Thyroid patients call the bluff

There’s almost 4000 e-signatures so far on our federal petition, but hypothyroidism affects 3 to 5% of the Canadian population, and that’s millions of people.

So, it’s time for a rant.

It’s time to rally the troops of well-educated thyroid patients and enlightened doctors. It’s time to reason with the masses that blindly trust the current system. It’s time to point out the fallacies of the dogmatic endocrinologists who staunchly defend the current TSH paradigm at all costs…

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Hypothyroidism is an epidemic that we cannot eradicate, but we can and must manage it better given our advanced knowledge at this time.

Why have the guidelines for hypothyroid therapy not changed much since the 1980s?

Meanwhile, research on the power of the T3 hormone and the shortcomings of standard therapy have rendered many old biological assumptions highly questionable if not utterly obsolete, as demonstrated elsewhere on this website.



Given the percentage of our population on thyroid medication and the standard practice of monitoring by TSH alone, it is quite possible we could have at least a million Canadians living for the rest of their lives with suboptimal T3 thyroid hormone levels without knowing it.

Thyroid hormones affect every organ and system in our body, and that’s why doctors say hypothyroid symptoms are non-specific.

Sadly, this very same excuse doctors use to justify not investigating thyroid levels further is actually the most logical reason to investigate them further.

Research on the health effects of T3 hormones show that suboptimal T3 levels even within reference range can worsen other diseases.

This makes it absolutely crucial to rule out suboptimal T3 in a person who may be forced to live with a relatively static T3 level for the rest of their life given a static dose of meds.

Suboptimal-T3 thyroid patients are not only suffering daily from chronic hypothyroid symptoms, but are also more susceptible to secondary health conditions like depression, infertility, cognitive difficulty, weight gain, skin diseases, kidney liver and heart diseases, and chronic fatigue.

Secondary conditions require secondary medications and additional medical visits and tests.

  • How is that affecting our economy?
  • How is that increasing the burden on our Health care system as our population ages?
  • How is that affecting families and individuals?



Consider the many errors in medical reasoning that have led to our current state of hypothyroid therapy.

1. The red herring: Distraction

The doctrine of the supposedly linear relationship between TSH and T4 hormones has overwhelmed attention to the most powerful thyroid hormone, T3.

The power of TSH over the healthy thyroid gland has blinded medicine to the impotency of TSH in the patient dependent on a hormone pill.

The focus on improving the sensitivity of the technology of the TSH test to detect levels down to 0.001 mIU/L has distracted us from asking these fundamental questions:

  • “what exactly does TSH tell us and what does TSH fail to tell us about thyroid hormone status across the entire body?”
  • “what other health conditions, medications, and even diets can powerfully manipulate TSH levels so that they no longer reflect thyroid hormone levels?”
  • “which biologically necessary roles does TSH continue to play in a patient without a thyroid gland to stimulate?”

The greater abundance of the T4 hormone in bloodstream has overshadowed the power of the less abundant hormone, T3. Yet it cannot minimize the power of T3 to say that the thyroid gland secretes only 7-15% T3 hormone.

Medicine currently likes to justify T4 monotherapy by saying that the thyroid gland secretes only 20% of our daily supply of T3, and that 80% of T3 is converted from T4.

Yet T4 has limited non-genomic effects and no proven genomic effect within the thyroid hormone receptor. However abundant it is, it is relatively impotent; its main role is to float around awaiting conversion to T3 — or Reverse T3.

In contrast, consider the power of T3 alone.

2. The irrelevant measuring stick

Every organ and tissue in our body defines hypothyroidism as T3 insufficiency, not as a statistically determined T4 deficiency. Even in premature babies, low T3 in serum is associated with later developmental delays.

Any educated doctor would know that hypothyroidism is not caused by TSH excess, but high TSH is merely the healthy pituitary gland’s response to low T4.

Yet we have committed a biological fallacy by redefining the state of hypothyroidism not by the thyroid hormone needs of the human body, but by the TSH response to hypothyroidism before therapy.

TSH was the measuring stick we chose to idolize above all others in the 1980s, and it redefined hypothyroidism according to the lens we choose to see it through, rather than the biological phenomenon itself.

Nowadays doctors seem to think of TSH as a thyroid hormone, since the TSH test is commonly referred to as a “thyroid function test.” But wait, TSH does not enter thyroid hormone receptors.

The pituitary gland is certainly not omniscient about T3 and T4 hormone levels in the brain, joints, or bone marrow.

The conversion of T4 to T3 in the pituitary gland is different from the rate of conversion in other parts of the body.

Why, then, was TSH chosen?

  • TSH is a cheap way to screen the population at large and detect the obvious, extreme cases of thyroid gland dysfunction.
  • TSH was chosen at a time in history before the Free T3 test was refined.

Careful research in the past few decades, employing Free T3 testing, has proven TSH is unable to guide medication and dosage decisions in patients once they are on any form of thyroid medication.

3. Faulty cause-effect logic

Thyroid medication directly manipulates the TSH in a person with a dysfunctional thyroid system, and yet we judge the success of therapy by the skewed results of this medical manipulation of a pituitary gland secretion.

To magnify this cause-effect logic error, we even interpret the TSH by a reference range based on a healthy population that is not taking thyroid medication. This system is neither logical nor evidence-based.

Textbooks acknowledge that TSH testing cannot identify a patient whose TSH secretion does not fit the statistically expected response to low thyroid hormone levels. That’s why TSH alone can’t detect central or “secondary” hypothyroidism caused by pituitary – hypothalamus failure.

Yet we have minimized such cases of incorrect diagnosis based on TSH as “rare” while we have disabled the medical system from proving or even discovering how frequently TSH fails to identify signs and symptoms of suboptimal T3 in the average hypothyroid patient on therapy.

4. Faulty policy based on incomplete research methods

Unbiological reasoning has poisoned the research literature on thyroid therapy as well.

The lack of TSH by itself cannot render a thyroid patient hyperthyroid, nor has low TSH ever been proven to play a causal role in osteoporosis or heart disease.

On the other hand, We know that excess T3 causes osteoporosis and heart disease, and T3 deficiency causes fragile bones and heart disease. Of this there is no doubt.

Yet despite this knowledge, studies that have not measured T3 have concluded that low TSH alone puts thyroid patients at risk.

Why do these studies have power? The sheer number of their research participants to create a statistically significant “association” between a single marker (TSH) and a disorder.

Unfortunately, these studies have no foundation in any proof of an underlying direct biological cause-effect relationship between low TSH and these disorders.

As a result of these sweeping studies, guidelines now caution doctors not to permit low TSH in hypothyroid patients on therapy.

What this fear-mongering policy has effectually done is put patients at risk of suboptimal T3 that can be far more harmful than a suppressed TSH on thyroid therapy.

If only the studies on the direct effects of T3 hormone were as powerful to influence policy to bring real improvements to patients’ lives!



Thyroid patients’ careers are not at stake for calling the bluff on endocrinologists who defend the TSH paradigm’s medical compromise.

  • Instead, our health is at stake.
  • Hypothyroidism is a lifelong condition.

These facts gives thyroid patients a strong motive to learn and the rest of their lives to educate themselves.

We can now read scientific articles on Pub Med, too. We can learn the vocabulary and concepts. Many of us even hold advanced degrees and have advanced literacy skills in spite of our struggle with hypothyroidism.

Dear Doctors, skim the other posts and pages of this website to see that we are not mindlessly consulting “Dr. Google” but the scientific journals and research studies that create and refine our collective medical knowledge. This knowledge belongs to us too.

Educated thyroid patients can see through these flaws in medical reasoning.

Thyroid patients who have won access to successful therapy now have the energy to fight for their brothers and sisters — to maintain access to the tests and medicines they may need in future.



We know thyroid therapy is far from simple, even though the fundamental basis of euthyroidism is as simple as T3 sufficiency from the perspective of the organism.

Our medical system must change policy to dig deeper than pituitary TSH levels interpreted by a measuring stick based on people with healthy thyroid glands.

Monitoring the TSH alone is as absurd as going to a hockey game and paying attention to the outspoken fan in the upper bleachers instead of the location of the puck and the players on the ice.

We must begin to pay due respect to the queen of all thyroid hormones, triiodothyronine, T3, and acknowledge the T4 hormone as her servant.

Without functioning thyroid gland tissue, the TSH-T4 feedback loop is no longer a perfect and flexible loop, it is a broken loop.

Pituitary TSH is a dethroned king. In the patient with a dysfunctional thyroid gland, TSH is now reduced to a one-way response to a static thyroid drug with immense power to distort hormone ratios and relationships.

Thyroid hormone sufficiency is best assessed by interpreting the relationships among T3, T4, and TSH in the context of a patient’s thyroid hormone therapy, other relevant thyroid hormone sufficiency markers, symptoms, other health conditions, and other medications.

Each patient absorbs thyroid medications differently, metabolizes them differently, transports them differently into organs and cells beyond the bloodstream, and can even have different levels of response at the thyroid hormone receptor level in some organs but not others.

Therefore we must keep all thyroid drug options accessible on the market and open to prescription for patients who do not metabolize the standard T4 medication into sufficient active T3 hormone.

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