A healthy heart happens with T3 in the mix!
Are you hypothyroid and have gotten a diagnosis of Atrial Fibrillation, or have frequent palpitations, or a high heart rate, or other diagnoses related to your heart?
Now granted, one could have inherited a heart problem of any kind due to genetics, or there can be other reasons you need to discover as the cause. So it’s important to go with your doctor’s guidance!
But many thyroid patients have discovered that their heart issues were directly related to being hypothyroid, or having problems with their cortisol or iron levels contributing to continued hypothyroidism. So just in case, read on….
Janie’s mother was a good example
I had never heard of anyone in my family of origin who had heart disease…until my mother found herself with clogged arteries, high blood pressure and a rising pulse. In her 60’s, she had to have an angioplasty. I remember thinking how odd the entire scenario was…until several years later when I became a Thyroid Patient Activist!
Turns out that the risk of heart-related problems and coronary heart disease can go hand-in-hand with either undiagnosed or undertreated thyroid disease!
And that was my mother: treated with Synthroid her entire life, which we now know leaves all-too-many with lingering hypothyroid symptoms of our own degree and kind. She suffered from depression, poor stamina, afternoon fatigue…and finally culminating in the above. Bingo.
And with patients being dosed by the TSH lab test (which we know leaves us hypothyroid), or treated with Synthroid, levothyroxine, Eltroxin and other T4-only meds (which leaves us hypothyroid to our own degree and kind), no wonder we, as informed patients, started seeing heart problems crop up in each other!
Why do our hearts suffer?
The answer for many appears to be from low levels of T3 (Triiodothyronine), the active thyroid hormone. Your heart’s health and your entire cardiovascular system is highly dependent on adequate levels of T3 for its well-being. T3 improves contraction and thus cardiac output, for one. So if it’s low, output goes down.
T3 keeps your metabolism running well, which helps clear out excess arterial fatty deposits. So if its low, cholesterol and fatty acids go up.
Or if you can understand a biological explanation of what T3 does for your heart: “Bioactive T3 is a powerful regulator of inotropic and lusitropic properties of the heart through their effects on myosin isoforms and calcium handling proteins in particular.” (http://circ.ahajournals.org/content/122/4/385.long)
A good explanation of what poor levels of T3 can do to the heart comes from this article:
…the heart is particularly vulnerable to reductions in biologically active T3 in plasma because cardiomyocytes have a negligible capability to generate T3 from locally converted precursor T4. Consequently, when circulating T3 is low, the myocardium may become relatively hypothyroid.
But my doctor says T3 is dangerous for my heart!
To the contrary, there are many studies which underscore that the use of T3 (and can apply to NDT since it has direct T3) has been very positive for heart and cardiovascular health. For example, this study states the following:
Clinical studies have shown that mild forms of thyroid dysfunction, both primary (subclinical hypothyroidism and subclinical hyperthyroidism) and secondary (low T(3) syndrome) have negative prognostic impact in patients with heart failure. In these patients, the administration of synthetic triiodothyronine (T(3)) was well tolerated and induced significant improvement in cardiac function without increased heart rate and metabolic demand.
Another study found positive results with T3, stating:
Altogether, our data indicate that short-term administration of substitutive doses of synthetic L-T3 state reduces activation of the neuroendocrine system and improves LV SV in patients with ventricular dysfunction and low-T3 syndrome.
This study reveals that T3 plays a key role in repairing a damaged heart:
The potential of TH (thyroid hormones) to regenerate a diseased heart has now been tested in patients with acute myocardial infarction in a phase II, randomized, double blind, placebo-controlled study (the THiRST study).
In fact, research has shown that low T3 can mean a negative outcome in cardiac patients:
…low T3 concentrations are a strong independent predictive marker of poor prognosis in cardiac patients and might represent a determinant factor directly implicated in the evolution and prognosis of these patients.
Then why am I told that using T3 or NDT in my thyroid treatment could be dangerous or cause arrythmias?
The problem with T3 is in the word “excess”, such as is found with chronic Graves disease or hyperthyroidism. Excess T3 or excess NDT could increase the heartrate in harmful ways as well as your systolic blood pressure. But ironically, so can low T3. And no one is talking about taking excess amounts of T3 in the treatment of hypothyroidism.
But my heart rate went way up when I was raising my Natural Desiccated Thyroid or T3 to treat my hypothyroidism…
If upon raising NDT or T3, one only then finds themselves with a high heartrate, we have found that usually points to an cortisol or iron issue. So it’s important to test BOTH of those–cortisol via saliva, NOT blood, and ALL FOUR iron labs.
Seven reasons for a high heartrate:
Summary of graphic. Seven reasons for having a heart problem for a lot of thyroid patients include a cortisol problem, having inadequate levels of iron, being on T4-only like Synthroid or Levo, having a high reverse T3 (RT3), being undiagnosed hypothyroid or held hostage to the TSH lab test, Hashimoto’s, or Lyme, EBV, etc.
What about the A-fibrillation I was diagnosed with?
FYI: Atrial fibrillation means your heart’s two upper chambers will beat irregularly and you might feel a sudden pounding or racing of your heart. It will cause poor blood flow, meaning you could feel tired and weak as a result. It can also cause heart palpitations. (Not all heart palpitations are the result of A-fib, by the way. See below.)
Danish researchers found that even mild hyperthyroidism can increase your risk of having atrial fibrillation. And with Hashimotos driving you into a hyper state, plus some patients having both antibodies to Hashi’s and Graves disease, it might be related to A-fib in some patients.
Another presentation titled Atrial Fibrillation in Hypothyroidism found that hypothyroidism itself can lead to A-fib
A 2009 study found that subclinical hypothyroidism might increase the risk of transient atrial fibrillation.
Bottom line, no matter what the cause, A-fib has serious consequences if it’s not addressed upfront, so work with your doctor. And with any treatment your doctor finds for your A-fib, patient experiences show us that being on the right thyroid treatment (which too many patients found is not T4-only), and treating any cortisol or iron issues, may also be key to avoiding A-fib.
One word of caution…
I, Janie, have Mitral Valve Prolapse (MVP). That means the mitral valve on my heart is very sensitive. And before I started on NDT, I would get palpitations here or there in response to stress or activity. So when I started on NDT, I got a lot of palps. And with each raise, I got palps. But they always subsided within 5 days after each raise, and went away. And we have all learned to start on smaller amounts of NDT (like one grain) and raise in smaller amounts (like 1/2 grain) to allow our T3-starved hearts time to adjust to this wonderful and powerful hormone. Today, I RARELY get palps anymore as compared to those I got before I got on NDT, so my experience confirms that T3 in my treatment made a huge difference in my heart!
Bottom line, as you switch to NDT, or use T3-only in your treatment, work with your doctor while teaching him about the efficacy of T3 to your heart!