About us


The Canadian Thyroid Patients’ Campaign is a science-focused thyroid therapy advocacy and awareness campaign co-led by a grassroots group of Canadian thyroid patients.

For many people, a thyroid disability is a lifelong chronic disease that profoundly affects all aspects of our physical and mental health, quality of life, and our contributions as citizens.

We believe all thyroid patients should be able to obtain accurate and complete diagnosis, complete and relevant thyroid testing, as well as unprejudiced and individualized adjustments to optimize their thyroid therapy.

We believe good science ought to be the basis of therapy. Our scientific knowledge is still very incomplete, and scientific prejudices and paradigms often get in the way. We foster genuine dialogue within the context of evidence-based thyroid therapy and evidence-based thyroid advocacy.

Our aims

  • Promote public dialogue about the experiences of thyroid patients as individuals and as a diverse group.

  • Promote deeper public knowledge of the science of thyroid hormone health and thyroid gland health.

  • Challenge contemporary policies and clinical guidelines that limit thyroid testing.

  • Fight against the limitations our doctors face to conform to oversimplified clinical thyroid education, practice guidelines, policies and flowcharts.

  • Challenge thyroid pharmaceutical prejudice against any regulated T4- or T3-prescription-based hormone medication available on the market

  • Persuade national and provincial governments to acknowledge thyroid disease as a chronic illness. With chronic disease status comes funding for research.

  • Challenge thyroid research to uphold the highest standards of scientific integrity, ethical integrity, and logical argumentation to reach conclusions.

  • Engage in international collaboration in thyroid patient advocacy.

What is evidence-based thyroid activism

What do Canadian thyroid patients struggle with?

So many things! These challenges are not in priority order.

  • Medical dismissal and misunderstanding of the body-wide symptoms of thyroid hormone imbalance and its influence on many other health conditions. We are a disease placed in an impossible category. The immense and far-reaching power of thyroid hormones is apparently too much for our most intelligent doctors to handle. ALL the major symptoms and signs of thyroid hormone imbalance have now been misclassified as “nonspecific” to our disease!
  • The tyranny of the TSH test and laboratory reference ranges over our diagnosis and therapy
  • Cost-cutting campaigns that limit our access to thyroid hormone tests
  • Medical prejudices and myths that limit our range of pharmaceutical options for therapy
  • Official therapy guidelines that are based on a biased and selective review of evidence and research, not a full and objective assessment of evidence
  • Lack of awareness of the T3 hormone’s powerful role in human health, and its central role in thyroid disease and optimizing thyroid therapy
  • Price increases, drug shortages, and lack of market diversification for synthetic T3 and desiccated thyroid medication.
  • Lack of awareness of thyroid autoimmunity, including the health effects of all thyroid antibodies and the interactions among several autoimmune disorders
  • Lack of research conducted on thyroid patients maintained on long-term therapy
  • Lack of studies on the health outcomes of thyroid therapy that differentiate patients by Free T3 levels, disease / gland status, and antibodies.

Read our Campaign Statement for more information on our challenges and stance.


Our messages express injustices and harms

We each have a moral responsibility to cry out against systems and beliefs that harm any human beings.

Our visual memes and verbal claims may at times seem very aggressive or accusatory, but our complaints are ethically and scientifically justified, and our suffering is real.

Harm includes taking away someone’s voice and freedom of choice among safe and effective therapy options, and the right to adjust doses and therapies to alleviate suffering from chronic thyroid symptoms and worsened chronic diseases. This harm happens in oversimplified thyroid medical education and it happens in in doctor’s offices.

Harm includes taking away someone’s equal right to basic health care, such as thyroid hormone testing, thereby discriminating against the uniqueness of one’s individual thyroid disability and therapy. It is fundamentally discriminatory to assume that one oversimplified therapy model works safely and effectively for all patients with a thyroid disability. This harm happens at the level of provincial lab testing policies and colleges of physicians and surgeons who regulate, discipline and punish innovative thyroid health practitioners.

Harm includes justifying systemic discriminatory policies by means of unscientific prejudices, employing discriminatory research methodologies, and performing biased, selective literature reviews to reinforce a rigidly defended status quo. These practices occur at the level of scientific research, as researchers apply their chosen paradigms to disease definitions, research questions, methodologies, and analysis of data. It happens at the level of medical associations, such as the therapy guidelines written by the American Thyroid Association.

We always make an effort to back up our claims with appropriate scientific evidence, references, and reasoning in our blog posts.

We do not target individual people. For example, we never wish to attack individual doctors who may have good intentions and open minds.

For whom do we advocate?

If your health is challenged by a thyroid hormone imbalance or a thyroid disease, whether temporary or permanent, mild or severe, we advocate for you.

There are three general categories of thyroid patients:

1. Autoimmune thyroid diseases (AITD) patients

These can cause progressive and permanent destruction of the thyroid gland itself and other tissues in the body.

  • Hashimoto’s thyroiditis is caused by two anti-thyroid antibodies (Thyroglobulin antibody, TGAb, and Thyroid Peroxidase antibody, TPOAb) that induce thyroid inflammation (goiter), nodules, and ultimately cause gradual follicular cell death and fibrosis over many years or decades. Death of too much thyroid tissue can result in various degrees of permanent hypothyroidism, which can cause or worsen multiple chronic diseases such as heart failure and depression. This is the most common form of AITD.
  • Graves’ Disease is caused by TSH-receptor “stimulating” antibodies (TSAb) that overstimulate active thyroid gland tissue to secrete excess thyroid hormone. Chronic hyperthyroidism can result in severe damage to organs such as bones and heart. Likewise, chronic hypothyroidism during mismanaged thyroid therapy (before or after thyroid gland removal or radioactive iodine therapy) can damage any and all tissues and organs in the body and worsen any chronic disease.
  • Atrophic thyroiditis is caused by TSH-receptor “blocking” (TBAb) and “cleavage” antibodies in addition to the antibodies that characterize Hashimoto’s and Graves’ disease. When the blocking and cleavage antibody act together, it causes progressive thyroid gland atrophy and fibrosis, which can lead to severe hypothyroidism as the gland itself shrinks and shrivels up while dying. As long as enough thyroid gland tissue remains (before complete atrophy), changing antibody activity stimulation can bring about “remission” to euthyroid status, phases of hypothyroidism, and phases of hyperthyroidism over many years.

These are not really three separate autoimmune diseases.

They are merely three predominant clinical manifestations of “thyroid autoimmunity.”

Even though you can’t be hypothyroid and hyperthyroid at the same time, a patient in any single AITD category has a risk of also having the antibodies that are characteristic of the other two.

2. Patients with other thyroid pathologies

Other gland failures can also result in permanent thyroid hormone imbalances that must be treated. These patients may or may not also have autoimmune thyroid disease in addition:

  • Thyroid Cancer, before or after a full or partial thyroidectomy that requires thyroid hormone therapy.
  • Central or hypothyroidism due to hypothalamus or pituitary failure or drug effects. These patients cannot secrete enough bioactive TSH to stimulate a healthy thyroid gland.
  • Congenital hypothyroidism, such as birth without a thyroid gland, or defects in thyroid hormone transport.

3. Patients with a temporary thyroid condition

  • Benign growths or nodules on the thyroid gland that require thyroid surgery or removal. Growths and nodules must be monitored for signs of cancer.
  • Pregnancy and post-partum hypothyroidism and hyperthyroidism may be temporary.
  • Infectious thyroiditis can cause thyroid pain and temporary hyperthyroidism, but may be temporary.
  • Low T3 Syndrome (non-thyroidal illness, NTIS) can cause those who have healthy thyroid glands to experience severe thyroid hormone imbalance and T3 deficiency. Severe and long term T3 deficiency can hasten death and worsen the critical illness that triggered them. Only in those who survive is it temporary. Survival depends on the reawakening of TSH-stimulated T3 gland stimulation.
  • Unfortunately, due to discriminatory definitions of NTIS syndrome that have excluded the vulnerable thyroid-disabled population from study, we lack scientific studies of NTIS incidence and recovery rates in the thyroid-disabled population.

Campaign emphasis

At this time, our thyroid patients campaign is focusing on improvements to lifelong therapy for hypothyroidism, while not ignoring hyperthyroidism and other thyroid conditions.

  • The vast majority of patients with a thyroid disease diagnosis will become hypothyroid.
  • While hyperthyroidism and many gland disorders are temporary, severe damage to the thyroid gland itself is usually completely permanent and lifelong.
  • Patients whose treatment for hypothyroidism is mismanaged and misunderstood may suffer chronic symptoms and signs of hypothyroidism in tissues throughout their body regardless of a normalized or even low TSH hormone secretion from the pituitary gland.

However, we will from time to time discuss issues in hyperthyroidism, thyroid cancer, thyroid gland health, Low T3 Syndrome and thyroid hormone sufficiency in general.

Thyroid disease is chronic, not cured

What kinds of thyroid medications do we advocate for?

ALL of the thyroid hormone pharmaceuticals. All patients should have the right to explore each of them and decide which therapy modality works best for them or which combination at any ratio:

  • Synthetic T4 (Levothyroxine, Synthroid, Euthyrox)
  • Synthetic T3 (Liothyronine, sold in Canada as Cytomel by Pfizer). Both regular and slow-release T3 are also available in powder form from compounding pharmacies.
  • Desiccated Thyroid Extract (DTE / NDT, sold in Canada as ERFA Thyroid), which contains both T4 and T3
  • Compounded thyroid medications. Powdered forms of T4 and T3 and desiccated thyroid are available at licensed compounding pharmacies across Canada.

According to science, the hormones ALL these medications provide are completely “bioidentical.” Thyroid pharma: Bioidentical yet harmful?

Therefore, there is no scientific rationale for pharmaceutical prejudice for or against any of these preparations. Pharma prejudice refuses a paradigm shift in thyroid therapy

However, individualized therapy is necessary. Each patient’s body will respond differently to a particular type, brand, dosage, and ratio of thyroid hormones.

T4 and T3 pharmaceuticals operate in very different ways and must be dosed and optimized differently.

Some thyroid patients convert T4 into T3 very efficiently, and some convert T4 poorly. Some will fare poorly on T4 alone, and others will not require any T3. Non-active ingredients and bioavailability (how much hormone can be absorbed) can make even two brands of synthetic T4 unequal.

Contrary to popular belief, there is no single T4:T3 ratio of secretion and no single rate of conversion, even when the thyroid gland is completely healthy. See The two T4-T3 ratios that confine thyroid therapy

Different types of thyroid disease and their progression will influence therapy. Genetics, concurrent health conditions, pregnancy, menopause, aging, diet, and nutrient deficiencies can interfere or assist.

Therefore, patients and doctors require the freedom to choose among all thyroid hormone pharmaceuticals and to combine them as necessary to provide the ratio and dose of T4 and/or T3 hormone in blood that works best for the patient’s body.

Thyroid hormone pharma-Denies-biology

Anti-discrimination in thyroid therapy

Doctors and medical systems should not limit thyroid testing or care based on non-medical categories such as income level, gender, age, education, ethnic background, skin color, religion, or geographic location.

Likewise it is discriminatory to place _medically unnecessary_ limitations on thyroid patients’ care based on their concurrent health conditions, disabilities, pregnancy status, or even patients’ dietary needs or preferences.

Likewise, a thyroid health policy that enforces T4 monotherapy as the standard of care for all hypothyroid patients is discriminatory against all who are “poor converters” of T4 hormone. Likewise, it is discriminatory against poor converters to force them to endure a limited supply of T3 within T3:T4 combination therapy. Less T3 than they need, especially in the presence of more T4 hormone than they can metabolize properly, can lead to a reduced quality of life and health for the rest of their lives. These patients’ suffering from medical ignorance and discrimination is unnecessary and preventable.

Thyroid patients suffer from T4 Monotherapy

It’s not that T4 monotherapy itself is flawed, but the current therapy paradigm that deploys it is flawed.

We call the current therapy paradigm the TSH-T4 paradigm.

A “TSH monotesting” policy goes hand in hand with T4 monotherapy.

“TSH monotesting” is the practice of considering TSH the only test required for the vast majority of clinical decision making in thyroid therapy.  Free T4 testing will be used as an adjunct only when TSH is in the “subclinical” zones below and above reference.

This TSH-T4 paradigm is discriminatory against many types of thyroid patients.

  • It is discriminatory against hypothyroid patients on therapy who are poor converters of T4 hormone into T3.
  • While T4-dominant therapies may maintain pituitary TSH secretion in the normal range, a level of T4 hormone that normalizes TSH cannot protect patients from tissue hypothyroidism beyond the pituitary gland.
  • It is discriminatory against patients who experience an elevated TSH but “normal” T4 levels. In this therapy model, the right to begin thyroid therapy is often withheld until TSH achieves an arbitrary level above reference range and/or until Free T4 drops below a reference boundary defined by the local laboratory. These patients may suffer unnecessarily from genuine hypothyroidism due to insufficient delivery of T3 hormone to cells.
  • It is discriminatory against patients whose TSH secretion is permanently or temporarily compromised by health factors other than their thyroid hormone supply in blood.

TSH is not an omniscient hormone.

TSH secretion levels do not signal T3 sufficiency in organs and tissues throughout the body. 

TSH is a localized tissue response based on the unique T4-T3 conversion rates that occur only within the hypothalamus and pituitary.  There are a wide variety of T4-T3 conversion rates in tissues throughout the body, and all of the tissues exchange their hormones in two directions with the common reservoir in bloodstream.

TSH will not elevate in response to insufficient T3 levels in bloodstream or tissues beyond the pituitary. As long as the hypothalamus and pituitary gland can convert sufficient T4 into T3 locally and/or obtain enough T3 from bloodstream to meet its local needs, these two glands really do not care how low your T3 level goes in blood. These two organs don’t care if some of your organs require MOST of their T3 from blood. Ultimately, these two organs don’t care how hypothyroid the rest of your body is.

TSH also adjusts to other physiological factors besides thyroid hormone supply.

As for health risks of an isolated low TSH, there is still no proof that low TSH alone can directly cause harm to bones or the cardiovascular system.

Thyrotoxicosis is not physiologically defined by TSH. It can only be caused by the presence of hyperthyroid levels of T4 and T3 in bloodstream, and its primary evidence will be multiple signs and symptoms of hypermetabolism in tissues.

While an isolated low TSH may define a “biochemical” category of “subclinical hyperthyroidism,” this is a laboratory test definition, not a physiological definition. In biology, a low TSH cannot either “cause” or “define” the pathological state of thyrotoxicosis.

Our website & blog

We engage in three types of communication:

  • Advocacy (raising awareness; calls to action; articulating our stance; recommendations, policy analysis, response to policies; news and trends)
  • Patient community support (mutual encouragement, self-advocacy tips)
  • Thyroid disease and therapy education (reviews of scientific articles and other relevant publications)
  • Continuing medical education and policy education is important for all involved in thyroid therapy, whether you are a thyroid patient, citizen, or health professional.

Many of our posts are shared on Facebook and Twitter along with images / memes sized for both media.

Please read our full Terms of use regarding the limitations of our website.

Patient support group (Facebook)

Our support group had been running for several years before our campaign began.

The “Canadian Thyroid Support Group” operates separately from our Campaign at https://www.facebook.com/groups/CanadianThyroidSupportGroup/ 

In the support group, patients take the initiative to learn from each other. We are very aware that we are not doctors and we are not offering official medical advice, but we build knowledge together. Patients face different challenges in different parts of this country. Each person’s thyroid journey is unique, including their response to thyroid medications. We often link or cite resources for each other.

Campaign history

We began in July 2018 with a Facebook campaign and website. We spearheaded a Canadian federal petition to Health Canada in 2018, which received 5644 verified e-signatures. Our petition was read in Parliament by MP Diane Finley on January 28, 2019.

Long after the petition campaign, we have continued to develop our website and promote our campaign with original articles, visual memes, and videos. Our supporters respond, share, and comment on our communications as we build momentum.

Government responds to thyroid petition

Who are we?

Our campaign has an Advisory Group consisting mainly of thyroid patient leaders from a Canada-wide private online patient support group.

We are not affiliated with the Thyroid Foundation of Canada.

We are not affiliated with any pharmaceutical companies or medical associations.

We strive to maintain a patient’s perspective as we promote or critique thyroid research, guidelines, and trends in thyroid therapy.

Main spokesperson

Our main Campaign researcher and writer is Tania Sona Smith.

When we become an official organization with named public leaders and a board of directors, we will post our organization information and our names and profiles.

Meet campaign researcher

Read more about Tania Smith in several posts:

We are building, and we need you.

Our movement is still gaining momentum and followers. We are in the process of becoming an official registered organization, though it’s a slow process involving volunteers, many of whom still suffer from thyroid disease and the imperfections of thyroid therapy.

Do you have skills and energy and inspiration to use them? See posts that discuss ways you can help:

Contact us

See the links on the right sidebar:

  • Join us on Facebook
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  • Subscribe to this website’s Blog

Use our Contact link (in the header above) to email canadian.thyroid.patients@gmail.com

You can join us