is lying is to overdose a person on 1000-500 mcg of T4 and then testing their blood 2, 4, and 6 hours after a dose. “Published data suggest that a serum FT4 peak at 2 hours rising above the upper limit of the normal range (more than 25 pmol/L) with an increment of more than 20 pmol/L suggests poor adherence to treatment, or pseudomalabsorption in most cases (281–285), but unfortunately, there are no well-established standards for this test.”

The proof suggested here does not involve the TSH decreasing. It involves the T4 rising tremendously, which would be expected if the patient absorbs well, whether they have TSHR blocking antibodies or not.

This mode of proof is similar to the witch trials in the seventeenth century, which involved drowning a woman to see if her body floats or not. They truly have no idea that another reason besides absorption could be the problem.

She’s a liar if she absorbs her meds. If she absorbs, well then, there is no scientific explanation. Either way you save faith in TSH.

Given the challenges of performing such a complicated test that can prove malabsorption, most patients are accused of noncompliance after routine testing.

Merely having a discordant TSH-T4 result can’t prove that noncompliance caused it.

You can’t know for sure, based on a single TSH and FT4 test result, that a thyroid patient was not taking her T4 properly for the previous 6 weeks to 3 months. You also can’t prove that a patient is not taking her thyroid meds if the FT4 level is high enough to show that she has been absorbing T4 hormone, and FT4 results are consistent enough to show she has absorbed at the same rate she normally absorbs it.

This explanation erodes the doctor-patient relationship rather than investigates scientific causes.

The thyroid therapy literature makes it easier to sacrifice trust in a patient’s sanity and honesty than sacrifice faith in TSH.

This theory presumes that a thyroid patient either won’t be troubled by any hypothyroid symptoms caused by forgetting to take her pills, or that her increased hypothyroid suffering will exert no negative feedback on her forgetful behavior.

The theory also presumes a conscious sneakiness or deviousness on the part of the thyroid patient to try to cover up her noncompliance in the days before a test.

How could this theory account for any but the most rare cases of devious and forgetful thyroid patients who don’t mind the suffering they bring on themselves by underdosing and then overdosing, test after test?

Promoting this theory in guidelines contributes to the general impression among doctors that thyroid patients are unstable people who can’t even handle taking their pills once a day.

You can imagine Biondi and Wartofsky shaking their heads or rolling their eyes as they write “The prevalence of noncompliant hypothyroid patients has been reported to be between 30% and 80% despite the simplicity of L-T4 replacement therapy and its once-daily oral administration.”

This insulting belief is confirmed by researchers’ occasional comments on the unacceptable inconvenience and near impossibility of expecting a patient to comply with dosing more than once a day within long term T3-T4 combination therapy.

If we can’t take one T4 pill per day, the theory goes, nobody can expect us to comply with 2 or 3 doses of T3 per day even if we remove hypothyroid symptoms by doing so.

I challenge thyroid researchers to prove that your theory is a plausible explanation for _producing_ the most extreme high TSH – high T4 test results in the first place.

Where are the experimental studies that mimic the hypothesized TSH noncompliance and explain how swiftly a shift from noncompliance back to compliance can affect T3, T4 and most importantly, TSH? How much of a decrease followed by increase in dose is required to create different degrees of TSH-T4 discordance? Have those studies ruled out the presence of TSHR blocking antibodies by measuring them?

Such studies do not yet exist, or they would have been proudly announced and cited in this article and literature that resorts to the insulting patient-noncompliance hypothesis.

If you want to prove such a mistrustful hypothesis, here is an easier way. Why not spring a sudden thyroid test on such a patient? Secretly book a lab test for her, and on the morning of the test day, urge her to immediately get tested. If she is being forgetful or purposefully noncompliant, she might not comply with the order to get suddenly tested. If she does comply with the test, you may well be able to catch her low T4 level in her supposedly noncompliant phase before she tries to be more compliant.

AND … use a TBII test at the same time to rule out the TSHR blocking antibodies.



I am having a hard time understanding the neglect of this research topic given its importance and broad implications.  I am tempted to believe that its revolutionary paradigm-shifting potential is the reason why it’s neglected.

The autoimmune cause of atrophic thyroiditis (AT) has been studied since the 1980s and explained in many articles (see the note at the end of my references).

High TSH has been an object of inquiry for a very long time. But this potential cause of high TSH gets neglected. The strong association between high TSH and atrophic thyroiditis and the known connection between AT and the TSHR blocking antibody should have made this an area of research long ago.

A landmark 2017 study claimed this antibody’s relevance to autoimmune thyroid diagnosis and therapy.

Diana et al’s 2017 article’s title is “Prevalence and clinical relevance of thyroid stimulating hormone receptor-blocking antibodies in autoimmune thyroid disease.”

Their abstract deserves to be inserted here in full.

OBJECTIVE: “The prevalence and clinical relevance of thyroid stimulating hormone (TSH) receptor (TSHR) blocking antibodies (TBAb) in patients with autoimmune thyroid disease (AITD) was investigated.”

METHOD: “Serum TBAb were measured with a reporter gene bioassay using Chinese hamster ovary cells. Blocking activity was defined as percentage inhibition of luciferase expression relative to induction with bovine TSH alone (cut‐off 40% inhibition). All samples were measured for TSHR stimulatory antibody (TSAb) and TSHR binding inhibiting immunoglobulins (TBII).”

RESULTS: “A total of 1079 unselected, consecutive patients with AITD and 302 healthy controls were included. All unselected controls were negative for TBAb and TSAb. In contrast, the prevalence of TBAb‐positive patients with Hashimoto’s thyroiditis and Graves’ disease was 67 of 722 (9.3%) and 15 of 357 (4.2%). Of the 82 TBAb‐positive patients, 39 (48%), 33 (40%) and 10 (12%) were hypothyroid, euthyroid and hyperthyroid, respectively. Ten patients were both TBAb‐ and TSAb‐positive (four hypothyroid, two euthyroid and four hyperthyroid). Thyroid‐associated orbitopathy was present in four of 82 (4.9%) TBAb‐positive patients, with dual TSHR antibody positivity being observed in three. TBAb correlated positively with TBII (r = 0·67, P < 0·001) and negatively with TSAb (r = –0·86, P < 0·05). The percentage of TBII‐positive patients was higher the higher the level of inhibition in the TBAb assay. Of the TBAb‐positive samples with  > 70% inhibition, 87% were TBII‐positive.”

CONCLUSIONS: “Functional TSHR antibodies impact thyroid status. TBAb determination is helpful in the evaluation and management of patients with AITD. The TBAb assay is a relevant and important tool to identify potentially reversible hypothyroidism.”

Studies prior to 2017 have estimated that TSHR blocking antibodies are found in 10% of Hashimoto’s patients, and this large 2017 study confirmed the estimate at 9.3%.

For this very reason, the TSHR blocking antibody at least ought to be an area of research in hypothyroidism, which is far more prevalent in the population than hyperthyroidism.

It is puzzling that this 2017 research article with such strong policy-based conclusions did not create waves. It needs to be re-emphasized in 2019 by a mere atrophic thryoiditis patient with a non-medical PhD.

Since this 2017 study was published in an immunology journal, not an endocrinology journal, will anyone other than me and Dr. Diana’s research team be puzzled by this research gap, lack of dissemination, and lack of impact on thyroid therapy policy?

In my own case, misdiagnosis of my TSHR antibody and misguided therapy contributed to the neglect of my chronic low T3 and my uncontrollable and illogical TSH, and ended in a severe health crisis that drove me to emergency three times. My illness was eventually resolved by my own research and a doctor willing to believe in the evidence.

A TBAb test, or even a TBII test (which Diana et al’s abstract clearly states is consistent with TBAb test results) could have helped put me in a select category consisting of about 9.3% of Hashimoto’s patients and 4.2% of Graves’ patients.

It’s amazing to ponder how many articles discuss the AT variant of Graves’ disease and yet how ignorant our medical systems remain of the existence of atrophic thyroiditis.

If this level of ignorance is so widespread, then how many doctors are ignorant of the cause of spontaneous gland atrophy? how many have never heard of TSHR blocking and cleavage antibodies? how many have never heard of an ultrashort feedback loop? As a result, how many doctors do not have enough knowledge to deduce the clinical implications of TSHR antibodies?

Who, among the research endocrinologists focused on autoimmunity, could not see that thyroid diagnosis and thyroid therapy can be compromised by testing TSH alone and then blaming everything else but TSHR antibodies for a discordant result, when this antibody is such a major candidate for its influence on TSH?

Why has there been such widespread medical ignorance for so long?

It could be because most of the studies of the blocking TSHR antibody have originated outside of the US.  Many studies of AT and the TSHR antibody are from researchers in Japan and Korea. Yet they have published in English and in several major thyroid journals to disseminate their knowledge widely.

It is also puzzling that the ultrashort feedback loop, a theory proven by advanced research in Graves disease, is not discussed in the literature about AT. Acquired atrophic thyroiditis (AT) is known to be a variant of Graves disease, so its antibody variant should engage the same ultrashort feedback loop.

In other words, why wouldn’t anyone who is an expert in this area consider that TSHR autoimmunity could cause of TSH oversecretion if TSHR autoimmunity can cause TSH hyposecretion?

By now we should have had several studies of TSHR blocking antibody levels in the blood of hypothyroid patients containing an excessively high TSH for their T4 level. Someone should be asking this question: Among such patients, what is the prevalence of a positive TBII or TBAb test result?


TSHR blocking and cleavage antibodies are not measured because one of their most noticeable effects, thyroid atrophy, is not measured.

Thyroid atrophy is unnoticed because it is not routine for a doctor to use their hands to physically palpate a thyroid gland in a patient’s neck at diagnosis, and because non-inflamed thyroids don’t get ultrasounds.

In my own case, my former doctors were likely mystified by my high and fluctuating TSH despite high-normal T4. My lab test history shows that they decided to try to keep my FT4 from going over range. While they ignored my high TSH and did not try to lower it even though it was almost always high, when my TSH was suppressed in one test result, they cautioned me about the health risks of low TSH and reduced my dose slightly, which was then followed by a spike in TSH far above reference. Subsequent dose adjustments were unable to control my TSH.

Because of a failure in data collection, my unique autoimmune diagnosis was delayed to the end of 13 years of T4 monotherapy, when I experienced three months of cardiovascular distress after at least three years and 9 test results showing chronic below-reference T3 levels.

I obtained a thyroid ultrasound through a strange series of events. I swiftly got referred for a carotid artery ultrasound when I had unexplained light-headedness during walking and driving and I arrived at my chiropractor’s office in distress with an irregular resting pulse rate and blood pressure measurements. The neck ultrasound showed mixed plaque in my carotid artery. This plaque was an unusual finding for my health status and age, but it could have been due to chronic low T3 and perhaps the lower heart rate, reduced blood flow and high cholesterol that went along with it. I then complained to a different doctor of neck discomfort and a feeling of tightness or swelling, and I couldn’t tell whether it was my thyroid gland or my unexplained cardiovascular symptoms. Then I finally got my first thyroid ultrasound.

It required a patient’s research and initiative to arrive at a correct diagnosis by means of clinically relevant tests. I self-advocated for the testing that resulted in data collection, and I paid for specialists and tests the medical system wouldn’t pay for. Even the many Graves’ disease genetic risk polymorphisms I found in my own analysis of 23andme raw data strengthened the accuracy of a diagnosis of atrophic thyroiditis.



What is the use of medical research if so much of it has been unable to educate the medical system about the TSHR blocking antibody and has been unable to influence testing policy?

What is the use of specialized medical education if it cannot equip endocrinologists to question dogma?

Whenever ignorance supports a religiously defended status quo, it is incredibly difficult to dispel.

Trust in TSH’s accurate response in thyroid therapy is a continually defended and reinforced status quo.

When faced with a mismatch between TSH and thyroid hormones, baseless accusations of a patient’s noncompliance appear rational.

The complex truth of TSH unreliability is very uncomfortable.

When scientific knowledge threatens the dominance of TSH-only testing policy, it is too tempting to dismiss or underestimate its importance, even if the words “clinical relevance” are in the title of an article.

At the level of the individual health practitioner, blind trust in guidelines prevents them from diagnosing their own ignorance.

At a system-wide level, TSHR antibody ignorance works in a similar way as the evidence-discarding and penny-pinching policy of preventing Free T3 and Free T4 testing.

Any data that might undermine trust in TSH-only policy is deemed “unnecessary” data.

It’s a way of hiding all TSH-questioning data.

If thyroid experts in endocrinology really knew what they should know about autoimmune thyroid disease (if they carefully read thyroid research and pondered it), they would be forced to admit the truth.

Failure to use the TBAb or TBII test (TSH binding inhibitory immunoglobulin test) in hypothyroidism perpetuates ignorance about the 9-10% prevalence rate of the TSHR blocking antibody in Hashimoto’s.

TSH is not reliable as a judge of thyroid hormone status in persons with Graves disease antibodies, whether they are euthyroid, hypothyroid, or hyperthyroid.

It takes intellectual courage and moral courage for endocrinologists to stand up and say “we should do something to stop this widespread ignorance. We should stop acting on our past ignorance because we know better.”


Medical guidelines and thyroid pharmaceutical inserts should add blocking and stimulating TSHR antibodies to the LONG list of known health conditions, substances and medications that can make the supposedly “sensitive and specific” TSH test result unreliable and inaccurate.

As I’ve outlined in this post, these antibodies are powerful, complex and unpredictable.

They are present not only in Graves’ disease but also a significant number of hypothyroid people with Hashimoto’s antibodies.

The antibodies mimic and block TSH action wherever TSH receptors are found, including the pituitary gland itself.

Pituitary glands are not wired to respond correctly to T3 and T4 in the presence of TSHR antibodies.

They have the power to deceive even the pituitary gland about how much TSH it’s secreting.

They can distort TSH secretion.

TSH can have a very abnormal relationship to T4 levels over time, as I’ve illustrated here by my own lab test history.

These antibodies add one more reason to encourage measurement of Free T3 and Free T4 to optimize thyroid therapy.

If you want to know what the patient’s thyroid hormone status is, you need to directly measure both thyroid hormones, not just trust in the response of TSH.

Thyroid patients are painfully waiting for endocrinologists to move forward with moral and intellectual courage.

Study and ponder your own research publications.

Disseminate your hard-earned knowledge of the TSHR antibody.

Inform doctors that a significantly shrunken thyroid gland, not shrunken since birth and not caused by surgery, is a clear sign that TSHR blocking and cleavage antibodies have had their inevitable effect on the thyroid gland.

Teach them about the ultrashort feedback loop on TSH secretion and how two types of TSHR antibody can interfere with it.

Use your scientific knowledge to inform clinical practice guidelines.

Resist the blind policies that forbid full thyroid hormone testing and antibody testing.

These are the policies that make accurate thyroid diagnosis elusive and standard therapy misguided and ineffective in thyroid patients like me.

  • Tania S. Smith


Biondi, Bernadette, & Wartofsky, L. (2014b). Treatment with thyroid hormone. Endocrine Reviews, 35(3), 433. https://doi.org/doi: 10.1210/er.2013-1083

And three further subsections:


Kakita, T., & Odell, W. D. (1986). Pituitary gland: one site of ultrashort-feedback regulation for control of thyrotropin. The American Journal of Physiology, 250(2 Pt 1), E121-124. https://doi.org/10.1152/ajpendo.1986.250.2.E121

Toni, R., Jackson, I. M., & Lechan, R. M. (1990). Thyrotropin-releasing-hormone-immunoreactive innervation of thyrotropin-releasing-hormone-tuberoinfundibular neurons in rat hypothalamus: anatomical basis to suggest ultrashort feedback regulation. Neuroendocrinology, 52(5), 422–428. https://doi.org/10.1159/000125623

DIETRICH, J. W., TESCHE, A., PICKARDT, C. R., & MITZDORF, U. (2004). Thyrotropic Feedback Control: Evidence for an Additional Ultrashort Feedback Loop from Fractal Analysis. Cybernetics and Systems, 35(4), 315–331. https://doi.org/10.1080/01969720490443354

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Kumar, S., Iyer, S., Bauer, H., Coenen, M., & Bahn, R. S. (2012). A Stimulatory Thyrotropin Receptor Antibody Enhances Hyaluronic Acid Synthesis in Graves’ Orbital Fibroblasts: Inhibition by an IGF-I Receptor Blocking Antibody. The Journal of Clinical Endocrinology & Metabolism, 97(5), 1681–1687. https://doi.org/10.1210/jc.2011-2890

Kung, A. W., Lau, K. S., & Kohn, L. D. (2001). Epitope mapping of tsh receptor-blocking antibodies in Graves’ disease that appear during pregnancy. The Journal of Clinical Endocrinology and Metabolism, 86(8), 3647–3653. https://doi.org/10.1210/jcem.86.8.7704

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NOTE: In general, I have drawn on my wider reading on Graves’ autoimmunity and Atrophic Thyroiditis. See my larger Atrophic Thyroiditis bibliography. It’s a Google Sheet linked to an earlier post on Thyroidpatients.ca — BIBLIO: Atrophic Thyroiditis

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