Key passages from “Thyroid and the Heart” (Grais & Sowers, 2014)

From “Thyroid and the Heart” by Ira Martin Grais MD and James R. Sowers MD. The American Journal of Medicine, 2014-08-01, Volume 127, Issue 8, Pages 691-698.

My commentary is at the end of the post, following all the excerpts.

From the Abstract

Thyroid hormones modulate every component of the cardiovascular system necessary for normal cardiovascular development and function. ….
The goal of this review is to access contemporary understanding of the effects of thyroid hormones on normal cardiovascular function and the potential role of overt and subclinical hypothyroidism and hyperthyroidism in a variety of cardiovascular diseases.

  • Thyroid and cardiovascular function are intimately linked.
  • When thyroid dysfunction is known or suspected, cardiovascular disease or risk should be assessed.
  • When certain cardiovascular diseases, such as atrial fibrillation or sinus bradycardia occur, thyroid function should be assessed.
  • Cardiac and peripheral vascular function, including cardiac and endothelial mediated vasorelaxation, is partly dependent on thyroid hormone signaling.
  • Subclinical thyroid dysfunction also can be associated with cardiac disorders and merits clinical screening.

Clinical Significance

The relationship of thyroid hormonal abnormalities and cardiovascular disease goes well beyond the risk of atherosclerosis in association with hypothyroidism and the risk of atrial fibrillation in individuals with hyperthyroidism.

The 2 organ systems are intimately linked by their embryological anlage, and the ubiquitous effects of thyroid hormone on the major components of the entire circulatory system: the heart, the blood vessels, and the blood, as defined by the flow law ( Figure 1 ).

Thyroid Hormone Effects on the Cardiovascular System

The major effects of thyroid hormones on the heart are mediated by triiodothyronine (T3) ( Figure 2 ).

  • T3 generally increases the force and speed of systolic contraction and the speed of diastolic relaxation.
  • T3 decreases vascular resistance, including coronary vascular tone, and increases coronary arteriolar angiogenesis.


Thyroid hormones can promote both physiological and pathological myocardial hypertrophy.

Mechanisms of Thyroid Hormone Effects on the Vasculature

It has been known for 2 decades that T3 exerts direct effects on vascular smooth muscle cells to promote relaxation. [….]

T3 stimulates nitric oxide (NO) production […]

T3 reduces vascular smooth muscle cell contraction by decreasing [Ca 2+ ] i as well as Ca 2+ sensitization.

Thyroid Hormones and Heart Failure

The role of low thyroid hormone function in promoting heart failure and the potential benefits of thyroid hormone replacement have been reviewed extensively. In this regard, heart failure can lead to the downregulation of the thyroid hormone signaling system in the heart. In the failing heart, decreases of nuclear TR levels occur. In addition, serum levels of T4 and T3 are decreased with heart failure in the context of the nonthyroidal illness syndrome. [….]

Animal studies and a limited number of human trials indicate that increasing thyroid hormone action, either by increasing T3 receptor levels or serum levels of T3 hormone itself, can improve cardiac function without significant detrimental effects.[….]

While atherosclerosis and atrial fibrillation are most commonly related to abnormal thyroid function, numerous other cardiac conditions also have been related to thyroid dysfunction. These include

  • pericarditis,
  • pericardial effusion,
  • cardiac tamponade,
  • sinus bradycardia and tachycardia,
  • atrioventricular block,
  • torsade de pointes ventricular tachycardia, typically with a long QTc;
  • left ventricular systolic and diastolic dysfunction,
  • heart failure,
  • high output congestive state,
  • cardiomyopathy,
  • mitral valve prolapse (in particular with autoimmune thyroid gland disorders),
  • endothelial dysfunction,
  • dyslipidemia,
  • and both systolic and diastolic hypertension.[….]

Hypothyroidism decreases endothelial-mediated vasorelaxation and vascular compliance and thus, elevated diastolic blood pressure.

Lowered peripheral vascular resistance in hyperthyroidism increases blood volume and venous return. This can lead to what is called “high output failure” when a more accurate term is a congestive state.[….]

While these cardiovascular disease abnormalities have been described with overt thyroid dysfunction, some are increasingly recognized as being associated with subclinical hypothyroidism and subclinical hyperthyroidism.

Even high normal thyroid hormone function is associated with a slightly increased risk for developing atrial fibrillation.


Hypothyroidism is characterized by depressed levels of T4 and T3, with compensatory high levels of thyroid-stimulating hormone. In seeking the classic clinical manifestations of this condition such as

  • fatigue,
  • sluggishness,
  • hoarse voice,
  • constipation,
  • delayed distal tendon reflexes,
  • and skin changes,

the clinician should also evaluate patients for cardiovascular manifestations of hypothyroidism. The most common are

  • diastolic hypertension,
  • sinus bradycardia due to sinus node dysfunction,
  • and failure of the sinus node to accelerate normally under conditions of stress such as caused by fever, infection, or heart failure.

Other cardiac manifestations may include

  • heart block,
  • pericarditis,
  • pericardial effusion,
  • and rare cardiac tamponade.

Additionally, in chronic hypothyroid states there is

  • increased risk of atherosclerosis often associated with dyslipidemia (hypercholesterolemia) and hypertension.

Less common are

  • cardiomyopathy,
  • endocardial fibrosis,
  • and myxomatous valvular changes.

The coronary artery disease accompanying hypothyroidism may be preexistent or be aggravated by the thyroid dysfunction, especially as peripheral vascular resistance increases. The hypertension associated with hypothyroidism may be asymptomatic or attended by overt myocardial ischemia, including angina pectoris or myocardial infarction. [….]

Typical electrocardiographic changes that can be seen in hypothyroidism include

  • sinus bradycardia,
  • a prolonged QTc (which can result in torsade de pointes ventricular tachycardia),
  • low voltage,
  • and the rare instance of atrioventricular block.

Some of the salient cardiovascular changes that can occur when hypothyroidism is present are

  • sinus bradycardia,
  • decreased cardiac output,
  • diastolic hypertension,
  • increased myocardial oxygen demand due to increased afterload,
  • long QTc with increased risk of torsade,
  • increased risk of atherosclerosis due to dyslipidemia (increased total cholesterol, increased low-density lipoprotein cholesterol, decreased low-density lipoprotein receptors, hypertension, and elevated homocysteine levels),
  • some evidence for increased abdominal aortic atherosclerosis and increased intimal-medial carotid thickening,
  • and decreased myocardial perfusion, which can resolve with thyroid replacement therapy.

Some of these changes are risk factors for coronary artery disease, some relate to the flow law, and some are prime determinants of left ventricular function and myocardial oxygen demand.[….]

For hypothyroid patients with stable coronary artery disease, one should use lower doses of L-thyroxin and increase the dose slowly. For example, one may consider starting at 12.5 μg orally daily and increasing the dose every 6 weeks. The lowering of peripheral vascular resistance with thyroid hormone replacement also can ameliorate the myocardial ischemia in patients with hypothyroidism.[….]

Approximately 4% of patients with hypothyroidism develop pericarditis [….]

Subclinical hypothyroidism is defined as a state with high TSH with normal blood levels of T4 and T3. Here the thyroid dysfunction is compensated for by the greater stimulation of the elevated TSH level. Despite normal levels of thyroid hormone, such patients are at somewhat increased risk of atherosclerosis. [….] Left and right ventricular systolic and diastolic dysfunction also have been described in subclinical hypothyroidism […]


The clinical symptoms and signs of hyperthyroidism include

  • systolic hypertension,
  • increased left ventricular mass,
  • exercise intolerance,
  • angina pectoris, and
  • systolic murmurs.

Complications include

  • atrial fibrillation with its risk of stroke, and
  • high output and
  • heart failure.

Atrial fibrillation, especially in the presence of preexistent heart disease, can result in clinical heart failure. This heart failure may be due to an associated rapid ventricular response, which, when sustained, can lead to tachycardia-mediated cardiomyopathy. The loss of atrial contractile function and decreased diastolic filling time due to the tachycardia may cause increased filling pressures, further contributing to this cardiomyopathy.

Atrial fibrillation and atrial flutter management presents unique challenges in patients with associated hyperthyroidism. [….]

While sinus tachycardia is the most common arrhythmia seen in hyperthyroidism, the incidence of atrial fibrillation ranges from 2% to 20%, with prevalence increasing with age.


Thyroid hormone affects virtually every anatomic and physiologic component of the cardiovascular system. In the presence of heart disease, pericardial disease, heart failure, or arrhythmias, overt or subclinical thyroid dysfunction merits a high level of clinical suspicion.

My Commentary

I am thankful for the important information shared above. However, the article as a whole (admittedly, largely as a reslult of biases and blind spots in the literature it is reviewing) has some serious shortcomings.


This article provides helpful information about hypo- and hyper- thyroid hormonal effects on the cardiovascular system. 

It provides important cautions about administering T4 to hypothyroid patients with certain cardiovascular symptoms. It recommends starting at a very low dose of T4 and increasing very gradually.

I do not believe this information is emphasized enough to health care providers.

In my own experience as a thyroid patient, many doctors were completely unaware of how my vascular symptoms of vasospasm, vasoconstriction and intermittent claudication in adjacent limbs could have been affected by my hypothyroid condition. This article makes it clear that Low T3 and hypothyroidism can affect the cardiovascular system. 

The only thing tests could find wrong with me was my hypothyroid state of Low T3 and high TSH, my extremely tiny and atrophied thyroid gland, some mixed plaque in my carotid artery (way too soon for a 46 year old female), and high LDL cholesterol (despite good HDL and triglycerides).

In addition, caution regarding T4 supplementation was extremely relevant in my case. My blood vessels repeatedly responded negatively to even slight raises in T4 that I took during my illness in the attempt to re-normalize my TSH.

Therefore, this information should be shared and distributed more widely.


Only one early section in the article emphasized the centrality of the T3 hormone. 

It rarely acknowledges the problem of “thyroid hormonal dysfunction.”

Elsewhere, the frequent repetition of “thyroid dysfunction” in the context of TSH levels places undue emphasis on the dysfunction of the thyroid gland itself. 

It is stated that

The goal of therapy is a euthyroid state with normal thyroid-stimulating hormone (TSH) and, of course, improvement in myocardial ischemia and cardiac function (Hypothyroidism section, para. 4). 

This sentence seems to imply that merely normalizing the TSH will result in improvement in cardiac function. However, according to the article itself, that the more crucial hormone that directly improves cardiac function is the T3 hormone. 

In cases of hormone metabolic dysfunction, normalization of TSH does not result in appropriate T3 levels. The connection between TSH and T3 only applies when hormone metabolism is functioning normally. Many things can go wrong between TSH secretion and T3 uptake. 

  • When TSH stimulates the thyroid gland, at least 80% of hormone the thyroid gland secretes is in the form of T4, and a maximum of 18/19% T3.
  • Even a healthy thyroid gland cannot secrete enough T3 to satisfy the body’s needs. The vast majority of our body’s required T3 is converted from T4 within our organs and cells on an “as needed” basis.
  • T4 is merely a storage hormone. When an organ requires more T3 or less T3, it must convert the appropriate amount of T4 into more of the active T3 hormone by removing one iodine molecule. It does this through the enzymes we have identified as “deiodinases” (type 1 and 2) active in organs and cells.
  • Each organ and bodily system has different demands for T3 under different conditions, for energy production within its cells.
  • Sufficient Free T3 levels in serum make T3 equally available to all organs, which is especially important for organs like the heart that are very inefficient at converting T4 to T3 locally. 
  • During transport, T3 in blood directly affects the health, integrity and behavior of blood vessels throughout the body.

Like other organs, the pituitary gland manages its own conversion of the storage hormone T4 to active T3. It converts this from serum at its own rate, independent from other cells in the body.

Therefore, normal TSH is a signal of the pituitary gland’s ability to produce its own sufficient supply of T3 from adequate T4. The pituitary gland is blind to T3 levels outside of itself.

The pituitary gland is protected from thyroid hormone metabolic dysfunction that may exist throughout the body. The pituitary gland does not contain any Deiodinase Type 3, which is the enzyme that can deplete and block T3 in the rest of the body. 

Deiodinase type 3 is responsible for converting T4 to “Reverse T3” which fits into T3 receptors but is inactive. The higher the Reverse T3 levels, the more inactive RT3 molecules can block nuclear receptors and uptake of T3. To make matters worse, the same deiodinase type 3 that converts T4 to RT3 also catabolizes T3 to inactive T2 before it can reach the cell nucleus. Thus, an overactive Deiodinase Type 3 can significantly harm the body — outside the pituitary gland. 

Becasue the pituitary gland is shielded from the effects of Deiodinase Type 3, it may secrete a “normal” level of TSH while the rest of the body may be in a hypothyroid state due to thyroid hormone metabolic dysfunction.

As shown in this article, Subclinical hypothyroidism, defined as a “high” TSH in the presence of “normal” T3 and T4 levels, is the thyroid literature’s most common attempt at acknowledging a thyroid metabolic disorder. However,

  • High TSH is only one way among many that thyroid hormone levels can be imbalanced in relation to each other.
  • Low Free T3 levels should be of much greater concern than high TSH, since the only organ that requires TSH is the thyroid gland. TSH is a signalling hormone, while T3 is the active hormone. The entire body requires sufficient free T3 in serum to supply organs, such as the heart, that are very ineffective at converting T4 to T3.
  • The diagnosis of subclinical hypothyroidism can be made without testing for levels of Reverse T3. Without testing RT3, the root causes of the hormonal imbalance cannot be revealed or ruled out.  Subclinical hypothyroidism is a superficial marker.
  • The level of TSH at which a patient is considered “hypothyroid” has been debated and has changed drastically over the past 15 years. Lab range cutoffs have varied based on what researchers, health organizations, and labs believe to be a “high” TSH.

High TSH alone is not a biologically reliable indicator of thyroid metabolic dysfunction.

Instead, a thyroid hormonal metabolism dysfunction can be better diagnosed by focusing on two relative indicators:

  • Free T3 levels in serum in relation to Free T4 levels. If T4 is high but T3 is low, it may be a sign of a T4>T3 conversion problem caused by insufficient activity of Deiodinases type 1 and type 2.
  • Free T3 in relation to Reverse T3 levels in serum. An extreme FT3/RT3 ratio can verify a metabolic dysfunction with Deiodinase Type 3.

However, I suspect that most thyroid experts do not want to diagnose a metabolism disorder becaue acknowledging such a disorder may justify the use of T3 medication.

The use of T3 medication (such as Cytomel) is only indirectly mentioned, and is treated with suspicion in this article: 

Animal studies and a limited number of human trials indicate that increasing thyroid hormone action, either by increasing T3 receptor levels or serum levels of T3 hormone itself,* can improve cardiac function without significant detrimental effects. It is currently unclear if long-term administration of thyroid hormone** to patients in heart failure will be well tolerated and will lead to increased survival. This can only be determined by long-term randomized controlled clinical trials.***

*This can be done by administering T3 directly.

**Which thyroid hormone, T3 or T4?  It matters. 

If you administer more T4 to a patient whose overactive Deiodinase Type 3 converts T4 to Reverse T3, you may be harming them by blocking and depleting their T3.

*** Controlled trials of T3 are only beginning to be conducted in heart patients suffering from LowT3. Truly more work needs to be done in this area, but it is logical to try supplementing T3 when T3 is low and cannot be converted in sufficient amounts from T4.




Acne on T3-only therapy for hypothyroidism

This article does not review research articles. It only details my careful personal experience and N=1 trials with acne while on T3-therapy for hypothyroidism.

(For the reasons why I had to switch to T3-only, see some of my other posts.)

Phase 1: Transitioning through T4/T3 combination therapy

As soon as I started transitioning from T4-only (Synthroid) therapy to T3-only (Cytomel) in April 2016, I started getting acne rosacea, within days of starting T3 at 5mcg while still on 100mcg T4. Every two weeks I increased T3 by 5mcg and lowered T4 by 20mcg. While my overall health gradually improved, my acne got worse in phases.

Phase 2: Adjusting T3-only dose and timing

Eventually after the 2-month gradual transition, I was finally on T3-only, and my acne gradually improved as I slowly increased my 3 daily doses in increments of 2.5 micrograms/day every two weeks. I stopped increasing T3 doses when my careful daily measurements of body temperature, heart rate, and other direct signs of hypo/hyper-thyroidism showed that I had reached an ideal T3 replacement dose. By that time, the general skin redness had almost disappeared from the “butterfly zone” and I was experiencing fewer and less frequent outbreaks of tiny whiteheads.

However, even on the ideal dose of T3, some acne still remained on chin, nose and forehead. The red little dots left in the skin after gently popping whiteheads still took too long to heal, and I was still getting occasional breakouts of whiteheads.

Continue reading “Acne on T3-only therapy for hypothyroidism”

Vascular chest pain with T4 (Synthroid) fixed by T3 therapy: A patient narrative

In this post, I’ll give you a narrative that is focused on my own experience as a patient who developed vascular pain symptoms in direct relation to T4-treatment (Synthroid).

  • The health crisis began in February 2016.
  • Gradual transition from T4 to T3 therapy began in April 2016.
  • Full recovery was achieved on T3 only by September 2016
  • Health has been maintained on continued T3-only therapy as of Jan. 2017.

Health background

Continue reading “Vascular chest pain with T4 (Synthroid) fixed by T3 therapy: A patient narrative”

Low-T3: The huge and horrible gap in thyroid research

Many studies have been done on patients whose T3 levels are below lab reference ranges despite a TSH and T4 within range. Most of them have discovered that low serum Free T3 is a dangerous factor to have when one is ill: it is often an independent predictor of morbidity and mortality in patients with organ failure such as heart disease, liver disease and kidney disease. (See my review in this post on the Dangers of Low T3.)

The problem is that such research studies usually exclude patients diagnosed with hypothyroidism.  Why?  They always say it is to avoid confounding factors. Researchers have been mainly intrigued by the puzzle of hormonal dysregulation in patients who have a normal, functional thyroid. Studying hormone dysregulation in people with abnormal thyroids is less paradoxical and potentially more complicated.

Continue reading “Low-T3: The huge and horrible gap in thyroid research”

The dangers of Low T3

At the heart of much supposed “controversy” in endocrinology is the role of T3 thyroid hormone testing and T3-based treatments for hypothyroidism.

Perpetuating this “controversy” is the continual restatement in research articles that T3 and T4-T3 combination therapy (of which Natural Dessicated Thyroid is a sub-type) is a “controversy.” Repeatedly saying it is controversial only serves to reinforce the controversy and dismisses it, if the persons stating it are not doing anything to resolve it.

Meanwhile, clinical practice shows little sign of an actively debated controversy. Most doctors conform to the T4-only recommendations for best practice because they are easy and cheap.  Adjusting Synthroid dosage to TSH levels to “normalize the TSH” has turned into a simple game of numbers that leaves many hypothyroid patients symptomatic and at risk.

As I show in my review of a journal article by Abdalla & Bianco (2014), biology teaches that a healthy plasma T3 level must be defended, and the TSH cannot be trusted to indicate adequate T3 levels.

The dangers of low-T3 in any patient can be logically hypothesized from many studies of “Low T3 Syndrome” and “Sick Euthyroid Syndrome” and “subclinical hypothyroidism”

A recent journal article (Rhee, et al, 2015) included a table outlining the associations between Low T3 and morbidity/mortality: Continue reading “The dangers of Low T3”

T3 Thyroid hormone is a biological priority

Plasma T3 defense league
Image adapted from “Superheroes” by Martin Kas, April 26, 2008, from

Among the many excuses commonly heard from doctors about NOT measuring the T3 thyroid hormone and NOT treating hypothyroidism with T3-therapy are that “the half-life of T3 is too short” and “T3 levels vary based on too many factors.” These arguments serve to minimize the importance of the T3 hormone.

However, this 2014 article refutes these excuses:

Abdalla, S. M., & Bianco, A. C. (2014). Defending plasma T3 is a biological priority. Clinical Endocrinology, 81(5), 633–641.

  • It teaches the biological priority of T3 over all other thyroid hormones. TSH, T4 and the deiodinases merely serve to protect and regulate healthy T3 levels.
  • It emphasizes the mechanisms that protect long-term stability and homeostasis of T3 levels in the body and refutes the misconceptions based on its short half-life.
  • It stresses the medical importance of testing T3 serum levels and treating chronic dysregulation of T3 hormones to attain the biological standard of T3-based euthyroidism.

The T3 hormone remains of paramount importance, despite the complex biological factors that can interfere with T3 metabolism and inactivation.

Continue reading “T3 Thyroid hormone is a biological priority”

Diclofenac and Celecoxib inhibit T3

Caution, if you take either of these common Non-Steroidal Anti-Inflammatory (NSAID) drugs and have Thyroid T3-hormone issues, or problems in your blood vessels!

In my recent research I found a 2016 article with this title: “Evidence that diclofenac and celecoxib are thyroid hormone receptor beta antagonists.” (Zloh, et al, 2016)

They analyzed the molecular structure of these drugs to confirm their “TRβ antagonistic properties.” They also measured “changes to Triiodothyronine (T3) induced vasodilation of rat mesenteric arteries” with these drugs.

They found these two drugs “significantly inhibited T3 induced vasodilation compared to controls.”

Inhibition of vasodilation is obviously NOT the effect you want if you have atherosclerosis or any problems with blood vessel spasms or constriction.

I was recently put on Diclofenac to resolve my chest arthritis AND at the same time, I was starting T3 therapy to resolve chest pain from vasoconstriction. Obviously the combination of these two therapies was contradictory.

In contrast, they tested naproxen and it did not have this TRβ inhibitory effect.


Zloh, M., Perez-Diaz, N., Tang, L., & Patel, P. (2016). Evidence that diclofenac and celecoxib are thyroid hormone receptor beta antagonists. Life Sciences, 146, 66–72.

Why is it so difficult to get thyroid disease diagnosed and treated?

We rely on doctors and technologies to prevent and treat illness. But dysfunction can occur in the medical system, not just in the human body it’s supposed to treat. Image: “2008.11.25 – The physician,” by Adrian Clark, November 25, 2008, from

I’ve created a series of blog posts that tells my story and outlines the six challenges I’ve faced as a hypothyroid patient with hormone-conversion dysfunction and various other health conditions that were worsened by this.

This post provides my summative reflections on the experience.

At almost every turning point in my experience with Hashimoto’s thyroiditis, I have had to do my own research and take initiative to ask my doctors for tests that should have been done years earlier.

On top of my hypothyroid symptoms (during treatment as well as pre-treatment) and the fact that chronic hypothyroidism increases risk for other health issues (such as heart problems), I have struggled with systemic barriers in the health care system, as explored by these posts:

If it has been this challenging for me, a very curious and assertive patient with a PhD and access to research databases to take initiative in my own thyroid health, how hard must it be for patients without such ornery character traits, advanced research education, and/or research resources?

Continue reading “Why is it so difficult to get thyroid disease diagnosed and treated?”

Issue 6: Lack of referral to an endocrinologist who understands

If you are lucky enough to get referred to an endocrinologist, will they understand the importance of T3? Image: “Doctor Hand,” by, September 8, 2009, from

This series of 6 blog posts tells my story and outlines the six challenges I’ve faced.

This post focuses on the fact that most family doctors are not equipped to test for or treat underlying hormonal thyroid dysfunction that may occur despite “normal” TSH and T4 levels.

Unfortunately, it also describes a disappointing consultation with an endocrinologist.

It is important for thyroid patients to have access to a specialist who can interpret abberant thyroid test data and manage conditions such as chronic Low-T3 in patients treated with Synthroid.

At almost every turning point in my experience with Hashimoto’s thyroiditis, I have had to do my own research and take initiative to ask my doctors for tests that should have been done years earlier.

On top of my hypothyroid symptoms (during treatment as well as pre-treatment) and the fact that chronic hypothyroidism increases risk for other health issues (such as heart problems), I have struggled with systemic barriers in the health care system:

  1. Delayed diagnosis of hypothyroidism
  2. Misdiagnosis of thyroid-related depression
  3. Ignorance of Hashimoto’s autoimmunity
  4. Lack of regular (or any!) thyroid ultrasound testing
  5. Lack of testing for Free T3 and Reverse T3 levels
  6. Lack of referral to an endocrinologist who understands

Continue reading “Issue 6: Lack of referral to an endocrinologist who understands”

Issue 5: Lack of testing for Free T3 and Reverse T3 levels

Every organ and every cell requires T3 hormone for proper function. In fact, T3 is so important that all other thyroid hormones exist mainly to protect and regulate our T3 levels. Reverse T3 mimics the molecular shape of T3 but has no effect other than plugging up cells’ T3 receptors.  Healthy levels of T3 and Reverse T3 prevent thyrotoxicosis, but if RT3 dominates T3, it can lead to T3 deprivation, which leads to a very poor prognosis in acute or chronic illness.

This series of 6 blog posts tells my story and outlines the six challenges I’ve faced.

This post focuses on the importance of regularly testing “T3” and “Reverse T3” hormone levels in the blood of hypothyroid patients to ensure that therapy is achieving its ultimate goal of adequately replacing the most important thyroid hormone, T3.

At almost every turning point in my experience with Hashimoto’s thyroiditis, I have had to do my own research and take initiative to ask my doctors for tests that should have been done years earlier.

On top of my hypothyroid symptoms (during treatment as well as pre-treatment) and the fact that chronic hypothyroidism increases risk for other health issues (such as heart problems), I have struggled with systemic barriers in the health care system:

  1. Delayed diagnosis of hypothyroidism
  2. Misdiagnosis of thyroid-related depression
  3. Ignorance of Hashimoto’s autoimmunity
  4. Lack of regular (or any!) thyroid ultrasound testing
  5. Lack of testing for Free T3 and Reverse T3 levels
  6. Lack of referral to an endocrinologist who understands

Continue reading “Issue 5: Lack of testing for Free T3 and Reverse T3 levels”