Tania Smith has written an excellent review of an important paper by Anderson et al (in Thyroidpatients.ca) which has described a major study relating AF to thyroid hormones levels, and mercifully including FT3 with FT4 and TSH. It shows that AF linkages to the various hormones are much more tenuous than currently believed
Anderson, 2020: Thyroid hormones and atrial fibrillation
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diogenes
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I’ll be sending it to mine... Whether he takes the time to read it or not (and I suspect the latter) is up to him, but he won’t be able to say he wasn’t informed!
The study mainly looked at patients not under therapy, but also included T4-therapy patients as a separate sizeable group. In both cases, high FT4 was linked to a higher possibility of AF, but TSH was noninformative and there was no such relation with FT3 so long as it remained in its reference range. So what this tells me is that, if in a patient with problems for T4-T3 conversion, aggressive monotherapy with T4 to FORCE a sensible FT3 is attempted (with a corresponding low TSH), it will cause elevated FT4 and the corresponding greater likelihood of AF. It therefore argues against such an approach and therefore indirectly (without saying so) would suggest combined therapy so as not to give this problem (so long as FT3 is in its reference range). That is, FT4 need not be above the range or high up, if the need for a given T4 dose is mitigated by the added T3.
A thing we should all keep in mind when reading these studies. They only explain the overall risk in a patient group for a particular problem; they do not apply in the same way to an individual in that group.You cannot as an individual have 10% AF; you either get it or you don't. And the low extra risk means that most do not get AF in these circumstances. So, as always it is or should be a decision by the patient having been told the risk, to act as they feel is best. I think doctors in these situations ought to advise and honestly display the risk if there (I mean to give the actual figure and not "you will get AF"), but not dictate that they are therefore going to impose on the patient what they personally think is best.
So whichever well known Endo, can't remember if it was Toft or Lowe, is quoted many times on here as saying slightly over range T4 is not a problem is/was wrong ?! I need high/over T4 to convert enough T3 and I do have Afib.
I have recently talked about this with my Endo but there are implications for cardiac patients. I have always done very well on Levo but I do need levels that make most GP's panic ! My late husband was on T3 and Levo and it was a constant juggling act to stabilise his levels and when he went in for cardiac surgery his T3 was stopped which I believe contributed to his death 4 weeks later, so I'm reluctant to rock my boat by changing. I will see what my Cardiologist thinks.
Good Stuff . I shall stick it under my Gp's nose, since i seem to need my FT4 at 20 -22pmol[7.9-14] 200% through the lab range at the moment , and trying to lower it left me constipated and asleep.
Thanks for posting this Diogenes, it’s the opposite argument endo uses to try to prevent my daughter from staying on T3 - she has AF which I’m sure gets worse on too much T4 (when they have tried to remove the T3 telling her it’s the T3 that is risky). Incredibly useful
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