An excellent article on Healthing.ca by Postmedia Network journalist Karen Hawthorne provides a wealth of insight into hypothyroidism in a short article. I think it’s so well-written that it deserves an award for excellence in journalism.
This is an article worth discussing and amplifying.
I know that a journalistic article must be short. It can’t include everything, and I had a lot to say in my interview that could not be included. So I’m offering my selected paraphrases, quotations, and additional commentary, in my characteristic manner. I go on short forays into the relevant thyroid science.
I also have sincere praise and thanks to offer in response to Hawthorne’s representation of the perspectives of Laz Bouros and Dr. Sana Ghaznavi, the other two interviewees featured in this article. We’re in this together.
My interview excerpts, and beyond
The article begins with information and quotes from an interview with me, Thyroid Patients Canada founder and president, Tania Sona Smith. Last year, I posted a social media Change dot org Petition to grant thyroid disease official “chronic disease” status in Canada and to include thyroid disease in our national chronic disease surveillance program.
I’m so glad that our unofficial petition inspired Hawthorne. Someday I’d like to launch an official federal petition to the Public Health Agency of Canada, and now thanks to Hawthorne’s article, I know who to ask for help in that endeavor!
Karen Hawthorne asked me why I founded Thyroid Patients Canada back in 2020. Of course, a lot of it had to do with my own diagnosis and treatment story. That’s where long-term passion comes from.
But some of my passion also comes from my skills and insight as an academic in the humanities who deeply respects scientific inquiry. As an academic in communications studies who is interested in both the science and the “rhetoric of science,” I read deeply in the published thyroid science. I started reading back in 2016 when my treatment difficulties became a health crisis. I saw from my experience AND my reading that hypothyroid treatment was not sufficiently based on publications in thyroid science, but on biased traditions and dogma that cater to the professional limitations and preferences of physicians.
In my case, prior to diagnosis, the fatigue and unexplained depression caused by hypothyroidism was severe. It made it unsafe to drive, as described in Hawthorne’s article. I didn’t realize until 13 years later that my severe symptoms were likely caused by complete atrophic thyroiditis and/or TSH-receptor-blocking antibodies prior to atrophy. My first ultrasound in 2016 revealed my thyroid was 0.5 mL in volume. No wonder back in 2003 my TSH was over 150 mIU/L at diagnosis with no goiter. I didn’t even have an elevated TPOab in 2016, so I’m not a Hashimoto’s patient.
Yes, hypothyroid etiology (cause) matters in hypothyroid therapy, contrary to science-blind conventional medical opinion. Conventional diagnosis likes to put all cases of acquired hypothyroidism in one bucket labeled “autoimmune hypothyroidism.” No, thyroid atrophy is not “late-stage Hashimoto’s,” as I explain in my article reviewing the science on atrophic thyroiditis. Unlike my peers with Hashimoto’s, I’m more like a rare Graves’ disease patient who flipped from hyper to the hypothyroid side, or like a Graves’ patient whose TSH-receptor antibodies continue to manipulate TSH after a total thyroidectomy. This partly explains why my TSH was very unreliable in response to FT3 and FT4 (Paragliola et al, 2019; See “The TSAb stimulating antibody can lower TSH despite euthyroid status.“).
As I explain in Hawthorne’s article, during standard levothyroxine, my treatment was also complicated by a secondary thyroid problem that now has a name. My lab results manifested what is now being proposed as a syndrome “resistance to exogenous thyroxine” (Lacamara et al, 2020). This condition makes TSH rise unreasonably high per unit of normal or high FT4, and it often coexists with an extremely low FT3/FT4 ratio. In fact, the extremely abnormal hormone ratios, including ratios with the much-maligned Reverse T3 (RT3) hormone, provide the fingerprint of this diagnosis. Hormone ratios matter.
Before Lacamara’s article identified the manifestations of this syndrome, this discordance between a high TSH and high-normal FT4 had often been attributed to patient noncompliance. But you can’t induce the telltale set of hormone ratios seen in Lacamara’s study by not taking your levothyroxine meds properly. I feel insulted by the fact that my physicians likely misattributed my TSH misbehavior to missed doses followed by extra doses before a lab test. No, I was extremely compliant because my mental health depended on not missing a single dose. Dear physicians, when you don’t know what is going on, keep an open mind as you do research. And ask the patient. Don’t blame the patient in secret and keep your unproven accusation to yourself.
In 2016, when I fell into an unexplained illness with cardiovascular manifestations and a high RT3, my body’s poor response to standard hypothyroid treatment interfered my job as a university professor. It eventually cost the healthcare system several emergency visits and expensive tests for daily recurrent chest pain.
Finally, the mysterious random chest pain syndrome was resolved by reversing my chronic T3 deficiency — by including thyroid hormone, T3 (liothyronine) in my hypothyroid treatment. Why didn’t any physician think of vascular problems due to endothelial dysfunction? Because they didn’t learn in medical school that a T3 hormone deficiency may have a harmful influence on vascular integrity. Apparently that’s learned by reading the science.
I’ve learned a lot from my diverse fellow thyroid patients since my own thyroid treatment malfunction in 2016. I believe we need more than one thyroid patient organization that functions as a “voice of thyroid patients in Canada” — and globally.
Whenever I have a little time beyond my day job and private responsibilities, I confidently and publicly advocate for patients based on science, and I advocate for better thyroid science.
We need more science on hypothyroid treatment that truly supports patients and changes rigid, outdated, anti-T3 and symptom-dismissing policies. If LT4 monotherapy treatment was implemented as early as the 1970s, why was a 2014 ATA hypothyroid treatment guideline confessing to so much ignorance about crucial issues, such as the clinical impact of variations in T3 levels during treatment? Too much hypothyroid therapy research has been T3-blind or fearful of T3’s power. A lot of it has attempted to defend traditional TSH-normalized LT4 monotherapy rather than truly defending the health and well-being of all patients.
But there’s a lot of good thyroid science that ought to be celebrated. Drawing on a bibliography I provided by email, Hawthorne points to two of the most important recent publications in the field of hypothyroidism, the international consensus statement on combination T4-T3 therapy (Jonklaas et al, 2021) and Dr. Antonio Bianco’s new book, Rethinking Hypothyroidism, published in 2022. But the work of scientist Rudolf Hoermann and team on hypothyroid therapy is among the best because it reveals the weaknesses of what I call “TSH-only-ism” and highlights the value of Free T3 testing. I highly recommend a 2023 interview of Hoermann on Endocrine news by D. Bagley in July 2023, “A Second Opinion: A novel approach to treating hypothyroidism shifts the focus from TSH levels.”
Insights from Bouros and Ghaznavi
But my experience and insights weren’t the only feature in this article. Hawthorne also asked Canadian endocrinologist Dr. Sana Ghaznavi and the Thyroid Foundation of Canada’s president, Laz Bouros, to comment on the need for the Public Health Agency of Canada to monitor thyroid diseases. They agreed Canada ought to add thyroid to its chronic diseases list.
Bouros is quoted as explaining that the symptoms of incomplete thyroid treatment are a heavy burden for some individuals. Thanks for reporting that. I would agree based on my role as administrator in an online patient support group with over 2000 patients.
My question to Canadian physicians, citizens, and our government is, wouldn’t the symptomatic burden and comorbidities of many poorly treated hypothyroid individuals be a burden for Canadian society as a whole? I think of how my challenges cost the healthcare system, and I paid for supplementary healthcare, while it disrupted my personal and professional life. Luckily I was a fairly healthy 46 year old at the time; I cannot imagine what it would be like if I had been a hypothyroid patient over 60 with heart failure, or a young pregnant mother with a toddler to manage. How do problems during hypothyroid treatment affect families, employment, communities, comorbidities, emergency visits, hospital admissions, and mortality rates? These issues deserve more than superficial research approaches of the past. So much thyroid research is designed to conceal or minimize the problems faced by a minority.
In the article, Dr Ghaznavi points to the problems caused by Choosing Wisely’s unwise campaign to cancel FT3 and FT4 tests during levothyroxine treatment whenever the TSH is normal:
“What’s troublesome about that is that if you’re not checking for low T-3, you’re not going find the percentage of patients who even though their TSH is normal, their T-3 is overtly low. That guideline has to be updated to say, ‘in patients that are otherwise feeling well, it’s okay to continue to do the TSH alone.’”(Dr. Ghaznavi, in Hawthorne, 2023)
Ghaznavi is right. TSH alone might be fine most of the time for most patients who aren’t symptomatic. However, I hesitate. I’m still concerned about the asymptomatic thyroid patient with a chronically low FT3 or low FT3/FT4 ratio. They’re walking on thin ice. What happens when a severe illness of any kind causes them to lose even more of their T3? I was in that situation in my final 3 months of Levothyroxine monotherapy. I could not recover without LT3 treatment.
I’m also proud of Ghaznavi for explaining how she treats patients with two LT3 doses a day.
We each have a different response to LT3 treatment. Whereas one patient of Ghaznavi’s may be symptomatic by 2pm, another patient may differ in their metabolic clearance rate of T3 hormone and their simultaneous T4-T3 conversion rate. I happily dose 4-5x a day to even out the peaks and valleys of my current treatment with fast-release LT3 monotherapy.
Ghaznavi’s complaint against considering hypothyroidism “fixed” by TSH-normalizing LT4 treatment should be echoed:
“I think by saying that it isn’t a chronic disease is just feeding into this narrative that if you don’t have a functioning thyroid, we give you T-4. If your TSH is normal, then you’re normal. Everything fixed. But that’s a total oversimplification of something that’s physiologically a much more complex problem to solve.”(Dr. Ghaznavi, in Hawthorne, 2023)
Hear hear! Like diabetes, thyroid disease is not fixed or cured by treatment. It’s just managed, well or poorly, deeply or superficially. Since thyroid hormones are needed by all tissues and organs, thyroid disease is a multi-system disorder, not just a problem that affects the function of a single gland.
It’s so refreshing to hear Ghaznavi’s emphasis on symptoms, FT3 levels, and LT3-inclusive treatment. I’m so surprised to hear this coming from an endocrinologist, after reading many decades of science in which endocrinologists preach and defend a narrow-minded, rigid, outdated dogma that oversimplified and cheapened thyroid disease management as a mere matter of TSH management. Thank you!
My commentary on Ghaznavi’s points is to elaborate more on the complexity and individuality of thyroid hormone transport and metabolism. The complexity explains why plasma T3 levels matter AND why merely normalizing biochemistry does not necessarily make this chronic disease and its symptoms or health risks disappear. Ineffective treatment can still exist when all three hormones are in their normal ranges. That’s because each person’s individual setpoint, or therapeutic window, may be located in a narrow individual range within those population ranges, as shown by Hoermann et al’s excellent longitudinal research published in 2019. During an average of more than 5 patient years of LT4 monotherapy, each individual had a different FT3 level at which hypothyroid symptoms appeared or disappeared:
When looking at the individuality of this graph, why would you force a patient with a high setpoint to live with thyroid hormones in the low end of range, and vice versa? Why would you dismiss a single burdensome symptom when a strategic dose adjustment may make symptoms “absent”? And what do you do when there’s hardly any distance between symptomatic and asymptomatic FT3 levels, as with the short lines in the graph above? It’s not sustainable in lifelong therapy. For them, I suggest including LT3 to widen the therapeutic window.
Unfortunately, we can’t see their concurrent FT4 in this graph above. The concurrent FT4 and efficiency of T4-T3 conversion plays a major role in determining one’s need for more or less FT3 in circulation.
We at Thyroid Patients Canada sincerely thank Karen Hawthorne for her excellent journalism. We thank Laz Bouros and Dr Ghaznavi for raising their voices with mine and our organization in a chorus calling for change.
In the context of the horrible things going on with restrictive LT3 treatment policies, TSH-only-ism and anti-LT3 attitudes in the UK right now (I’ll say more about that later), this article is a breath of fresh air. So encouraging.
Let’s embrace the complexity and individuality of thyroid diseases and their treatment. Thyroid disease is not as simple as we all want it to be. You can’t say hyperthyroidism is more complex than hypothyroidism, or that diabetes is more complex than thyroid disease. If we accept these complexities and listen to the best thyroid science and the patient, we have more chance of succeeding together at thyroid therapy.