Thyroid Patients Canada: Looking back on 2020, entering 2021

The year 2020 has been a productive year for our organization of thyroid patients and our website, despite the challenges we all faced on a global scale.

In this post,

  1. HIGHLIGHTS: I’ll briefly mention our organizational milestones of the year.
  2. TOP 10: Then I will give links, visuals, and introductory summaries of our 10 most popular posts of 2020, according to WordPress viewing stats shown in a screenshot as of today, December 31, 2020.

To conclude, I’ll talk about my hopes for patient activism & physician activism as we move into 2021 and beyond.

Organizational milestones

We’ve come a long way from our beginnings in July 2018 as the “Canadian Thyroid Patients Campaign.” We decided to register our organization as “Thyroid Patients Canada.”

On February 11, 2020

Read more: “Thyroid Patients Canada becomes nonprofit corporation.”

In April, 2020

We launched our private, patients-only, international “Thyroid Patients Canada Support” group on Facebook. Read more: “Welcome to our new Support Group.”

See our Group information pages and memes in the main menu under “Groups.”

The private Facebook support group has grown steadily and is now at 620 members.

Our faithful members and Support group moderators do their best to follow our aims to “1. Share wisely. 2. Seek evidence. 3. Reason carefully,” as we’ve outlined in an introductory video, various posts and pages.

As our organization’s president and researcher, I participate when I can, but it’s certainly not an “Ask Tania Smith” forum — it is a place for collaborative peer learning, and many patients provide intelligent tips, links to relevant scientific articles, suggestions of things to mention to doctors, and encouraging comments.

Website growth and readership

To date, since our beginning in mid-2018, the website has had 202,919 views and 109,417 visitors.

In 2020, the website had 148,600 views and 84,636 visitors. The visitors grew more than 3x over 2019.

Our readership is international. Visitors come predominantly from the following countries: United States, Canada, UK, Sweden, Australia, India, Norway, Germany, Denmark and Finland.

Top 10 posts of 2020

Here are the stats for the most popular posts. I’ll give links and brief summaries of each below.

#1. 7 ways to raise TSH without reducing thyroid dose.

(January 21, 2020) 11,239 views this year.

You’ve just come to your doctor for your annual check-up. Either you feel fine and you want to get a renewal of your current thyroid prescription, or you feel rather hypothyroid and you’re hoping to get an increased dose.

But your doctor has been trained to say, “Your TSH is just below reference (or too low in reference). I’m going to have to reduce your thyroid medication.” The current therapy guidelines say so.

Your heart sinks. You predict months or a year of increased brain fog and fatigue.

…. In this post, learn 7 ways you may be able to prop up a lazy TSH to prevent a harmful thyroid dose decrease.

#2. RLC Labs issues Nature-Throid and WP-thyroid recall for subpotency.

(August 28, 2020) 5,521 views this year.

Earlier this year, Acella’s NP thyroid was found to be superpotent (over 110% on the T3 content), and they issued a voluntary recall.

Now, as of August 25, 2020, Nature-Throid and/or WP-Thyroid are sub-potent, so their manufacturer RLC Labs is issuing a voluntary recall.

UPDATE SEP 6, 2020: “The products are being recalled because testing of samples from  six (6) lots  by the U.S. Food and Drug Administration found the samples to be sub potent. The product may have as low as 87% of the labeled amount of Liothyronine (T3) or Levothyroxine(T4).” (FDA notice ) We still do not know whether it is the T3 or the T4 and which hormone (s) it was in the Nature Throid and the WPThyroid.

#3. Thyroid therapies: What my life is like in the T3-monotherapy wheelchair.

(August 28, 2019) 4,417 views this year.

[This is a biographical post by Tania S. Smith, the main researcher and writer for Thyroid Patients Canada.]

Here, I’ll use my own personal example to discuss a few dimensions of T3 monotherapy, which I envision as a “wheelchair.” I’m drawing on the fictional analogy I developed in an earlier post, where I imagined thyroid disease like crippling foot disease.

  1. The therapy of 100% T4 can be seen like a walking stick or cane.
  2. Next in complexity comes a walker, which represents a rolling, adjustable T3-T4 combo.
  3. When the first two options fail, which they do for some thyroid patients, the last resort for safe, effective treatment is 100% T3 medication, which is like a wheelchair.

Here I’m discussing long-term full thyroid replacement T3 monotherapy.  This means that a person relies on T3 medication for for 100% of their thyroid hormone supply, usually without any measurable T4 in circulation.  I’m not talking here about combining T3 with T4 or desiccated thyroid — that’s for another post.

I’d like to use my experience and scientific knowledge of T3 monotherapy to help other people understand why people like me need it, how we use it, what life is like, and how it functions uniquely as an adaptation that can be therapeutic.

#4. No, 25 mcg of L-T3 Liothyronine isn’t equivalent to 100 mcg L-T4.

(September 19, 2019). 4,317 views this year.

In thyroid therapy, how many micrograms of Cytomel (T3) are equivalent to how many micrograms of Synthroid (T4)?

In this post, I summarize what five (5) historical thyroid science sources had to say about this equivalence between 1968 and 1976, at a time when researchers and clinicians were very familiar with the use of these medications as monotherapies and combinations.

#5. Cancer scientists point finger at T4 & RT3 hormones.

(February 5, 2020) 4,016 views this year.

For many decades, scientists have been studying the effect of thyroid hormones in promoting cancer proliferation.

Confusion and contradictions often arise in “cancer & thyroid” research reviews because the relationship between cancer and thyroid hormones is very complex. […]

Fortunately, Aleck Hercbergs and Paul J. Davis and colleagues have been doing research that clarifies the effect of T3 versus T4 hormones in the context of cancers. […]

In Hercbergs and team’s recent preclinical study, cancer patients who were beyond all other hope were able to extend their survival by significantly reducing their circulating T4 hormone and also the variable RT3 concentrations that it brings. They replaced these hormones with synthetic T3 hormone, which provides the active form of thyroid hormone that can maintain life and health even in the absence of T4. […]

In 2019, a helpful review of this innovative cancer therapy and its history was published:

  • Hercbergs, A. (2019). Clinical Implications and Impact of Discovery of the Thyroid Hormone Receptor on Integrin αvβ3–A Review. Frontiers in Endocrinology10

In this article, I’ll showcase the work Hercbergs and team have been doing in the science of T3, T4, RT3, and Tetrac activity at the integrin receptor, and the science’s specific relevance to cancer therapy. I’ll also discuss some of the barriers preventing this clinically-tested T3-dominant therapy solution from taking hold in cancer therapy and in thyroid therapy in general.

#6. Free T3 peaks and valleys in T3 and NDT therapy.

(November 25, 2019). 3,942 views this year.

Lack of knowledge about Free T3 peaks and valleys contributes to failure and frustration in T3-based therapies, including desiccated thyroid and T3-T4 combination therapy. […]

So many times, I’ve thought to myself, “I really wish all doctors who prescribe T3 or NDT medication understood the science behind the T3 dosing effect.”

In fact, even thyroid patients taking T3 or NDT should know the Free T3 dosing curve because it strongly influences their symptoms and lab results. Yes, you might be hypothyroid for half the day or more, and your lab tests might tell an uninformed doctor you’re thyrotoxic when you’re not.

This post displays one graph of normal TSH, FT4 and FT3 circadian rhythms, and then six graphs showing Free T3 fluctuations after doses of T3. You can learn a lot just by simply scrolling through and eyeballing these graphs. To help intelligent thyroid doctors interpret and apply them, I summarize their research context and give some commentary.

Once you understand how T3 behaves in isolation, you can apply your knowledge to various T3-T4 combinations and NDT dosing.


  • NORMAL Circadian rhythm, no thyroid medication
    • Russell, 2008 – the natural TSH, FT3 and FT4 curves
  • When does a thyroid patient need T3 dosing?
  • The T3 Dosing curve
    • Saravanan et al, 2007 – Combination T3-T4 therapy, hypothyroid result
    • Jonklaas et al, 2015 – A single overdose of 50 mcg T3 in euthyroid people
    • Saberi & Utiger, 1973 – A single dose of 50 mcg T3 in hypothyroid people
  • T3 Dose-splitting effects on FT3 / T3 levels
    • Ben-Shachar et al, 2012 – 1x a day versus 2x a day, 3x a day
    • Busnardo et al, 1980 – 3 times a day, euthyroid with suppressed TSH
    • Celi et al, 2010, 2011 – 3 times a day, hypothyroid with normal TSH
  • Blood test timing
  • Lessons learned

#7. Remissions and fluctuations in autoimmune thyroid disease: TRAb.

(April 5, 2020) 3,397 views this year.

Stories of complete remission from autoimmune hypothyroidism circulate on internet forums. Stories of significant fluctuations in thyroid status that allow one to reduce thyroid medication or require a major increase—these also circulate. […]

So, how common are remission and fluctuation in thyroid status?

They are more common in autoimmune thyroid disease than most people realize. This article provides scientific evidence that these tales of autoimmune remissions and even “flip-flops” between hyper- and hypothyroidism do occur.

However, remissions and fluctuations in thyroid status do not occur for the reasons that many people say they do, namely, the reduction and/or disappearance of TPOAb or TGAb antibodies. A different set of thyroid antibodies are responsible for thyroid status fluctuations.

In this post, I’ll share scientific information about the two TSH-Receptor antibodies (TRAb):

  • the TSAb (stimulating) antibody and
  • the TBAb (blocking) antibody

These antibodies can be found at different prevalence rates in all three subtypes of autoimmune thyroid disease: Hashimoto’s thyroiditis, Graves’ Disease, and Atrophic thyroiditis. […]

After equipping you with with understanding and examples, I conclude with tips about safely discovering whether you might be in remission while on therapy for hypothyroidism. It’s best to be aware of these antibodies’ existence in case an unexpected fluctuation in thyroid status happens to you someday, or happens to someone you know.

#8. The THIRD type of autoimmune thyroid disease: Atrophic Thyroiditis.

(December 27, 2018) 2,565 views this year.

Do you know about the THIRD type of autoimmune thyroid disease?

Atrophic thyroiditis may coexist with Hashimoto’s and can occur in people with Graves’ disease. In some estimates, approximately 10% of Hashimoto’s patients carry the blocking antibodies associated with Atrophic Thyroiditis (AT) (Fröhlich & Wahl, 2017).

But Atrophic Thyroiditis is not simply a subtype of Hashimoto’s. Paradoxically, it’s more related to Graves’ disease, even though Graves’ disease causes hyperthyroidism and Atrophic Thyroiditis is an extreme form of hypothyroidism.

As I explain in this article, many myths and general ignorance exists regarding this form of thyroid disease because thyroid autoimmunity is not as simple as it seems.

Atrophic Thyroiditis is caused by a different set of antibodies than Hashimoto’s and Graves, but it is genetically and immunologically related to Graves disease.

Atrophic Thyroiditis has a different prognosis than Hashimoto’s, causing TSH-blocking effects as soon as the antibodies appear. It often leads to far swifter process of thyroid gland destruction. It can affect both maternal and fetal health during pregnancy. It can occur at any age, even in early childhood.

Despite its severity and influence on health, atrophic thyroiditis not easy to diagnose because of widespread medical ignorance and myths, the absence of goiter, the frequency of antibody fluctuations, and problems with testing technologies and test ordering practices.

You may often hear the mantra that “thyroid antibodies don’t affect treatment,” but that’s false with regard to Graves’ disease antibodies, and it’s also false with regard to Atrophic Thyroiditis antibodies. The antibodies that are part of this thyroid disease can significantly interfere with lifelong thyroid therapy, if or when the antibody persists, or reappears long after thyroid atrophy has decimated the thyroid gland.

#9. Anderson, 2020: Thyroid hormones and atrial fibrillation.

(September 30, 2020) 2,409 views this year.

Atrial fibrillation is a cardiac rhythm disorder that significantly elevates the risk of stroke as well as stroke severity. Thyroid hormone excess caused by hyperthyroidism is often named as one of the risk factors for atrial fibrillation.

However, it does not require excess thyroid hormone above the reference range to elevate risk of atrial fibrillation. Significant risk exists even within the normal range, and below reference range.

A team of researchers led by Jeffrey L. Anderson published the results of a large study in the Journal of Cardiovascular Electrophysiology, January 2020. They examined the medical charts of 174,914 patients over an average of 7 years. They tabulated their TSH and thyroid hormone tests and incidents of atrial fibrillation (AF).

[…] The best this research can do for thyroid patients today is to release the stranglehold on harmful AF-thyroid-hormone-risk fears and mythologies that stand in the way of T3-T4 combination therapies, and to raise key questions for future research.

The study raises four implications:

  1. Question thyroid therapy dogma that accepts high-normal FT4 and low FT3
  2. Quell fear of AF in T3-inclusive therapies
  3. Measure the most vital thyroid hormone, FT3
  4. Conduct research on treated thyroid patients’ AF risk

#10. Flexible-Ratio T3, T4, and NDT Combination Thyroid Therapy.

(September 5, 2019) 2,385 views this year.

Here I bring thyroid science into a discussion of effectively adapting and managing the most flexible form of thyroid therapy, T4-T3 combination therapy.

This is a model capable of adapting to an individual’s unique thyroid disability and response to thyroid medication.

Finding an individual’s optimal combination therapy is medically necessary when conventional T4 monotherapy fails to treat hypothyroidism due to poor T4-T3 conversion or poor T4 absorption, and when a patient can’t tolerate or manage the delicate balance of T3 monotherapy. 

Just as monotherapies don’t work for everyone, one magical T3:T4 ratio in medication won’t work for everyone. The idea of the “physiological ratio” modeled on statistically average thyroidal secretion rates is a medical idol based on a misreading of the scientific evidence (see our satiric post on Pilo et al, 1990: “Meet a person with the perfect T3:T4 thyroid secretion ratio“).

Instead of adhering to a rigid recipe, the whole purpose of combination therapy is to be flexible enough to adapt to the individual’s unique needs and metabolic handicaps, just as a real thyroid gland compensates for shortfalls in T4-T3 conversion.  

Some patients will do fine with the 1:4.2 ratio found in desiccated thyroid, while others will need more T3 than desiccated thyroid provides, and some will need less. Knowledge of the science behind what we’re doing helps us adapt our ratio, dose, and even the timing of our doses, to achieve better health outcomes.

Conclusion: Into 2021 and the future

[Review last year’s reflective “Thyroid Warriors” post from December 2019: Healthier thyroid warriors: Our fight is not over.“]

At the beginning of 2021, as President of Thyroid Patients Canada, here are my hopes for patient activism and physician activism to improve thyroid therapy in Canada and internationally.

1. Patient activism in 2021: Our knowledge is our hope.

As patients, I believe our hope for optimal thyroid treatment rests in the soundness of our knowledge of our own thyroid condition and thyroid science.

We have to know more about thyroid than most of our doctors do. Our knowledge is not only our hope, it’s our shield and armor in self-defense. We can’t depend on the medical profession to notice when there’s signs of a problem or to know what to do about it.

If you go to a hospital emergency unit, it’s a roll of the dice whether you’ll be assigned to a doctor who understands your thyroid condition or treatment enough to know how it may relate to your emergency.

The patient herself (or himself) is the only trustworthy line of continuity among doctors. Even the best thyroid doctors (See “Thank you, good thyroid doctors!“) sometimes retire. Move away. Or we ourselves must move to a different location. Our own knowledge of our thyroid condition is our foundation as we go through our lives with thyroid disease.

  • Do you have a unique thyroid condition, or a nonstandard therapy approach that you benefit from? Ask your doctor to write a letter about your thyroid & related diagnoses, and to put this in your medical file. Keep a copy somewhere safe. Ask them to explain in writing the rationales for any non-standard thyroid therapy. Otherwise you may suffer regressions in your care as you move between doctors, or if you end up in hospital and your good doctor cannot be reached in a hurry.

We have to know how current guidelines, when they are mistaken for absolute laws, can narrow our treatment. In North America, we’re still dealing with the narrow and prejudicial American Thyroid Association guidelines from 2012 and 2014. See my series of posts in which I critique them by way of a “back-room paraphrase” and verbatim quotation, saying in a down to earth way what they mean and what their reasoning appears to be: 2014 ATA thyroid therapy guidelines: 1. Levothyroxine ; 2. Ethics ; 3. Desiccated thyroid ; 4. Using Synthetic T3 ; and 5. Research

Thyroid treatment policies can change for the better, or the worse. Hopefully guidelines can change for the better, but the UK experience with the new “NICE” guidelines in 2020 saw a narrowing of care. We must remain vigilant and ready to speak up on behalf of our patient community.

Thyroid tests get cancelled. Patients have to speak up publicly to protest the decision making process and rationale. See posts that reveal the unscientific bases of these decisions:

There’s a lot of myths out there circulating among patients and doctors. Some of the largest myths — both in conventional medicine and alternative medicine — concern Reverse T3 hormone test, and that’s why I have many posts about this hormone, trying to clarify misunderstandings and point to its appropriate use.

This is why it’s been my vision from the start, and as I continue, to ground everything I say in thyroid science. I try to be very clear whenever I’m making a hypothesis, or talking about knowledge I’ve gathered from my own or other patients’ experiences in support groups.

Thyroid science belongs to us, the patients, as much as it belongs to doctors and researchers.

Published scientific literature in databases like PubMed, despite its flaws, is our foundation, our shared scientific inheritance among patients, doctors, policymakers and researchers.

When we argue for changes or improvements in our own therapy or in policies affecting thousands of us, this body of publications is our main common ground.

If we want changes, we can’t just cite a celebrity doctor’s website, a patient’s group, or book — unless it is grounded in citations and references of this body of literature. We have to point to published scientific evidence, just like doctors and medical associations have to, to justify any changes.

Science is a method, too, not just a body of literature, and a scientific mindset can be helpful as we help ourselves and each other find our “individual optimal” thyroid hormone levels and doses in thyroid therapy. Even when we analyze our own therapy, we ought to take a scientific approach and keep records of our own data, considering confounding variables.

Scientific vocabulary can be challenging, but some concepts are absolutely essential. For example, patients ought to be capable of using the word “deiodinase” and know why the deiodinases are so important to thyroid hormone health. We ought to know the different parts of the thyroid hormone journey from secretion/dosing to transport, metabolism, signaling, and bloodstream hormone levels.

We often aren’t educated like diabetes patients are to manage our own disease and treatment. We’re usually just handed a pill and told it will solve our problems (ha!).

But we can still embark on a journey of lifelong learning. Science can help us understand, and therefore to co-manage, our lifelong chronic health condition as it may change through our life.

2. Physician activism in 2021: Fight for us!

Our organization is more than just a place for patients. We know that doctors come to our website and find value in it. I get emails.

We often make appeals to you, dear physicians, in your offices (or on Zoom) when you see us. But that’s not enough to make changes happen. We also need to have a voice in public venues like this, where our power relationship is not in the way, and where you don’t feel personally involved. Here in public we can talk with all of you as doctors, collectively, about our thyroid diagnosis and thyroid therapy.

Here on this website, I as a patient often address you on behalf of many other patients, speaking as a collective “we.” I will continue to educate, support, and persuade you as doctors to be, like the thyroid gland itself, a “shield” of our thyroid hormone health. (See “The thyroid gland is a T3 shield. Defend the unshielded.“)

We call on you to stand by us and believe us when other doctors would dismiss the severity of our symptoms and attribute our health problems to nonthyroidal or psychosomatic causes. The best of you know that thyroid hormone signaling and metabolism occurs everywhere, in every organ and tissue, and that the TSH alone can’t speak for the thyroid status of any other organ or tissue.

We need you, dear physicians, to be our advocates in professional settings where we are voiceless and powerless. We call on you, physicians, to take courage and fight for our health more than just protect and advance your personal careers.

We call on you to protect and stand by your fellow physicians when they are arraigned by medical authorities for being visionary nonconformists who actually help their patients by going beyond the guidelines. Guidelines are consensus documents embedded in history, and research can prove their guidance misguided immediately after they are published. Guidelines are not absolute laws, and they can be used as weapons by people who want to instill fear and gain power.

Any thyroid patient who has ever been helped by a physician will have a deep respect and gratitude for all good thyroid doctors. What is a good thyroid doctor? See our post “Thank you, good thyroid doctors!” for a list of features.

At the same time, any thyroid patient who has been through thyroid disorder misdiagnosis, delayed diagnosis, or mistreatment has a right to complain publicly against doctors who publish materials that twist or overlook thyroid science, or that denigrate patients, leading to grave harm and suffering. (See an especially sickening example that deserved our rebuke: “2019 ATA article engages in patient-blaming and doctor-shaming.”).

I have hope, and I believe many others do as well, that many a “bad thyroid doctor” can admit their mistakes and become a “good thyroid doctor.” But it will take a lot more than just a science-based blog by a thyroid patient’s organization to make that change happen.


Tania S. Smith, PhD,
President, Thyroid Patients Canada,
and thyroid science analyst

4 thoughts on “Thyroid Patients Canada: Looking back on 2020, entering 2021

  1. Thank you so much! You are doing us a great service! I haven’t found a higher quality, more detailed thyroid resource anywhere!

  2. Love this site! It’s so refreshing to find a scientific research based thyroid resource. I’ve been exploring the site and reading of the articles. Is there any information how to switch from NDT to synthetic T4 and T3. I’ve read many people do a straight conversion ie. 2 grains on NDT would be 76 mcg of T4 and 18 mcg of T3 but that seems almost too easy. Thank you!

    1. Thanks for your kind feedback Beth! Yes here are the links.

      In part 1, I do a critique of the dose conversion charts in current product monographs for T3 and for ERFA desiccated thyroid, and then I give the conversion charts from history. Some of the charts show the average doses on T3 mono vs. T4 mono vs NDT.

      It comes with a part 2 post on modern science on dose equivalency, which includes data on T3 monotherapy versus T4 monotherapy, and it ends with implications for T4-T3 combination therapy.

      I also have a separate post on the NDT – LT4 dose equivalency tables that came out of a clinical trial by Hoang in 2013 — the problem is that they were using a narrower range within the TSH reference range as their therapy target, and they permitted some people’s FT4 to fall below range on desiccated thyroid!!

      Most modern trials that try to work out thyroid dose equivalencies force people onto poorly optimized therapy by a TSH normalization target alone. They simply do not care about adjusting doses within FT3 and FT4 reference ranges to remove hypothyroid signs and symptoms on EITHER medication regime, over a longer term period. Many trials have a bias toward the regime the patient was on for a long time before they enrolled in the clinical trial, which had the higher likelihood of being optimized to fit the patient’s long term well being.

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