Hypothyroidism and High Blood Pressure (Part 3)

This is the third episode discussing the connection between hypothyroidism and high blood pressure. Today we discuss Beta Blockers. There are a number of beta blockers on the market. Many of them have an impact on thyroid physiology.

Metoprolol seems to be the beta blocker with the least impact on thyroid hormone physiology. Propranolol seems to be the beta blocker with the most dramatic impact on thyroid physiology. So much so that it is used as a treatment for hyperthyroidism.

Propranolol and many of the other beta blockers can induce cellular hypothyroidism by inhibiting Deiodinase 1 and 2, increasing Deiodinase 3, and reducing the metabolism of reverse T3.

Studies have shown that decreases the conversion of T4 to T3. It is reduced levels of T3 in your cells that causes hypothyroid symptoms.

Propranolol increases reverse T3 (rT3). Possibly by increasing the conversion of T4 to rT3, and by reducing it’s metabolism and clearance from the body.

What is interesting is that T4 will often rise, and TSH does not appear to be influenced by Propranolol. So consider you are put on a beta blocker. After a period of time you start to have low thyroid symptoms; tired, fatigue, weight gain, edema, dry skin, etc. You see your primary who runs a TSH with fT4 reflex panel.

Since the beta blocker does not influence TSH it may look normal. If it is high and fT4 is run, it to will be normal or possibly high because beta blockers raise T4 levels.

You will be told you don’t have a thyroid problem because these two labs are normal. If however a comprehensive thyroid panel was run to include T3 and rT3, we would be able to see that the beta blocker is inducing a cellular hypothyroid state.

This is a case of Drug Induced Hypothyroidism. The beta blocker induces the hypothyroid state as well as hide the impact because limited thyroid panels are often performed.

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Papers:
PMID: 1688102, 3967459, 885993