Hypothyroidism and AFib

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While it is well known that hyperthyroidism can be a trigger of AFib, living completely without a thyroid in itself will cause it even if you are not overmedicated. I am trying to get study's on this, but most go by assumptions. An increase in AFib after thyrodectomy is documented, but then it is theorized that this is due to being overmedicated. I have been undermedicated for almost 15 years and suffer from sever AFib. Many studies linking hyperthyroidism with AFib don't look at thyroidless patients, but at people with overproducing thyroid. I found one study of labrats that were given a thyrodectomy. Some were overmedicated, some undermedicated and some were kept within range. AFib was in 76 percent of undermedicated rats and around 60 in overmedicated rats. Yet the assumption remains that if you have AFib you are overmedicated. Anybody knows of any study of actual people with total thyrodectomy that doesn't just assume that the higher incident of AFib is due to overmedication. I saw one that admits the link is there independent of TSH level.

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    I've read some studies on this too and will go back to my sources to see what has been tested with human subjects.  I think these studies are missing the whole picture.  For example, after thyroidectomy calcitonin is not replaced and calcium homeostasis is affected (high calcium could cause afib).  Additionally, if the thyroid is damaged there could also be parathyroid gland damage too.

    Magnesium, potassium, and calcium imbalances are common in most thyroid-treated individuals because the root cause of their autoimmune thyroid condition typically impairs nutrient absorption as well.  

    I'll see what I can find and post a link.

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    Here is a review article with relevant human references... http://www.hormones.gr/~osenia62/pdf/05batr.pdf

    It drives me nuts that calcitonin is not considered.  Calcitonin is produced by the parafollicular C cells in the thyroid gland.  If the thyroid is removed or damaged calcitonin is not produced.  Calcitonin acts to lower serum calcium levels by depositing calcium in bone.  When calcitonin is deficient there is no calcitonin regulated peptides to build bone density when calcium is high.  Hence, one would expect an increased risk of osteoporosis and high calcium-induced types of negative cardiovascular outcomes such as an increased risk of afib over time.

    Let's not forget the adrenal glands that are also affected by thyroid hormone replacement.  High cortisol alone will increase the risk of osteoporosis but when the adrenal gland burns out then epinephrine has to compensate, also increasing the risk of afib.

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