I was always under the impression that propanolol reduced thyroid hormones (peripheral conversion of t4-t3) and so also raised tsh.
Tsh is still not right at 2.5 despite on my usual dose when not taking propanolol. I’d been taking one a week (80 slow release), and said to Gp I thought it could be the propanolol.
He said they didn’t do that and looked it up and couldn’t find anything. But it does mention contraindications in both leaflets and I also found the comment about peripheral conversion here:
I refused to take Propranolol because it can become addictive and you have to wean yourself off it when you eventually stop the drug. My husband was given it for anxiety and ended up in hospital because his heart rate became too low because of this drug. The GP did not take in to consideration that he was a long distance runner and had a very low heart to start with. I got rid of his tablets and told him never to take them again because I thought his heart was going to stop. This is just my experience of the drug but I know other people get on fine with it.
As I understand it, Propranolol is not itself an addictive substance. But you can become psychologically dependent on it, because it can give a feeling of relaxation. Hence the reason why it's often prescribed for anxiety.
It is frequently used in the treatment of hyperthyroid symptoms. I was very grateful for it myself when I was rushed to A&E because of ongoing frequent episodes of SVT. As you say, your GP should have taken your husbands heart rate into account before prescribing.
My Pharmacist told me it was addictive so blame him. I have been friends with him for over 30 years since we met when we worked together in the hospital pharmacy
Propranolol decreases plasma T3 and increases plasma rT3 in a dose-dependent manner due to a decreased production rate of T3 and a decreased metabolic clearance rate of rT3, respectively, caused by inhibition of the conversion of T4 into T3 and of rT3 into 3,3'-T2. This inhibition of 5'-deiodination is not secondary to inhibition of thyroid hormone transport across the plasma membrane. Propranolol and its major metabolite, 4-hydroxypropranolol, are not directly responsible for these effects, but an unidentified metabolite of propranolol might be involved. beta-blockers ameliorate clinical symptoms and signs of thyrotoxicosis independent of the decrease of plasma 13, that is confined to beta-blockers with membrane-stabilizing activity, such as propranolol and alprenolol. The decrease of plasma T3, however, appears responsible for some of the metabolic responses to beta-blockers.
Beta blockers and corticosteroids that only inhibit the peripheral conversion of T4 to T3 interfere minimally with thyroid function test results. Propranolol hydrochloride (>160 mg/d), atenolol, and metoprolol tartrate produce small reductions in total T3 levels. ncbi.nlm.nih.gov/pmc/articl...
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Important Announcement – Subnormal TSH Secretion
Conversion
High TSH and T4 in upper range?
A suggested gift to a doctor diagnosing hypothyroidism or treatment.
