In Canada, approximately 3.0% to 4.6% (1.1-1.6 million of our 2017 population) have been diagnosed with hypothyroidism, based on recent prevalence estimates in the United Kingdom and the United States. 
Hypothyroidism affects significantly more women than men, and it affects patients of all ages. For many people, hypothyroidism is a chronic, lifelong condition. Most people with hypothyroidism have autoimmune Hashimoto’s thyroiditis, but some become hypothyroid after medical treatment for autoimmune hyperthyroidism (Graves’ disease) or after thyroid gland removal for thyroid cancer, goiter or thyroid nodules.
The effects of undiagnosed and poorly treated hypothyroidism are serious and can affect all organs and bodily systems. Patients on lifelong therapy can suffer disorders that are triggered or worsened by even mild levels of uncorrected deficiency. Low thyroid hormones have been implicated in depression and cognitive decline,  cardiovascular disorders, [5, 6, 7, 8] and diabetes. [9, 10, 11]
Furthermore, autoimmune thyroid disease often occurs in conjunction with other autoimmune diseases, which may remain undiagnosed if their relationship to thyroid autoimmunity is not understood. [9, 11, 12]
Over time, seemingly minor thyroid hormone imbalances can contribute to many other health disorders, and these disorders require additional tests, medications, and treatments. These health problems can hinder patients’ ability to pursue fulfilling careers and an active life. Inadequately treated hypothyroidism also affects patients’ families and workplaces and places a burden on communities.
Doctors and patients are continually reassured that hypothyroidism is simple to diagnose and treat. We are told that the current medical response to it is highly sensitive and fully effective. Unfortunately, autoimmune hypothyroidism is highly susceptible to a delayed diagnosis, and biochemical hypothyroidism and its signs and symptoms can persist despite TSH-controlled hormone treatment.
The underlying problem we face is the TSH-centered model of thyroid health that prevents us from measuring and treating the direct cause of hypothyroidism while on hormone therapy.
Hypothyroidism is directly caused by a deficiency of thyroid hormone, especially a deficiency of T3 hormone. But the level of active thyroid hormone, T3, is rarely verified in diagnosis and treatment. This is because in a perfect state of thyroid health, sufficient T3 will be produced from T4 hormone.
Also, in a perfect state of health, T4 hormone will be perfectly inversely associated with TSH secretion. Medicine currently assumes that the model of perfect hormone regulation in a state of thyroid health can and should be transferred, without any modification whatsoever, to the unnatural and imperfect states of thyroid disease and oral thyroid hormone dosing.
Medicine acknowledges that inappropriate TSH secretion is not the root cause of hypothyroidism but rather a secondary effect and signal of hypothyroidism prior to diagnosis and therapy. However, our medical system does not act on the basis of this underlying cause and effect.
We currently live in a medical mindset that attempts to resolve hypothyroidism by medically normalizing a pituitary TSH secretion. The sensitive, hourly adjustment of thyroid hormone levels is a task that TSH is able to do quite well in people with healthy thyroid glands who are not taking oral thyroid hormones. The fundamental mistake is the unfounded belief that TSH controls and responds to thyroid patients’ HPT axis in the same way as it does in other patients. This assumption has been seriously questioned in research, as we discuss in our Definitions section, Low TSH section and Reference range section.
It is difficult to understand how medicine has arrived at the belief that a daily inflexible dose of the largely inactive thyroid hormone, T4, is in any way a substitution for a living gland that secretes both T4 and T3, and that everyone will convert T4 into T3 normally. A hormone pill, however perfectly engineered, cannot ensure its own sufficient absorption through an individual patient’s GI tract, cannot ensure that proteins are ready to assist its transport across cell membranes, and cannot ensure the pituitary gland’s appropriate TSH response at all times. Most importantly for life-long thyroid patients, our medication cannot ensure sufficient conversion of T4 to T3 hormone in bloodstream and in our bodily tissues.
Why must we force the model of thyroid health to apply to the situation of thyroid disease and therapy? Why are we forcing a population-wide statistical normal range to apply to an individual whose set-point is far more precise within that range? Why can’t we acknowledge that the thyroid patient’s hormonal status is more fragile and subject to distortion and interference? See a more detailed discussion throughout our rationale sections.
As a result of applying the mathematical model of the healthy HPT axis to the altered state of artificial hormone therapy, our doctors’ critical thinking is overruled by flowcharts and mathematical reasoning based on the “normal” statistical reference ranges of people with normal thyroid glands who are not on thyroid therapy.
Due to the TSH-dominant paradigm that limits our health, the pituitary TSH measurement is the first and only test in such simplistic flowcharts. The TSH results overrule and limit all subsequent diagnosis and treatment decisions. 
Overall, this mechanistic mindset straitjackets doctors and harms patients. It works against doctors’ discernment and critical thinking that should be at the core of medical practice. Most harmfully, it interferes with the identification and resolution of thyroid disease and deficiency in those who have a TSH in the normal statistical range.
These guidelines and flowcharts have also overlooked valuable biomarkers and clinical measurements of hypothyroidism that were in common use decades ago. Some tests, such as ankle reflex speed, average basal body temperature and metabolic rate,  are highly correlated with the degree of tissue stimulation by T3 hormone, and are more direct measures of thyroid hormone sufficiency than any blood test can be. If we really want to save money and care for patients, these additional measures of hypothyroidism should be part of our guidelines.
In Canada, standard diagnostic flowcharts and guidelines do acknowledge many special conditions for thyroid testing and interpretation, such as thyroid cancer, pregnancy, lithium and amiodarone. However, provincial guidelines, such as those in Alberta updated in 2014,  do not mention the effects of corticosteroid therapies (such as prednisolone) and the many other drugs and substances listed in the product monograph for the medication. 
Nowhere do these guidelines for doctors acknowledge the unique long-term health needs of thyroid patients on therapy.
It appears to presume that L-T4 and a normalized TSH secretion will return us to full thyroid health.
But this is not true.
Not only has our “natural” hypothalamus-pituitary-thyroid axis been disrupted, but now our hormone levels, and often our test results, are vulnerable to harm and distortion.
The most powerful effect is the thyroid hormone therapy we are on, but other influences include the substances in our diet and environment, low-protein and low-calorie diets, and our other health conditions and their drug treatments.
Next section: Challenges: Testing, part 2
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