Questions about thyroid and COVID-19 risk

This is not just another blog post that tries to answer questions with authoritative statements about coronavirus from the World Health Organization.

This blog post is about ASKING good questions and thinking critically about how questions are being answered.

Our thyroid patient community has been asking, and many voices are trying to answer, this general question: “are thyroid patients at risk from COVID-19”?

We’ve been given trite and superficial answers that apply to everyone in a time of crisis: Even when the specific topic is thyroid diseases and thyroid hormones, all that some people can say is something that comes down to “go wash thy hands, isolate thyself, and stop asking selfishly about your unrelated silly little disease. Stopping this infection is more important than any other disease right now.”

Most of that answer is correct except for the “unrelated silly little disease” part. You don’t know if it’s unrelated, it’s certainly not sillier than diabetes or heart disease, and it is not little in terms of the numbers of people affected by it.

We’ve been given speculative “You may may be at risk…” answers that often preface practical suggestions. Some of these suggestions are myths that have little basis in science, and others that are so general and relatively harmless as to apply to everyone.

At their worst, they make us more worried and trick us into buying stuff or doing stuff to make us feel like we’re protecting ourselves.

At their best, they motivate us to employ wise foresight. We all need to do general things to prepare ourselves for a rough ride through virus era, no matter what chronic disease we may have.

We’ve also been given “There’s no evidence, so calm down” answers that preface overconfident reassurances based on no evidence. What we don’t know can’t hurt us, right? Hmm. Sounds like a response you’d give to a child.

Making someone fearful based on no evidence and making someone feel invulnerable based on no evidence are both equally based on … no evidence.

Asking the right questions soon is a crucial skill in the viral era. Scientists need to hear our questions today so they can design studies that understand the mechanisms tomorrow. We simply don’t have time to waste on superficial questions.

If we ask imprecise or childish questions, we will get trite, manipulative, or overconfident replies.

  • I’ll first give my own 3 answers to the question “Why are there no simple answers?”
  • After that, I’ll break down 3 sub-questions about COVID risk in general, followed by 4 key thyroid disease variables we should look at when asking about thyroid & coronavirus risk.
  • I’ll conclude by analyzing answers given by the British Thyroid Foundation.

I challenge thyroid patients and scientists to ask the right questions.

Why are there no simple answers?

First of all, thyroid disorders are diverse and very complex. There are at least 4 major variables: 1) etiology, 2) gland health, 3) biochemistry, and 4) tissue thyroid status. I’ve just posted in some detail about the scientific basis of these 4 ways of seeing / defining thyroid status.

Many problems result from not seeing through all four lenses and getting stuck on narrow views of thyroid biochemistry. The examples below demonstrate the problem with using the term “hypothyroidism” (or hyperthyroidism) and assuming it is one monolithic thing.

Secondly, viral infections of any type are also complex. There is the “innate” immune system and the “adaptive” immune system.

You also need to know which stages of viral infection may involve thyroid hormones: “Viral replication involves six steps: attachment, penetration, uncoating, replication, assembly, and release.” (Biology LibreTexts)

In the dysfunctional response of “autoimmunity,” “viruses can lead to autoimmune activation or induce tolerance,” and “the reaction of our immune system against the pathogen can cause organ damage (immunopathology) or lead to autoimmune disease.(Fousteri & Dave Jhatakia, 2019). If we already have autoimmune thyroid disease, we have genes that also make us susceptible to additional autoimmune diseases.

Thirdly, there are too many unknowns about how this particular COVID-19 virus affects people with various “comorbidities” (other concurrent diseases) in various human populations. Scientists are studying it frantically right now.

However, questions about hypothyroidism have not yet been asked. We’ve looked at other comorbidities, though, even liver disease.

[View full text of source]

Let’s break down the “risk” question.

It’s too vague to ask “are thyroid patients at risk from COVID-19”? There are many sub-questions in that single question. First, define “risk,” risk of what?

A) Are we more vulnerable to contracting this viral infection?

B) Are we at higher risk of having “serious complications” from this viral infection?

C) Are we at higher risk of death or permanent damage when suffering from complications from this viral infection?

A retrospective study was done on the Middle East coronavirus outbreak in Saudia Arabia, including all cases reported from April 2014 to August 2015 (Aleanizy et al, 2017).

[View the full table]

In this example, which is NOT about the virus we’re facing today, but which was indeed a respiratory coronavirus, hypothyroidism was just as frequent as “pneumonia,” and more frequent than “acute respiratory distress syndrome.”

In a later Saudi Arabian study published by Alqahtani et al, 2018, further data listed hypothyroidism again.

[view the study]

As you can see, in the Saudi Arabian studies of the MERS coronavirus outbreak of 2014-2016, the vagueness of the term “hypothyroidism” leaves many questions unanswered. The methods section in the 2017 article only said “Patient’s charts were reviewed for demographic information, mortality, comorbidities, clinical presentations and health care facility.”

  • How was their hypothyroid status defined?
  • Was their hypothyroidism being treated, and if so, was it treated well?
  • How many of the people in this list were hypothyroid but not diagnosed or treated?
  • How many of them experienced “Low T3 Syndrome” (nonthyroidal illness) despite having a healthy thyroid?

Let’s break down the “thyroid disease” variables.

The four major variables involved in defining thyroid disease are

  • 1) thyroid etiology (especially autoimmunity)
  • 2) thyroid and pituitary gland health,
  • 3) thyroid biochemistry, and
  • 4) tissue thyroid status.

These variables have been defined already in a previous post. Here I give scientists some research methods tips for answering these questions.

1. AUTOIMMUNITY: Are we at more risk IF we have above-normal anti-thyroid antibodies floating around in our blood?

To isolate this “autoimmunity” factor from thyroid biochemistry, you’d have to include ALL the relevant thyroid antibodies, not just TPO and TG, because Graves’ antibodies are found in 9-10% of Hashimoto’s patients (Diana et al, 2017; Fröhlich & Wahl, 2017).

  • TPOAb – anti-Thyroid Peroxidase Antibody
  • TGAb – anti-Thyroglobulin Antibody
  • TRAb – TSH-Receptor antibodies. Measure BOTH Graves stimulating (TSAb) AND Graves blocking (TBAb), so you have to use a TBII test as well as a TSAb test)

If you’re going to study this, you also have to include treated Graves’ disease and Hashimoto’s and Atrophic thyroiditis patients, because WE are the ones asking the question, and whose health is at question. It also helps to include us because you’re more likely to be able to rule out risk due to high or low thyroid hormones if you study treated patients.

2. GLAND HEALTH: Are we at more risk IF we have poor thyroid gland health and pituitary gland function?

To isolate this “gland health” factor, one will need to do ultrasound studies or have ultrasound records. Echogenicity and vascularity, as well as thyroid volume, are relevant factors.

One can also examine T4 and T3 levels and their rise or fall in relation to TSH, and programs like SPINA-Thyr can give a mathematical estimate of thyroid gland responsiveness to TSH.

But you can’t just study the thyroid gland. The thyroid gland is only one part of the HPT axis (hypothalamus-pituitary-thyroid axis). Examine pituitary function. Programs like SPINA-Thyr can even use TSH and FT4 data within the reference range to determine how well the TSH is responding to FT4.

Consider both pituitary TSH secretion and thyroid health in patients treated for hypothyroidism, not assuming a person with a damaged thyroid always has a normal TSH secretion rate. It takes some intelligence, but central hypothyroidism can be diagnosed during therapy for primary hypothyroidism.

3. BIOCHEMISTRY: Are we at more risk IF we are hypothyroid or thyrotoxic in biochemistry right now?

To answer this question, one has to know patients’ FT3 and FT4 levels and their FT3:FT4 ratios and then divide the study population into cohorts by their thyroid hormone variables. Cohorts are important lenses on data, so take care: don’t presume the FT3 and FT4 reference ranges define cohort boundaries. Find out where the cohorts “organically” fall, perhaps even mid-range, instead of assuming that cells treat our statistical reference range boundaries like speed limit signs.

One must include both thyroid hormones because “The thyroid hormones (THs), 3,3′,5,5′ tetraiodo-L-thyroxine (T4) and 3,3′,5-triiodo-L-thyronine (T3) play essential roles in both the innate and adaptive immune responses.” (Montesinos & Pellizas, 2019).

To answer this question, we should also ask about TSH hormone. In 2018, Klein wrote “It has been known for over three decades that thyroid stimulating hormone (TSH) is made by cells of the immune system.”

Again, include treated thyroid patients in studies of all 3 hormones, because WE are the people who are asking the question. Excluding us makes the study less irrelevant to those whose biochemistry is manipulated by medication and whose life and health depends on T3 and T4.

As an incentive for an intervention study to treat COVID-19, it’s easy to experiment with changes to our dose or medication type because we are already taking thyroid medication.

4. Tissue thyroid status: Are we more susceptible to non-recovery from COVID-19 serious complications if we can’t secrete enough TSH or don’t have a thyroid that TSH can stimulate?

“Nonthyroidal illness syndrome” (NTIS), also known as Low T3 Syndrome, is a common finding in almost all acute illnesses and many chronic illnesses.

This is a thyroid disease factor because recovery from nonthyroidal illness syndrome (NTIS) in all types of illnesses, from pulmonary failure to heart failure, is accomplished by TSH rising (which requires a healthy pituitary secretion ability).

In other words, during “RECOVERY” phase, natural recovery a high enough TSH to stimulate enough thyroid tissue to hypersecrete T4 and T3 to give a “refill” of the depleted hormones, especially the T3 hormone.

As you can see in the figure, TSH can even rise above reference during recovery.

What happens to people who can’t raise their TSH because they have central hypothyroidism?

What happens to people who have no thyroid gland that can respond to TSH by secreting T3 and T4 to refill their depleted hormones enough to recover?

Treated, thyroid-disabled patients have been routinely excluded from NTIS studies, mainly because its deceptive name “nonthyroidal illness” makes it seem like it has nothing to do with people who have a “thyroidal” illness. But a little research shows we are susceptible, and we don’t know what our risk rate is in any type of NTIS.

Now is the time to include treated thyroid patients, as well as “nonthyroidal” patients, in studies of coronavirus nonthyroidal illness.

Early Answers from the BTF

To be fair, we know it’s hard to give a helpful, intelligent answer.

As you can see above, there are 9 questions here: you can ask about 4 different variables for each of the 3 risks.

The British Thyroid Foundation said this on the version published March 9th, 2020:

“There is no reason to believe that people with thyroid problems (autoimmune or otherwise) are at any excess risk from coronavirus.”

[See the BTF coronavirus page archived on March 10, 2020 on]

As of March 25, the statement was updated to say this:

“Many people are asking whether having an autoimmune thyroid disease means you are immunocompromised. We can confirm it does not. The part of the immune system that’s responsible for autoimmune thyroid conditions is separate to the immune system that’s responsible for fighting off viral infections, such as COVID-19.” 

This very confident answer (their “not” is in bold text on their page), which intelligently distinguishes between innate and adaptive immunity, side-steps the question regarding the role of thyroid hormones and TSH in the innate immune system, and does not address the literature that has theorized autoimmune response to viral infections.

The March 25 updated BTF statement contained more information about biochemistry:

“There is currently no evidence that those with ‘poorly controlled’ thyroid disease are more likely to contract viral infections in general.

However, it is possible that patients with ‘uncontrolled’ thyroid disease (these are people who have very recently started medication or who do not take their thyroid medication as prescribed) may be at higher risk of complications from any infection. This is especially the case for those with an overactive thyroid (otherwise known as hyperthyroidism or thyrotoxicosis). We strongly recommend patients with thyroid disease continue taking their thyroid medication(s) to reduce this risk.”

[See the BTF Coronavirus page archived on March 29, 2020]

After this statement follows FOUR in-depth sections that address therapies for patients with hyperthyroidism, demonstrating an enhanced concern for this type of thyroid disease, and little to none for hypothyroidism.

Since this is the time to ask questions, I would inquire about this article, which seems to suggest the contrary — that higher thyroid hormone levels are helpful, rather than harmful:

  • Ishaq, M., & Natarajan, V. (2016). Integrated Stress Response Signaling Pathways Induced by Supraphysiological Concentrations of Thyroid Hormone Inhibit Viral Replication. Signal Transduction Insights, 5, STI.S39844.

The study abstract concludes by saying “This study offers a proof of principle of the concept that ISR [integreated stress response] activating agents like SPC [supraphysiological concentrations] of T3 and guanabenz can be potential antiviral agents.”

If high T3 inhibits viral replication, may we not ask the logical question about the converse, whether lower T3 levels foster viral replication?

If you examine this British Thyroid Foundation statement, you will also see that it does not address all the various aspects of risk, nor the four key aspects that define thyroid disease.

But we are in early days. Maybe they will revise their statement further.

We’re in this together, and so we have the right to challenge each other as “evidence-based” scientists and “scientifically-informed” patients.

There are 3 possible things one could mean when saying things like “there is no reason to believe…” or “we can confirm it does not,” or “there is currently no evidence that“:


Imagine a person elaborating on this stance:

“I understand the underlying biological theory of viral infection and it’s not rational or logical to think that thyroid status or thyroid autoimmunity makes any difference. These two biological systems do not directly interact with each other at all. They are like two ships passing in the night, oblivious to each other’s existence. It does not make sense to believe that they are related.

Is it truly not likely, given what is said above?


This stance would mean, in other words:

“We’ve conducted a lot of studies on populations in all demographic categories to investigate this question. We compared a control group with a thyroid disease group and found no higher or lower risk in people who are biochemically hypothyroid or in people with thyroid antibodies in circulation. We have worked our butts off trying to see if there was an association, but we came up with nothing. We have a ton of good data and we diligently ruled out any direct relationship.

It’s too early to insinuate such a thing in March 2020.


This is an honest elaboration of the meaning of this stance:

“We haven’t really considered this an important research question because we start with the presumption that it makes no difference. If we were worried about people, we would have done research. But we’re not concerned, so we’ve been sitting on our hands. We haven’t gathered any data, and we haven’t analyzed any data, so we can’t answer that question. We have been so unconcerned about this health issue that we prefer to remain utterly ignorant.

Nobody dares say it this way. But actions speak louder than words.

This is where we are really at.

Scientists have NOT yet considered all the pathways involved in the connection between viral infections and thyroid health conditions. They have NOT done a lot of research on these questions. They have NOT [yet] tried their hardest to look at thyroid patients’ risk, given the various complex aspects of risk and the various aspects that characterize thyroid diseases.

The biggest unasked, unanswered question is that of recovery from nonthyroidal illness syndrome (NTIS), also known as Low T3 Syndrome. This is a thyroid hormone health condition that involves great risk to life.

All patients who suffer from COVID-19 complications are at risk of NTIS and a difficult recovery regardless of whether or not they have a healthy thyroid gland or a thyroid disease.

Scientists in all medical disciplines, including thyroid endocrinologists, have been extremely neglectful to exclude all treated thyroidless individuals and central hypothyroid individuals from NTIS studies. It’s a shameful omission. Now is the time to prove that you truly are concerned for treated hypothyroid patients by including us in such studies.

Unasked questions lead to many, many more unanswered questions.

Let’s ask the right questions.


Aleanizy, F. S., Mohmed, N., Alqahtani, F. Y., & El Hadi Mohamed, R. A. (2017). Outbreak of Middle East respiratory syndrome coronavirus in Saudi Arabia: A retrospective study. BMC Infectious Diseases, 17.

Alqahtani, F. Y., Aleanizy, F. S., Ali El Hadi Mohamed, R., Alanazi, M. S., Mohamed, N., Alrasheed, M. M., Abanmy, N., & Alhawassi, T. (2018). Prevalence of comorbidities in cases of Middle East respiratory syndrome coronavirus: A retrospective study. Epidemiology and Infection, 147.

British Thyroid Foundation. (2020, March 9). Thyroid disease and coronavirus. British Thyroid Foundation.

Diana, T., Krause, J., Olivo, P. D., König, J., Kanitz, M., Decallonne, B., & Kahaly, G. J. (2017). Prevalence and clinical relevance of thyroid stimulating hormone receptor-blocking antibodies in autoimmune thyroid disease. Clinical & Experimental Immunology, 189(3), 304–309.

Fröhlich, E., & Wahl, R. (2017). Thyroid Autoimmunity: Role of Anti-thyroid Antibodies in Thyroid and Extra-Thyroidal Diseases. Frontiers in Immunology, 8.

Fousteri, G., & Dave Jhatakia, A. (2019). Viral Infections and Autoimmune Disease: Roles of LCMV in Delineating Mechanisms of Immune Tolerance. Viruses, 11(10).

Huang, C., Wang, Y., Li, X., Ren, L., Zhao, J., Hu, Y., Zhang, L., Fan, G., Xu, J., Gu, X., Cheng, Z., Yu, T., Xia, J., Wei, Y., Wu, W., Xie, X., Yin, W., Li, H., Liu, M., … Cao, B. (2020). Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet (London, England), 395(10223), 497–506.

Ishaq, M., & Natarajan, V. (2016). Integrated Stress Response Signaling Pathways Induced by Supraphysiological Concentrations of Thyroid Hormone Inhibit Viral Replication. Signal Transduction Insights, 5, STI.S39844.

Klein, J. R. (2018). Regulatory effects of immune system thyroid stimulating hormone β-subunit splice variant (TSHβv) on thyroid hormone secretion in mice. The Journal of Immunology, 200(1 Supplement), 100.1-100.1.

Montesinos, M. del M., & Pellizas, C. G. (2019). Thyroid Hormone Action on Innate Immunity. Frontiers in Endocrinology, 10.

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