Heart cells can only use a biologically active thyroid hormone (T3) that is not commonly tested nor prescribed in Australia.  If you do not have the correct amount of T3 getting into your heart an alarming array of signs and symptoms can develop with fatal outcomes.

Drs’ Klein and Danzi in the American Heart Association publication, Circulation* claim:

 

“low T3 is a strong predictor of all cause and cardiovascular mortality” and that T3 is a stronger predictor than age, poorly regulated fats or malfunctioning heart muscle.

 

Too much T3 in hyperthyroidism and Graves can be just as fatal as too little in hypothyroidism and Hashimotos.

Does the discussion leave you confused? Let’s do a quick thyroid recap:

  • Your brain talks to your thyroid via thyroid stimulating hormone (TSH).
  • TSH tells your thyroid gland how much hormone to make.
  • Your thyroid gland then releases into the body about 85% inactive hormone (T4) and 15% active hormone (T3).
  • Your liver, kidney, and skeletal muscle then make T4 useable by your body (biologically active) by turning it into T3 through a chemical reaction.
  • When you are under stress or your liver /kidneys are not operating as they should your body will sometimes decide not to make active thyroid hormone and to make reverse-T3 (RT3) that blocks active T3 from working!  If you are currently experiencing fatigue, stress and weight gain you may be producing too much RT3 and not enough active T3.

And the key point for this discussion, heart cells are not able to convert T4 to T3.  So if you do not have enough/ too much T3 in your heart – your life is at risk.

This conversation is not just relevant for thyroid patients though as a review of the evidence behind congestive heart failure concluded that approximately 30% of patients had low T3 levels.  And the decreased T3 level was found to be proportional to the severity of the heart disease.

In Australia when a thyroid problem is diagnosed TSH levels are closely monitored and if they are causing hypothyroidism or Hashimotos patients are given a synthetic form of T4 and not biologically active T3.

T3 levels are not routinely monitored with either the hyper- or hypothyroid in Australia.

In conditions of excess T3 hyperthyroid and Graves patients can develop:  palpitations, fast heart beat, exercise intolerance, breathlessness, blood pressure changes and atrial fibrillation.  Cardiac output may be increased by 50% to 300% over that of healthy people. The combined effect of increases in resting heart rate may lead to enlarged hearts and high risk of heart failure.

With not enough T3 Hashimotos and hypothyroid patients present with symptoms that are diametrically opposed to those described for Graves including: slow heart beat, mild hypertension, narrowed pulse pressure, cold intolerance, and fatigue. Unfortunately these patients also have a reduced ability to processed fats which commonly leads to high cholesterol levels and atherosclerosis a symptom picture commonly associated with serious and life threatening heart conditions.

Let me leave you with the good news: the researchers proposed thyroid hormone replacement treatment may in fact be able to reverse the risks.

Do you know your Goldilocks number?

Sonia

*Klein, I., & Danzi, S. (2007). Thyroid disease and the heart. Circulation, 116(15), 1725-1735.

 

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