The loss of thyroid clinical knowledge from Werner & Ingbar’s The Thyroid

The loss of thyroid clinical knowledge

Decades ago, a lot more doctors knew how thyroid hormone levels influenced all organs and tissues’ health.

It wasn’t all about the influence of thyroid hormones on the TSH.

It was more about the influence of truly adequate thyroid hormone levels on real health outcomes.

A lot more doctors learned and understood that if thyroid hormone levels were deficient or in excess, they would contribute to pathology in any or many organs and tissues across the human body.

They not only learned what to look for, but they understood some of the molecular biology behind the causes of thyroid symptoms and signs.

They knew how these hormones functioned to support body-wide human health.

As a result of this broad understanding, physicians who treated thyroid disease used to be far more attuned to the overall clinical presentation of their patients.

They used their deep knowledge of body-wide effects of thyroid hormone to assess whether a treated patient’s thyroid dosage or thyroid therapy modality was sufficient to achieve true euthyroidism, but not excessive enough to lead to thyrotoxicosis.

What has happened to this essential thyroid therapy knowledge?

It has been narrowed down into a mere superficial summary plus a few fragments.

Over the decades, doctors and endocrinologists have lost their deep and broad understanding of “the clinical manifestations” of thyroid hormone insufficiency and excess.

Today, the average doctor that treats thyroid disease hardly knows what real thyrotoxicosis looks like in a human body. They are told it exists whenever a TSH is low, so they gullibly believe it.

They also can’t recognize hypothyroidism when they see it, because either they don’t know what to look for, or a low or normal TSH number blinds them to it.

You can see this narrowing of thyroid knowledge in the changes in a key textbook, Werner & Ingbar’s The Thyroid, a major “bible” of clinical endocrinology, from 1986 to 2013.


In the 5th edition (1986) through 7th edition (1996), this textbook used to cover the effects of thyrotoxicosis in 17 different chapters on different systems or manifestations.

A parallel section on hypothyroidism had an equal number of chapters, 17, on exactly parallel topics.

Here’s the list of contents on hypothyroidism from the 7th edition in 1996:

7th edition chapter # SECTION C: Organ system manifestations of hypothyroidism
60 The skin in hypothyroidism
61 Connective tissue in hypothryoidism
62 The cardiovascular system in hypothyroidism
63 The respiratory system in hypothyroidism
64 The kidneys and electrolyte metabolism in hypothyroidism
65 The gastrointestinal tract and liver in hypothyroidism
66 The blood in hypothyroidism
67 The neuromuscular system and brain in hypothyroidism
68 The pituitary in hypothyroidism
69 The adrenal cortex in hypothyroidism
70 Catecholamines and the sympathoadrenal system in hypothyroidism
71 The male and female reproductive system in hypothyroidism
72 The skeletal system in hypothyroidism
73a Metabolic changes in hypothyroidism
73b Vitamin metabolism in hypothyroidism
74 Behavioral and psychiatric aspects of hypothyroidism
75 Myxdema Coma

In the 5th edition, these same “organ and systems manifestations” chapters covered these pages:

  • Thryotoxicosis, 17 chapters: p. 811 to 982 (171 pages)
  • Hypothyroidism, 17 chapters: p. 1125 to 1235 (110 pages)

Over the years, these sections were whittled down, and most of them are now gone.

In the year 2000, the 8th edition, they removed “Connective tissue” and “Vitamin metabolism.”

In the year 2005, the 9th edition, they removed “Metabolic changes.”

But the most recent edition in 2013, the 10th edition, view of thyroid hormone effects across the human body is much more narrow.
The 10th edition (2013) now only covers 6 systems or manifestations of thyrotoxicosis and an overview chapter. The parallel section called “Organ system manifestations of hypothyroidism” was also narrowed down from 17 chapters to 5 chapters plus a new overview chapter.

10th edition chapter # PART B: Organ system manifestations of hypothyroidism
39 [New chapter added]: Overview of the clinical manifestations of thyrotoxicosis
[Removed: Skin]
[Removed: Connective tissue]
40 The cardiovascular system in hypothyroidism
[Removed: Respiratory system]
[Removed: Kidneys and electrolyte metabolism]
[Removed: Gastrointestinal tract]
[Removed: Blood]
[Removed: Neuromuscular]
[Removed: Pituitary]
[Removed: Adrenal cortex]
[Removed: Catecholamines]
41 The male and female reproductive system in hypothyroidism
42 The skeletal system in hypothyroidism
[Removed: Metabolic changes]
[Removed: Vitamin metabolism]
43 Psychiatric and cognitive effects of hypothyroidism
44 Myxdema Coma

In the 10th edition, this is the coverage of this section:

  • Thyrotoxicosis, 6 chapters + overview: p. 434-486, (53 pages). 31% of the 5th edition’s section.
  • Hypothyroidism, 5 chapters + overview: p. 569-605, (37 pages). 32% of the 5th edition’s section.

The new overview chapter they’ve added provides very succinct summaries, such as a single paragraph on the muscoskeletal system that merely lists common conditions and provides citations.

The overview chapter lacks all detailed discussion of the cellular mechanisms by which these effects are achieved.

It rarely names any specific biomarkers for the pathologies — perhaps to discourage their measurement.

The chapter is sprinkled with happy stories about the magical disappearance of these symptoms and signs with proper therapy. For example, the discussion of hematology (blood disorders) ends with the vague sentence “The hematologic and hemostatic abnormalities described above all tend to resolve with adequate thyroid hormone replacement therapy.”

Hm, how do they judge adequate thyroid hormone replacement in 2013?

The introduction to this chapter defines hypothyroidism superficially as an elevated TSH and low T4, and the chapter NEVER mentions the T3 hormone.

It appears that the widespread belief is that no one on thyroid therapy with a normalized TSH is going to experience any of these symptoms and signs, and if they do, it can’t be due to their thyroid hormone levels, least of all their T3.

Such statements basically turn our very real hypothyroid effects during thyroid therapy into imaginary, impossible, or irrelevant phenomena.

They have disassociated the health effects from our supply of T3 hormone in blood and tissues. They did this in the very chapter that should have connected them.


We also know that the converse is also true — chronic or critical illness in one or more organs in the body can trigger profound dysfunction in thyroid hormone metabolism and action, even if it does not damage the thyroid gland itself.

This is the lesson of Low T3 Syndrome, now more commonly termed “nonthyroidal illness syndrome” or NTIS.

In Werner & Ingbar’s textbook, 5th edition, 1986, there was only one 26-page chapter on Nonthyroidal Illnesses (plural), p. 381-407, categorized under “Factors that control thyroid function.”

The narrow coverage of this topic in the textbook has remained narrow.

In the 10th edition, 2013, there is still only one chapter, half the length (14 pages), on Nonthyroidal Illness Syndrome.

This chapter is now categorized under a section renamed “the normal thyroid,” and is located many, many chapters away from the section on hypothyroidism.

This separation and categorization contributes to reinforce a fallacious belief and perception that this is a syndrome that never happens to any people with thyroid disease and especially not those who are taking thyroid hormone replacement. (This was proven untrue in the only study of classical nonthyroidal illness in six T4-treated men, Wadwekar & Kabadi, 2004.)

NTIS is a set of diverse medical conditions in which even people with healthy thyroid glands can undergo a bloodstream and peripheral deficiency in T3 hormone and a corresponding increase in Reverse T3.

Meanwhile the TSH is apathetically normal.

These are the most common features across all types of NTIS.

This textbook has never, ever acknowledged that they are just as common as features of failed T4 monotherapy in a patient who is a poor converter of T4 hormone, whose FT3 is below their individual healthy setpoint, whose RT3 is high-normal or elevated, and who may indeed collect illnesses that their TSH and their doctor are both equally unable to resolve by perpetually stimulating a dying, dead or missing thyroid.

The chapter acknowledges that when acute illness triggers T3 depletion, it may be adaptive in early phases, but it can become pathological in later “chronic” stages if the healthy-thyroid person cannot recover health by means of increased TSH secretion to refill the T4 and T3 deficit.

Nobody has ever acknowledged the existence of treated thyroid patients in whom this biochemistry is induced by therapy and remains chronic for the rest of their lives, for all they know.

The 10th edition acknowledges that nonthyroidal illness is diverse across many diseases or health status types: Fasting, mild illness, critical illness, surgical trauma and burns, chronic renal (kidney) failure, hepatitis (liver), HIV infection, and depression.

However, the treatment of this phenomenon treats the high risk of death from low T3 in a cold, heartless and objective manner.

It refers to what it admits to be “limited data” on the treatment of this disorder with T3 hormone as proof that therapy is in vain or has limited benefit, rather than admitting that people have been frightened away from trying increased doses of T3 or even doing clinical trials at all.

Overall, despite the strong association between disease, death and low T3 levels, the chapter imposes its own paradigm by asserting that T3 depletion is overall, adaptive.

It suggests that supplementing patients with TRH hormone will help their TSH return to normal and regulate their healthy thyroids.

They seem utterly oblivious to the fact that this TSH-boosting solution would fail to help anyone with a failed or missing thyroid recover from NTIS.


Bertrand Russell once said that “Change is scientific; progress is ethical; change is indubitable; whereas progress is a matter of controversy”

Science always changes, and to study change is important.

Scientific “changes” are not always ethical, or even evidence-based.

Has thyroid science really progressed, or regressed?

I believe the transformation of this “Fundamental and clinical text” over many decades illustrates the narrowing of some aspects of thyroid clinical knowledge at the expense of others.

This process is contributing to an artificial separation between other illnesses and thyroid disease and thyroid therapy.

It’s no wonder doctors do not see a treated thyroid patient’s thyroid hormone levels and their intimate connection to almost all other aspects of human health.

The field can maintain its worship of TSH by making it seem like common diseases that make TSH unreliable are miles and miles away from routine thyroid disease and therapy, when they are not in fact so far away.

The syndromes that deplete T3 levels are being framed as adaptive and benign. They may lower the human body’s healthy metabolic setpoint, but they can maintain that Low T3 far too long until it causes damage or death. The use of T3 in therapy is feared so much that they fail to use enough T3 (usually only enough to barely “normalize” T3) to truly help even the thyroid-healthy person recover from tissue hypothyroidism that could kill them.

Not only the knowledge of signs and symptoms, but the thyroid hormones themselves, are being thrown in the dustbin of oblivion, unmeasured and unregarded.

People’s lives are being thrown away along with them.

Braverman LE, Cooper D, eds. Werner & Ingbar’s The Thyroid: A Fundamental and Clinical Text, 10th ed. Philadelphia: Lippincott Williams and Wilkins, 2013.

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