Our medical system has invested so much in the TSH test that we’ve given it authority to override medical discernment about thyrotoxicosis.
The oft-repeated mantras that “TSH is the most sensitive and specific test” and “the only necessary test” have blinded many doctors to the diverse influences that can suppress or inflate TSH secretion.
Many doctors are reducing hypothyroid patients’ thyroid medication doses on the basis of a TSH number alone.
However, this TSH-centric view of thyrotoxicosis is inconsistent with the definition found in the most respected textbook in endocrinology.
Not only is a TSH-only definition of thyrotoxicosis unscientific, it is also harmful to patients on thyroid therapy.
Doctors’ uneducated kneejerk efforts to raise the TSH at the cost of true thyroid hormone health is one of the most frequent problems patients complain about in thyroid patient support groups.
In many cases the doctor’s decision to reduce thyroid hormones is quite shocking, as when the low TSH is directly contradicted by thyroid hormone measurements below reference or in the lower half of reference range. It is grossly anti-biological to make the muffled voice of a lower TSH silence the screams of low T3 levels and hypothyroid symptoms.
Doctors simply aren’t ordering the relevant tests or performing the physical examinations necessary to clearly discern what is going on. TSH alone cannot distinguish between hyperthyroidism, thyrotoxicosis and a falsely oversuppressed TSH, a side effect of thyroid hormone dosing that is not indicative of true thyroid hormone status.
This is causing unnecessary harm and suffering.
To clear things up, I go back to a foundational definition of thyrotoxicosis and advice on its diagnosis from one of the most authoritative textbooks in endocrinology today.
From that starting point, In a series of several posts, I follow their textbook and supplement it with medical research findings about the various factors that can cause thyrotoxicosis and/or manipulate the TSH to behave abnormally in relation to thyroid hormones.
Then it’s necessary to clear up the confusion about the symptoms and signs, some which also appear in both hypothyroidism and thyrotoxicosis. It’s vital to stop the dismissal of symptoms and signs that happens when doctors throw up their hands in frustration with them.
All of these things can help put lab test results in their proper place within the interpretive context of a patient’s clinical history and presentation.
OFFICIAL DEFINITION: THYROTOXICOSIS
The venerated bible of thyroid endocrinology, the massive, 1000-page textbook Werner and Ingbar’s The Thyroid, now in its tenth edition, explains very clearly that the pituitary suppression of TSH is not part of the definition of thyrotoxicosis.
The core definition hasn’t fundamentally changed since the co-editors of the textbook, Braverman and Utiger, explained this fundamental distinction at the opening of Chapter 28, “Introduction to Thyrotoxicosis,” in the 8th edition, year 2000:
“We use the term thyrotoxicosis to mean the clinical syndrome of hypermetabolism that results when the serum concentrations of free thyroxine (T4), free triiodothyronine (T3), or both, are increased. The term hyperthyroidism is used to mean sustained increases in thyroid hormone biosynthesis and secretion by the thyroid gland. Thus, the terms thyrotoxicosis and hyperthyroidism are not synonymous.”
Where is TSH in this definition? Nowhere.
Not only is a low TSH not the cause of thyrotoxicosis, it isn’t even a necessary or sufficient sign worthy of mention in the opening definition. TSH comes in later, when stipulating a distinction between subclinical and overt.
We also learn that thyrotoxicosis also isn’t the same as hyperthyroidism, even though people often use these words interchangeably.
In the 10th and most recent edition, Braverman and Cooper only slightly revised the first sentence of this definition. They clearly thought it was worth repeating and refining:
“We use the term thyrotoxicosis to mean the clinical syndrome of hypermetabolism and hyperactivity that results when the serum concentrations of free thyroxine (T4), free triiodothyronine (T3), or both, are elevated.”
Notice that the health outcome is specified as “the clinical syndrome of hypermetabolism and hyperactivity,” two words that emphasize the physiological response.
The main cause of this syndrome is serum free T4 and/or T3, described either as relatively “increased” in quantity, or as “elevated,” which adds the idea that these hormone levels in blood are above a standard set for normal.
The chapter lists and alludes to situations in which variation in response to an abnormal “elevation” of hormones doesn’t necessarily result in the syndrome of hypermetabolism, such as receptor resistance to thyroid hormone and HCG-inflated T4 levels during pregnancy.
When it does come into the chapter, TSH is always placed alongside both thyroid hormone measurements as a set, and the low TSH is not the main emphasis. Lab tests are secondary to the physical or clinical examination necessary for making a correct diagnosis 1) whether hypermetabolism is actually occurring in the body, and 2) its cause(s). Lab tests are not sufficient data when deciding what action to take, if any.
The TSH in thyroid therapy
The major problem with TSH-only diagnosis is the assumption that TSH behaves the same way and means the same thing in two very different situations:
1) before thyroid therapy begins and
2) during thyroid therapy.
Before therapy begins, the HPT axis is unbroken and functioning normally and without external interference, unless the hypothalamus and pituitary are compromised (central hypothyroidism). Therefore, outside of thyroid therapy, TSH is more likely to be an accurate reflection of thyroid hormone status.
But in the context of thyroid therapy, very paradoxical configurations of TSH, FT3 and FT4 are common, even without central hypothyroidism. Major distortions of the HPT axis are possible.
People with “untreated” and “treated” thyroid disease are two very different populations. The TSH can be misleading if interpreted using the “normo-thyroid” population’s reference range boundaries.
In thyroid therapy, the HPT axis is no longer a “closed feedback loop” working in both directions, both feed-forward to stimulate the thyroid, and biologically-generated thyroid hormone feedback to adjust TSH.
Instead, in thyroid disease and therapy, the HPT axis is a broken, unidirectional “open loop” in which thyroid hormone dosing interferes with natural T4:T3 ratios and levels and even circadian rhythms.
Nature has wired the TSH to respond to many other signals that the metabolic rate requires adjustment. TSH can be falsely oversuppressed by
- TSHR thyroid antibodies that interfere with pituitary TSH feedback,
- hCG hormone in pregnancy,
- other medications,
- other health conditions,
- dieting and fasting,
- exercising too much,
- and even by the effects of thyroid hormone dosing itself.
- (See a fuller explanation in “Targeting TSH? It’s not as specific or as sensitive as people claim.”)
The negative feedback loop on TSH secretion is subject to strong interferences from other biochemical signals besides T4 and T3.
Why wouldn’t TSH reduce when TSH-receptor thyroid antibodies acting on the pituitary make the pituitary think it’s secreting too much TSH? The ultrashort feedback loop that regulates TSH secretion has been known since the 1990s and is even so famous in science as to be named after its discoverers: the “Brokken-Wiersinga-Prummel Loop” (discussed by Dietrich et al, 2012). But do clinicians learn about this and how thyroid antibodies interfere? Unfortunately, no.
In addition, TSH is well acknowledged to be a hormone that amplifies even the most subtle, artificially induced changes in thyroid hormones. Why wouldn’t TSH also amplify the significantly shifted T3:T4 ratios and unnatural fluctuations caused by thyroid therapy plus thyroid disease?
New clinical research in thyroid therapy have proven that “Dosing and disease” can work together to unnaturally manipulate the TSH. In therapy, the main sign of the broken HPT axis is that TSH now has an abnormal relationship to T3, the most powerful and essential thyroid hormone. There’s a clear TSH-T3 disjoint that can become more and more extreme as thyroid tissue is killed or removed and more thyroid hormone must be dosed.
Most frequently, full “thyroid-replacement” doses in LT4 monotherapy can expose underlying handicaps in T4-T3 conversion, causing a low T3 together with an elevated T4, which can singlehandedly suppresses TSH despite the need for more T3 hormone. This is the TSH-T3 disjoint.
Therefore, decreasing the thyroid hormone dose just to increase the TSH can cause or worsen a FT3 deficiency and deepen a patient’s tissue hypothyroidism.
POSTS IN THIS SERIES
Some are yet to be published and will be linked when the links are published.
- Thyrotoxicosis? Many factors can lower TSH
- Thyrotoxicosis: Symptoms and signs
- Thyrotoxicosis can occur with high or normal TSH?
- TSH “can be very misleading” during thyroid therapy, say researchers
- How TSH ultrashort feedback works, and antibody interference
- Pregnancy thyrotoxicosis vs just a low TSH due to HCG hormone