Can Too Much Thyroid Cause Cardiac Arrest?

[leonardo]

I've been on a Ray Peat inspired diet for some years now including plenty of orange juice, milk, sugar, saturated fats and PUFA restriction. The results have been quite good and people are often surprised when I tell them my age. I've also tried different kinds of thyroid hormone from a variety of brands - Thyroid-S (from Sriprasit), Cynomel (Mexican Pharmacy) and Nutrimeds Bovine Thyroid.

A few months ago, I had a scary situation when my heart was beating too fast. The episode started after I got a new batch of Nutrimeds Bovine Thyroid (the previous batch had given me stellar results). I went to the doctor who suspected that it might be the strong coffee that I'd drunk that morning and aftenoon.

Anyway, after I dialled back on my dosage, things got to normal and I'm doing okay.

Today, I stumbled on this (rather-dated) article - High-Normal Thyroid Levels and Cardiac Arrest

I would like to know the consensus among the folks here about this study in particular and the issue of too much thyroid causing cardiac arrest in general.

Is there such a thing? If so, is it worth risking a thyroid dose if I have not been prescribed thyroid?

 

[DaveFoster]

Severe hyperthyroidism can lead to acute or chronic cardiac problems. You can get hypertension, tachycardia, sweating and heat intolerance with loose stools.

Dr. Peat has stressed the importance for doctors to monitor patients carefully in the context of a precarious physiological profile: for example, he names heart patients who receive small amounts of T3.

It sounds like you have a sourcing problem with your thyroid supplement, and its resolution should be a priority.

 

[leonardo]

thanks @DaveFoster.
I was wondering what the thoughts were regarding this specific sentence in that article:

"Researchers found that people with thyroid hormone levels at the high end of the normal range were 2.5 times more likely to die from sudden cardiac death, compared with people at the lower end of the range."

The article seems to suggest that even in the absence of a precarious physiological profile, elevated thyroid hormone levels are sufficient to predict that the odds of dying from cardiac arrest are more than double!

 

[Dan W]

I don't know what to make of the study, but I think the article's unfairly using the phrase "high levels of thyroid hormone" if you look at what was actually shown:

I'd have been more curious for them to look directly at connections between sudden cardiac death and *T3*. Both because you'd expect it to affect the heart more, and because it helps eliminate the question, "what's causing those participants to have unusually high free T4 in the first place?"

 

[Westside PUFAs]

I recall reading something about taking thyroid and it inducing congestive heart failure.

 

[Kartoffel]

The good old thyroid will kill you because it makes your heart beat too hard story. Apparently that story is still lucrative enough to embarrass yourself by publishing junk like this.

Thyroid. 2002 Jun;12(6):511-5.
Thyroid hormone metabolism in patients with congestive heart failure: the low triiodothyronine state.
Ascheim DD1, Hryniewicz K.
Author information
Abstract
Thyroid hormone has multiple effects on the cardiovascular system, ranging from molecular and cellular effects to the consequent hemodynamic alterations. Consequently, thyroid function has been evaluated in small cohorts of patients with advanced heart failure that indicate a significant prevalence of morphologic or functional thyroid disorders. We sought to determine the prevalence of altered thyroid hormone metabolism in a broad spectrum of ambulatory heart failure patients. Thyroid function tests were evaluated in 132 ambulatory patients (98 males, 32 females, mean age, 67 years) with left ventricular systolic dysfunction (EF < 35%) and New York Heart Association (NYHA) class I-IV symptoms. Hypothyroidism was defined as serum thyroid-stimulating hormone (TSH) > 4.25 U/mL and low triiodothyronine (T3) state was defined as T3 levels < 80 ng/dL, with normal thyroxine (T4) and TSH level. Seven percent of patients were found to have primary hypothyroidism and 34% have a low T3 state. Of patients receiving amiodarone, 21% had elevated TSH levels and 76% had low T3 levels. The prevalence of abnormal thyroid function correlated with NYHA class. There is an unexpectedly high risk of hypothyroidism and low T3 syndrome in patients regardless of treatment with amiodarone, which appears to correlate with disease severity that requires further investigation.

Am Heart J. 1998 Feb;135(2 Pt 1):187-96.
Thyroid hormone and cardiovascular disease.
Gomberg-Maitland M1, Frishman WH.
Author information
Abstract
Thyroid hormone directly affects the heart and peripheral vascular system. The hormone can increase myocardial inotropy and heart rate and dilate peripheral arteries to increase cardiac output. An excessive deficiency of thyroid hormone can cause cardiovascular disease and aggravate many preexisting conditions. In severe systemic illness and after major surgical procedures changes in thyroid function can occur, leading to the "euthyroid sick syndrome." Patients will have normal or decreased levels of T4, decreased free and total T3, and usually normal levels of thyroid stimulating hormone. This syndrome may be an adaptive response to systemic illness that usually will revert to normal without hormone supplementation as the illness subsides. Recently, however, many investigators have explored the benefits of thyroid hormone supplementation in those diseases associated with euthyroid sick syndrome. Thyroid hormone's effects on the cardiovascular system make it an attractive therapy for those patients with impaired hemodynamics and low T3. Thyroid hormone has also been considered a treatment for patients with congestive heart failure, for patients undergoing cardiopulmonary bypass and heart transplantation, and for patients with hyperlipidemia. At present there is no evidence suggesting a favorable treatment outcome using thyroid hormone supplementation for any systemic condition except in those patients with documented hypothyroidism.