I can't find any research that proves that TSH has a direct effect on bones. In fact there is a piece of research that shows that TSH does not have ANY effect on Bone Mass Density.
Thyroid Stimulating Hormone and Bone Mineral Density:
Evidence From a Two-Sample Mendelian Randomization
Study and a Candidate Gene Association Study
Nicolien A van Vliet,1 Raymond Noordam,1 Jan B van Klinken,2 Rudi GJ Westendorp,1,3
JH Duncan Bassett,4 Graham R Williams,4 and Diana van Heemst1
There is a very recent pieced of research that shows that EXCESS TSH has a negative direct effect on the heart.
H. Alonso a,1, J. Fernández-Ruocco b,1, M. Gallego a, L.L. Malagueta-Vieira c, A. Rodríguez-de-Yurre a, E. Medei b, O. Casis a,⁎
It seems to me that the evidence so far is that it is mostly the excess or lack of T3 that causes Atrial Fibrillation or Osteoporosis. Now we need to factor in the excess of TSH and together with the lack of sufficient that contributes to AF. Not the lack of TSH.
It seems to me that the doctors are so indoctrinated that TSH tells us everything that they cant see the wood for the trees. They very rarely consider T3 for anything, including well being and that the real cause of AF or OP in these circumstances is an excess of or lack of the correct amount for the individual patient of T3 - mostly.
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holyshedballs
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I think the link is between imbalanced thyroid hormones and osteoporosis/AF .. not TSH, as healthy bones require optimal T4/T3 ratio so that old bone can be dissolved or resorbed, & new can be produced to replace what was resorbed.
When thyroid levels are too low, both bone resorption & production decrease, resulting in possible osteoporosis. When thyroid hormones are elevated, bone absorption exceeds bone production with a net loss of bone mass, resulting in possible osteoporosis.
Also, issues such as elevated SHBG (commanly caused by elevated T3) may encourage lower levels of oestrogen resulting in possible osteoporosis, as might excessive use of hydrocortisone necessitated because of Hashi inflammation and which decreases bone formation & increases bone resorption. Also vitamin/nutrient deficiencies resulting from the typical malabsorption of the numerous low thyroid hormone induced gut issues.
But as doctors don’t/can’t routinely test T3, they are encouraged to use what is in their guide book …. a pituitary hormone ! ! ..
i m sure that OP and AF can be as a result of too much/too little T4 or T3. um also sure that although there is a risk of OP and AF, it is not as highas Endos make out. Very often, they just that "there is a risk" without quantifying the risk so that patients cant make an informed choice about their treatment plan.
I previously posted about the illogical reliance on TSH when T4 and T3 can be tested.
GPs and Endos seem to be locked into this illogical pardigm that TSH is the marker.
In that paradigm, TSH tells us how much T4 is in the blood not T4. TSH also tells us how much T3 is in the blood not T3. TSH apparently has a protective effect on bones when it doesnt and
It doesn't really even tell you how much T4 there is. You'll see people with low in range free T4 and only mid range TSH and people with low TSH and mid range free t4 and even people with sky high TSH and still mid range free t4. I suspect most people don't have a textbook perfect pituitary/hypothalamus/thyroid axis
I totally agree. Measuring TSH tells you how much TSH is in the blood. It can't tell you how much T4 or T3 is in the blood or how well T4 is converted to T3.
Given that T4 and T3 can be measured, I think that measuring TSH is only helpful in conjunction with measuring T4, T3 and TPO etc. Measuring TSH alone once treatment has begun is virtually useless as diogenes has very helpfully explained.
Particularly when the evidence shows that the lack of TSH does not affect bones.
So to insist that the TSH remains within the reference range when undergoing therapy is illogical.
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