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.
Unscientific myths about the significance of an isolated low TSH and kneejerk efforts to raise the TSH at all costs are among the most frequent problems noticed by patients who share lab test results and therapy experiences in online support forums.
Many doctors are reducing hypothyroid patients’ thyroid medication doses on the basis of a TSH number alone, which is the opposite of what the expert texts in endocrinology still recommend.
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.
In addition, when doctors do not understand the causes of thyrotoxic symptoms and signs when one or both thyroid hormones are elevated, patients have remained undiagnosed for thyroid disease, antibodies, nodules or tumors. Doctors simply aren’t ordering the relevant tests or performing the physical examinations necessary to clearly discern what is going on.
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.
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