A Follow-Up to the Blog Post - Physiological Replacement Therapy with T3 is Beneficial in Ischemic Heart Disease
I wrote a blog post recently entitled 'Physiological Replacement Therapy with T3 is Beneficial in Ischemic Heart Disease'. See: http://recoveringwitht3.com/blog/physiological-replacement-therapy-t3-beneficial-ischemic-heart-disease
Ischemic heart disease is caused by narrowed heart arteries and is also referred to as coronary artery disease or coronary heart disease.
The research paper referred to in the blog post does much to dispel the nonsense that many thyroid patients have to put up with from family doctors and endocrinologists about T3 use being dangerous and causing heart attacks. In fact the research shows quite the reverse.
In this blog post I am using some review material written by Canadian thyroid patient Tania S. Smith (with her permission).
This blog post provides a short analysis of the original research paper and may give some thyroid patients the information that they need to counter these incorrect arguments from their doctors. I have always known that T3 is a perfectly safe thyroid hormone to use when it is dosed correctly - at last we are seeing more research to back this up (there are other papers already - which I have referred to in other blog posts).
The research article that this and the previous blog post is based on is titled "The impact of thyroid hormone dysfunction on ischemic heart disease" by Madalena von Hafe and colleagues, May 2019, Endocrine Connections 8 (5).
Full scholarly article can be found here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6499922/
The PDF version of the article for printing is here:
Key points in the research article related to thyroid patients and T3 use
1. There has been overemphasis on hyperthyroidism and thyrotoxicosis by many doctors who believe that only excess T3 and T4 is bad for the heart. This article shows that the real thyroid hormone issue with respect to the heart is actually hypothyroidism (too little T3, possibly due to too little T4, but sometimes poor conversion of T4 to T3).
2. The article discusses T3 use extensively and even goes into the ways in which T3 therapy can reduce cardiovascular risk and promote healing.
3. It also states that the use of levothyroxine requires the preservation of peripheral deiodinase activity to convert T4 into the active hormone T3. It states that administration of T3 may be a better option [than T4] in patients with impaired conversion. The doctors openly acknowledge that impaired T4 to T3 conversion is actually a genuine issue with potentially serious consequences - cardiac issues and death in some cases.
4. The article discusses the improved health of patients treated with T3 thyroid hormone. These patients had severe heart issues (St-elevated myocardial infarction and non-thyroidal illness syndrome in acute coronary syndrome). The results of a study showed that T3 is safe and improved the heath of these patients with no side effects.
5. The authors discuss the importance of the T3 thyroid hormone, as it is the biologically active thyroid hormone. It also highlights how important a good conversion rate from T4 to T3 is!
6. The authors also make it very clear that T3 is the most important thyroid hormone and that it is 20 times more potent than T4! I state in my books that T3 thyroid hormone is at least 10 times as potent as T4, but that also T3 binds more easily to thyroid receptors than T4 - thus making it at least 10 times as potent (I was erring on the conservative side when I wrote that - I knew it was far more the 10x).
7. The article acknowledges that not all T4 is destined to become T3! T4 converts to some T3, but also to other thyroid hormones including reverse T3 (rT3). They do not go into rT3 too much but there is research that shows that rT3 is a T3-blocker, i.e. it actively slows metabolism when it goes too high (although the article does not refer to this I felt I had to state it).
8. The article makes it clear that it is T3 that is the thyroid hormone that is responsible for the major necessary effects on the myocardium (muscular tissue of the heart).
9. The article makes it clear that T3 does many useful things:
- it stimulates nearly all of the transporters and ion channels involved in calcium myocardial fluxes.
- it enhance[s] calcium uptake and release.
- it stimulate[s] both diastolic myocardial relaxation and systolic myocardial contraction.
- it upregulates α-MHC and downregulate β-MHC (heart muscle specific proteins).
- it increase[s] resting heart rate, cardiac contractility and venous tone almost immediately, increasing cardiac preload and cardiac output.
- it increases myocardial sensitivity to the adrenergic system by increasing the number of adrenergic membrane receptors.
- and other necessary effects.
10. The authors state that hypothyroidism (low T3 and T4 thyroid hormones) reverses or blocks the long list of good things from happening in the cardiovascular system. The hypothyroid state results in lower heart rate and decreased myocardial contraction and relaxation, with prolonged systolic and early diastolic time intervals, culminating in advanced stages of heart failure!
It is hypothyroidism, not T3 use, that cause heart failure!
11. This article finally admits that a low T3 syndrome IS a form of hypothyroidism. How could a syndrome characterized by a low thyroid hormone (T3) not be hypothyroidism? Just because TSH is not elevated and patients exhibit no 'clinical signs' of hypothyroidism, it is still possible to suffer a T3 deficit. Decades of endocrinology have seen Low T3 syndrome as not hypothyroidism. This article corrects that error.
12. Another revolutionary factor in this article’s discussion is that they discuss how other bad conditions take time to develop in the presence of hypothyroidism, e.g. insulin resistance and atherosclerosis.
13. The authors also admit that deiodinase Type 3 (D3), destroys thyroid hormone and leaves in its wake reverse T3 (rT3) hormone, and that this can be pathological. Yes, they actually use the word pathological. Recent studies show that expression of D3 is increased in some pathological contexts in a cell-specific manner, which are cancer, cardiac hypertrophy, myocardial infarction, chronic inflammation or critical illness.. They talk about the process by which this pathological over-expression of D3 and chronic inflammation and hypoxia lead to local cardiac hypothyroidism - in which the heart has even less T3 than you can measure in the bloodstream. In low T3 syndrome, by definition, blood T3 is already lower than the body needs it to be, and this article says T3 is even lower in the heart muscle itself.
14. The article makes it clear that a significant percentage of patients with acute coronary syndrome have NTIS [Non-thyroidal Illness Syndrome, a.k.a. Low T3 syndrome]. It also states that patients with ST-elevation myocardial infarction (STEMI) and alterations in thyroid function have almost a 3.5-fold increased risk of major adverse cardiac events, including cardiogenic shock and death, compared with patients with STEMI and no thyroid disorder.
15. Low T3 levels and/or high Reverse T3 at the time of the acute myocardial infarction (heart attack), has long-term effects on recovery 6 months later. The 1-year mortality increases.
16. They are so concerned with the risk of low levels of T3 and making heart surgery more successful that studies are looking into pre-treatment with T3 before going into surgery. The interest in the role of thyroid hormones cardio-protection is increasing.
17. Later sections in the article discuss thyroid hormone treatments. They are clear that all thyroid hormones are on the table, from levothyroxine to T3 to other thyro-mimetic compounds that target thyroid hormone receptors. This is music to my ears as I've been saying this for years and this is stated over and over again on my website and in 'The Thyroid Patient's Manual' book.
18. The Pros and cons of Levothyroxine and T3 therapy are discussed. The negative side of levothyroxine, again, is that the body needs to convert it to T3, which is less likely to happen in patients with poor T4-T3 conversion, which is common in heart failure and other heart conditions. The negative side of using T3, of course, relates to risk of overdose, i.e. a bad dosing protocol (which I protect against in my safe and careful protocol in the 'Recovering with T3' book). T3's very potency, its ability to heal, is its Achilles heel IF the dosing is not managed with care (which it can be).
19. Far, far more is written here about the studies that show T3's benefits, alone or in combination with T4, both in human trials and in animal studies. Even children -- yes children! -- are the objects of studies of T3 pretreatment for cardiac surgery.
20. In another research study they review, even a low daily dose of T3, a mere 1.2 micrograms per 100g in rats, confers benefits to their healing from heart attack, and the practical applications to humans are profound: Low-dose T3 might offer a suitable treatment option after myocardial infarction in patients who are intolerant to aerobic exercise training.
21. The authors also make it clear that tiny changes in thyroid hormone levels within the reference range, or not noticed in blood, are significant! Yes, symptoms and signs show the effect of thyroid hormone effect - not necessarily the lab results! They state that "Evidence suggests that the hypothyroid tissue state may be present independent of normal circulating levels of thyroid hormones. Therefore, it is important to identify a good biomarker of tissue hypothyroid-like state in order to treat patients effectively." What matters more than the reference range boundary is whether or not tissues like the heart muscle and blood vessels are getting enough T3. Even tiny doses can help.
22. Overall the research article makes it very clear that they see immense value in treating lower than needed T3 (even if it is within the reference range already). T3's benefits to the heart, and the protection and healing it offers during the crises of acute coronary events is too important to ignore. The authors state: "The results are promising so far; experimental and clinical studies demonstrate that thyroid hormones can limit ischemic injury, attenuate cardiac remodeling, and improve hemodynamics." When they use the term thyroid hormones the authors mean ensuring that the patients have enough T3.
23. Their final brief paragraph trumpets the declarations doctors need to hear. First of all: Low thyroid hormone levels are the main issue when it comes to cardiovascular tissue. It's not about TSH-based definitions of hypothyroidism, nor is it about a certain magic number. 'Low' thyroid hormone means 'low' from the perspective of the body, not from the perspective of some arbitrary statistical population reference range boundary. They state: "It is now recognized that even subtle changes in thyroid hormone levels can lead to adverse effects in the cardiovascular system. Experimental and clinical evidence suggests a close link between low thyroid hormone levels and poor prognosis in ischemic heart disease. This condition should therefore be regarded as a cardiovascular risk factor." Notice this - Low thyroid hormone levels, not necessarily high TSH, "should therefore be regarded as a cardiovascular risk factor."
I'll end with this quotation from the conclusion. This piece of research should pile up on top of many other pieces of research which demands action to change medical policies, practices, and research agendas in this direction: "Accordingly, thyroid hormone replacement therapy may yield improvements in lipid profiles, potentially reversing myocardial dysfunction and preventing the progression to heart failure. TH replacement treatment exhibits anti-ischemic and cardio-protective effects, acting as a promising target for ischemic heart disease. Moreover, subclinical hypothyroidism treatment and nonthyroidal illness syndrome constitute topics garnering increased interest; recent studies suggest that therapy with physiological doses of T3 are safe and provide beneficial effects on ischemic heart disease."
Many thanks again to Tania S. Smith whose longer articles I used to create this point based blog post.
P.s. if anyone wants to read Tania's original and longer articles on this please see: