The classification of hypothyroidism
The most problematic aspect of thyroid science today, according to eminent thyroid researchers Hoermann, Midgley, and their multiple co-authors, is overreliance on TSH in the classification of subclinical hypothyroidism and hyperthyroidism. [49, 50, 51, 52]
There is no debate over the biological fact that hypothyroidism is directly caused by a deficiency in one or both of the thyroid hormones T4 and T3, and this deficiency directly causes hypothyroid signs and symptoms and known pathological effects on bodily organs and symptoms.[53, 54]
Less widely known is the fact that the healthy human body is designed to carefully defend T3 hormone levels in serum, where it is needed by organs and systems that rely on this source. 
From the point of view of every cell’s thyroid hormone receptor, where only T3 is known to exert genomic effects, hypothyroidism is a T3 deficiency. [49, 56]
The perspective of the ATA guidelines
However, prominent guidelines documents, such as the 2012 guidelines for thyroid testing issued by the American Thyroid Association and the American Association of Clinical Endocrinologists (ATA Guidelines), have made TSH and its reference range the sole arbiter of the existence of thyroid hormone deficiency and excess.
As a consequence, the ATA guidelines have also dismissed Free T3 testing in hypothyroidism. Few seem to notice that they give insufficient and irrelevant reasons, citing the authority of medical articles from the 1980s and early 2000s, a problem which we discuss further in the section on Free T3 testing. 
TSH behaves differently in thyroid patients on L-T4 therapy
Researchers have analyzed data between patients on L-T4 therapy and controls, and they found that the FT3 – TSH relationship was distinctly different in the two groups. In those on therapy, T3 inversely correlated with TSH in a very linear manner across the upper half of reference range and beyond. But in controls, T3 was restricted to the upper-middle part of its reference range, while TSH also fluctuated narrowly in order to protect serum T3 consistency. Within normal TSH range, the L-T4 treated patients had significantly less T3 than controls.  In other words, the TSH will likely be lower in a hypothyroid treated patient at the same level of T3 hormone.
If TSH alone has to be the only judge for treated patients, then to be truly fair to them, the laboratory would have to provide an entirely different reference range just for patients on thyroid therapy, shifted toward a much lower TSH, in order to account for the skewed HPT axis that applies to their artificially-adjusted hormone status.
Unfortunately, the simplicity of an univariate TSH-dominant paradigm that applies to almost every adult is too attractive to leave behind. Current Canadian guidelines documents, boldly announce on the first page of guidelines that “Thyroid stimulating hormone (TSH) is the most sensitive and specific test for the investigation and management of primary thyroid dysfunction.” 
Such documents, revised in 2010 and 2014, dismiss T3 hormone testing in hypothyroidism by excluding it from diagnosis flowcharts as well as monitoring checklists in the majority of cases. [15 13 58]
Thus our country’s guidelines mimic the ATA and other international guidelines also developed on the basis of consensus, without attending to critical analysis of recent research on the central role of thyroid hormones, rather than TSH, in both health and thyroid disease.
The standard guidelines in many developed nations have created an echo-chamber that reinforces theories and practices based on an oversimplified and questionable biological foundation.
Thyroid hormone imbalance hiding under a normal TSH
The current overreliance on TSH results in our inability to see, and thus effectively treat, biochemical hypothyroidism that can hide under a normal or contradictory TSH. This can happen in a wide variety of health conditions that hypothyroid patients, as well as non-thyroid patients, can encounter during life.
In 2017, Chatzitomaris et al identified the altered states that lowered T3 in the presence of a normal or lower TSH, as “Type 1 allostasis.” The common and chronic Type 1 allostasis conditions include diabetes mellitus, caloric deprivation, depression, and exhausting exercise, and fetal life. More serious Type 1 allostasis conditions in which TSH can be blind to T3 deficiency are chronic heart failure, renal diseases, liver disease, pulmonary diseases, HIV infection, and critical illness in general. 
Conversely, Chatzitomaris et al identified as “Type 2 allostasis” conditions in which TSH does not accord with raised T3: Pregnancy, endurance training, obesity, adaptation to cold, acute schizophrenia, and post-traumatic stress disorder. 
In addition, in two states specific to hypothyroid patients, TSH does not elevate sufficiently to indicate a thyroid hormone deficiency, even when the pituitary and hypothalamus are healthy:
1) in the TSH-defined category of “subclinical” hypothyroidism, where we hesitate to treat with thyroid hormone a deficiency that TSH does not sufficiently acknowledge, a patient can suffer chronic hypothyroidism for years as the thyroid gland is slowly destroyed by an autoimmune process.
2) The second state is a T3- specific thyroid hormone deficiency. A hypothyroid state of abnormally low Free T3 in the presence of much higher T4 can be induced and/or maintained in some patients by L-T4 monotherapy treatment itself. [50, 60, 49, 61]
In fact, TSH has a very complex response to T3 and T4 hormone levels, responding to T4 and T3 in different ways and to a different degree under the artificial conditions of thyroid hormone therapy. 
Interference with TSH
To add to all these health influences a huge list of interfering drugs, substances and foods found in the product monographs for levothyroxine, why are doctors splitting hairs over a thyroid patient’s TSH of 0.4 and 1.0, and likewise, between a TSH of 3.5 and 4.0? Is there not enough proof that the pituitary gland cannot be relied on to be the arbiter of the thyroid status of a hypothyroid patient on therapy? If patients are depressed, or have arthritis, or are restricting calories and exercising too hard in the effort to lose weight, it will render their TSH even more unable to signal their hypothyroidism.
The TSH paradigm vs. T3 paradigm
A simple solution presents itself. Acknowledge that the “normal TSH” paradigm is harming the patients most at risk from its inflexibility, and return focus to the direct biological cause of hypothyroidism.
To ensure proper diagnosis and treatment, definitions of hypothyroidism must prioritize the patients’ thyroid hormone levels rather than the pituitary gland’s often delayed and potentially dysfunctional response to those levels. [63, 64]
The thyroid hormone levels, especially T3 levels, more directly influence the health of the entire body through biological processes that can only occur when sufficient T3 acts on the thyroid hormone receptors in every cell. 
In contrast, TSH has only an indirect influence by means of stimulating a functioning thyroid gland to secrete and mildly upregulating T4-T3 conversion, as we demonstrate in other sections. [66, 67]
Next page: Rationale: Reference ranges
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