This is a complex study of the effect of T3 on vasodilation academic.oup.com/endo/artic... . I do not have access to the full paper and anyway I'm not interested in the precise details!
T3 acts in a number of ways. Usually, it binds to thyroid hormone receptors (TRα1, TRβ1, TRβ2) which attach to a response element on the DNA to cause gene expression. This action usually takes several hours. T3 can also act directly on cells, either via a receptor or not. This study shows that T3 acting via TRα1 receptors causes vasodilation without gene expression. The essential point is that it shows that T3 causes vasodilation and hence people with low T3 may consequently have higher blood pressure. I’m not going to bother to get into studying this in detail as it will most likely be hard work and the basics are enough.
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jimh111
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All I need to hear when I’ve just recently added T3 to my T4 and have to keep an eye on my BP! I may look at article as I like to see the parameters of the study. Don’t want to be freaked by a study with 20 participants!
The details will be in the full paper. Most people will not notice a difference in blood pressure, I think this is so because we don't see lots of comments on BP. This study just shows that hypothyroidism may contribute to high BP.
Well, I think this is cheering, presumably it means that if our T3 is too low and corrected our blood pressure is then likely to lower, if it was high?
I have always had historically low bp and cholesterol until my thyroid issues started. My last bp had me pre hypertensive which is a massive jump from my previous baseline. I was wondering if the fact I am borderline with my medication could be causing it and if the Endo would look at it (spoiler - there was no interest from him). In the absence if actual Endo advice on this, since I am only 10% through range on T4 and 32% on T3 would increasing my medication help this? I am also struggling that the Endo that wants my surprised T3 to increase by the next blood test (am on combi T3/T4). Not sure how to balance the 2 things and don’t want to jeopardise my new nhs T3 supply which was a long time coming (and I think I only got because I am stable and relatively symptom free). Sorry if this hijacks the thread a bit!
Can't quite follow your comments but a general reply. It's reasonable that for some people at least hypothyroidism (defined as insufficient thyroid hormone action - or low fT3) will increase BP. I don't think we know at what level this loss of vasodilation occurs and it probably will vary from person to person. The only way to find out is to achieve clinical euthyroidism and see if BP improves.
I’m definitely using that word at my next, usual very fraught, telephone appt with my GP. It’s a shame it won’t be face to face as I would love to see his when I say it 😀
So, raise T3 and lower BP (which is a good thing). Raise T3 and lower TSH (which is also a good thing because you feel well). Sort of runs contrary to the belief that low TSH can cause heart problems (a bad thing). Anybody know what sort of heart problem you are supposed to get as a result of low TSH? I wonder if it is High BP driven? That wouldn't make sense with this mouse experiment. I developed high BP as soon as I had a TT and high T3 or low T3 did not have any effect, it just stayed high. Gosh, there is never any pattern to all these variables, which is probably why most endos stick to diabetes (just two variables to juggle - just have to think about a see-saw).
Low TSH usually (not always) indicates excess thyroid hormone and is associated with atrial fibrillation. A high TSH has a higher cardiac hazard ratio for cardiac problems and mortality but doctors never warn patients of the danger of having a TSH of e.g. 6.0. Both high and low TSH carries risks but we need to look deeper than TSH giving weight to signs and symptoms. Sometimes TSH is low due to insufficent hypothalamic or pituitary (thyrotroph) function.
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