Meet our campaign’s main writer, Tania Sona Smith

Meet campaign researcher

I’ve decided it’s finally time to put a human face and name behind our campaign so that media can contact us and know who to talk to.

Our campaign has experienced significant growth since we started in July 2018. I’ve made 79 blog posts on and this is my 80th. We also have 25 web pages containing our Campaign statement and its reference list. We now have over 1,000 page likes and many positive reviews.

It’s a scary step for me to put my name out there. As I’ve explained on our website, most of us in the advisory group, including myself, do not enjoy the stress of being in the public spotlight. I hope I will have the energy and wisdom to say the right things at the right time.

Given what has happened to thyroid doctors who don’t conform to narrow views, I fear backlash against my role in our campaign could be aimed at my thyroid doctor. In our climate of medical policing, I encourage you all to keep your doctors’ names out of the public light in our campaign unless they give permission or go public themselves.

Here, I’ll answer a few questions that people might have about me.

Who are you to speak for all thyroid patients?

I am a researcher and writer who defends and raises awareness of the thyroid hormone T3 in the context of overall thyroid hormone health, thyroid gland health, and other health factors.

Even if you only take T4 hormone in medication, or if you take no thyroid medication at all, your body still needs to secrete or convert enough of its own T3, and not too much T3, to be healthy.

Does every human being and every organ and tissue need optimal circulating and intracellular T3 hormone levels for health?


Are people with healthy thyroid glands at higher risk of death and continued illness when their T3 levels fall low and stay low during critical illness?


Are all thyroid patients’ T3 hormone levels at risk during thyroid disease and thyroid therapy — either at risk of excess or insufficiency, or unequal distribution among tissues?


Patient advocacy is not like a system of political representation. You don’t have to vote me into office for me to have a right to speak on your behalf as a fellow patient. I don’t need to have your type of thyroid disease or be taking your brand of thyroid medication to have empathy for you and to want the best for your treatment.

Because I speak out to defend and raise public awareness of your need for optimal T3, I do speak, indirectly, on your behalf, as a human being dependent on thyroid hormones.

I harp on and on about T3 hormone because I truly believe it is the main key to understanding and improving thyroid therapy and everyone’s thyroid hormone health. T4 and TSH and even the other thyroid hormone metabolites play their supporting roles, but nobody can survive without T3, and no one can thrive without well-regulated T3 signaling.

The T3 hormone has long been the most underappreciated and misunderstood thyroid hormone, and I believe this is the main reason why our disease and therapy is so misunderstood and poorly treated.

Maybe the fact that T3 hormone was co-discovered by a UK woman (Rosalind Pitt-Rivers) and a Canadian man (Jack Gross), rather than by a group of American men (in the scientific and social climate of the 1950s), has something to do with the way this important hormone has been treated over the years as a minor byproduct less worthy of measurement. (See “HISTORY: Rosalind Pitt-Rivers, the co-discoverer of T3 hormone“.)

Within the triad of T3, T4 and TSH hormones, T3 has the most powerful, direct influence on human health in every organ and tissue of our body. T3’s role in this triad shifts and responds in the context of thyroid gland health and thyroid therapy modality. This triad is also affected by other health conditions, medications, diet, lifestyle, and genetics. The triad shifts from fetal life to advanced age, within circadian rhythms, within pregnancy, within a monthly menstrual cycle, and as our body experiences the four seasons.

In the midst of this huge and complex system, if you don’t have a healthy thyroid gland to help you protect your T3 levels within the range that your individual body requires (which is not the same as the statistical reference range), your T3 is at risk of relative excess or deficiency.

Therefore, I believe all thyroid patients can benefit, indirectly from an advocate like me as I write publicly to support patients, physicians, and scientists.

Who are you as a thyroid patient?

I am quite an unusual thyroid patient.

No, I don’t have the most common type of thyroid disease, Hashimoto’s thyroiditis. I haven’t had thyroid cancer or thyroidectomy.

But I am thyroidless and severely hypothyroid without medication.

I have three rare conditions:

  1. Severe autoimmune Atrophic Thyroiditis, which can be called an “autoimmune thyroidectomy” because it took away my thyroid gland without surgery. (See my review of this variant “The THIRD type of autoimmune thyroid disease: Atrophic Thyroiditis“)
  2. Extremely poor T4-T3 conversion, although I do not have the classic DIO2 polymorphism, only two inactivating DIO1 polymorphisms, what looks more like an “SBP2 deficiency” described by Dumitrescu et al.
  3. Abnormal variation in TSH-FT4 relationships that, when plotted on a graph, fall in the zone of central hypothyroidism and then rise into the zone thyroid hormone (RTH). This is likely due to flares of the TSH-receptor stimulating and blocking antibodies.

I’ll summarize briefly.

As an Atrophic Thyroiditis patient, autoimmune attack by two variants of the Graves’ disease antibody has shrunk my thyroid gland down to a fibrosed flap of flesh about 0.5 mL in volume, according to ultrasound measurements. As evidence of near zero thyroid function, TSH does not stimulate thyroglobulin or FT4:

  • I have undetectable thyroglobulin protein over 4 test results, one of them when TSH was 6.17 mU/L (although mildly high TG antibodies are present)
  • Once, when TSH was 15.0 while underdosed on LT3 monotherapy, I had 0.5 pmol/L of FT4 (reference 10.0-25.0) in circulation, which is close to the assay’s lower limit of detection. However, this assay’s measurement may be unreliable because FT4 is <0.3 to 0.8 even when TSH is fully suppressed by euthyroid LT3 therapy.

I am also among the poorest of poor converters of T4 hormone into T3 hormone — an extreme statistical outlier with a stable FT3:FT4 ratio below 0.15 (mol/mol) while on LT4 monotherapy.

All three of my conditions caused my TSH test results to fluctuate from low to high above range on T4 monotherapy. My TSH had no logical relationship to my FT4 or FT3 thyroid hormone levels. TSH was a false guide for over a decade on standard therapy.

After up to 13 years of suffering with chronic low T3 and high-normal Free T4 while on standard thyroid therapy (Synthroid), I developed severe hypothyroid manifestations and an adverse cardiovascular response to T4 medication. I can no longer take T4 medication, not even desiccated thyroid (I tried it in 2017), without body-jolting cardiovascular spasms in my aortic branches.

While I suffered nonthyroidal illness with a high RT3 of 33 (8-25), I had an increased rate of thyroid hormone inactivation and my FT3 fell to 2.9 (3.5-6.5), but no one was willing to help me recover my T3 hormone. I sought a physician willing to dose me on T3 hormone.

For the better part of three years now (since Spring 2016) I have been happily maintained on a full thyroid replacement dose of T3 monotherapy.

I am truly “powered by T3” and T3 alone, since I maintain euthyroid status and overall health without little to no measurable FT4 or TSH in my body most of the time. Most people with untreated low FT4 and TSH would have “central hypothyroidism,” but my T3 levels are higher than normal, which compensates for the lack of T4 in circulation without causing thyrotoxicosis.

Living on T3 alone is something many people think is impossible or unhealthy, but I’m part of a worldwide network of people who flourish on LT3 therapy by necessity. Taking several doses of T3 every day is challenging. But I’m an adult, and it is under my conscious control, like a person dosing their own insulin as a diabetic. It can be a very effective last-resort therapy when all other thyroid therapy modalities and combinations have failed or cause harm, as they have in my case. I will say more in other posts in future. (See one of my personal narrative posts: “Thyroid therapies: What my life is like in the T3-monotherapy wheelchair“)

How do you know all this stuff about your own thyroid condition?

I have no formal medical or scientific education beyond high school chemistry. I am self-taught through immersion in thyroid scientific literature from the 1950s to the present.

Thanks to the better thyroid care provided by my current doctors, I have had the mental energy to analyze my laboratory test history, symptom history, and genetic test results in the light of my growing understanding of thyroid science.

I will have to write a separate post that provides the data and cites the scientific research that clearly confirms my diagnosis. I’m sure I’d be an interesting case to many curious thyroid doctors and researchers.

I believe rare cases of LT4 thyroid therapy derailment are more common than they appear to be. After all, my unusual thyroid conditions remained undiagnosed for a very long time. I dealt with symptoms through diet and supplements. I didn’t attribute most of my symptoms to thyroid, although I knew the cognitive and emotional symptoms were definitely thyroid. I blamed a lot on my other autoimmune condition that had an official diagnosis, ankylosing spondylitis. People can’t see something until they know what patterns to look for, and it’s too easy to blame the devil you know.


In part 2, I talk about the kinds of research I do in the scientific literature on thyroid, how I see thyroid patient advocacy, and my hopes for this campaign’s future.

See “Part 2: Meet our campaign’s main writer, advocate and researcher

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