The study below is very detailed and scholarly- it talks about the mechanism by which TSH helps to model bone. It's uncomfortable reading for me, as I have osteopenia after years (at least 20) of being TSH almost undetectable (around 0.01or 0.02).
You could say these are mice, we are people, but we share probably 97% DNA and we are mammals like them.
Here's an extract below:
Hyperthyroid-associated osteoporosis is exacerbated by the loss of TSH signaling
Ramkumarie Baliram,1 Li Sun,2 Jay Cao,3 Jianhua Li,2 Rauf Latif,1 Amanda K. Huber,1 Tony Yuen,2 Harry C. Blair,4 Mone Zaidi,2 and Terry F. Davies1
First published September 17, 2012 -
Brief Report Bone biology
The osteoporosis associated with human hyperthyroidism has traditionally been attributed to elevated thyroid hormone levels. There is evidence, however, that thyroid-stimulating hormone (TSH), which is low in most hyperthyroid states, directly affects the skeleton. Importantly, Tshr-knockout mice are osteopenic. In order to determine whether low TSH levels contribute to bone loss in hyperthyroidism, we compared the skeletal phenotypes of wild-type and Tshr-knockout mice that were rendered hyperthyroid. We found that hyperthyroid mice lacking TSHR had greater bone loss and resorption than hyperthyroid wild-type mice, thereby demonstrating that the absence of TSH signaling contributes to bone loss. Further, we identified a TSH-like factor that may confer osteoprotection. These studies suggest that therapeutic suppression of TSH to very low levels may contribute to bone loss in people.
Hyperthyroidism, a common health risk affecting approximately 1 in 100 individuals, is often accompanied by worsening osteoporosis, especially in postmenopausal women (1). There is compelling evidence from early in vitro and more recent mouse genetic studies that both thyroxine (T4) and triiodothyronine (T3) stimulate the resorption of bone by osteoclasts (2). This leaves no doubt that thyroid hormone excess is a major contributor to the profound bone loss and high risk of fracture in hyperthyroidism. Physiology tells us that high serum thyroid hormone suppresses the production of thyroid-stimulating hormone (TSH) from the anterior pituitary, although in subclinical hyperthyroidism, thyroid hormone levels can be normal, while TSH is low or undetectable. The osteoporosis associated with subclinical hyperthyroidism is therefore unlikely to arise from thyroid hormone excess alone (3).
We and others have shown that, in addition to its known function in stimulating thyroid follicular cells, TSH can act directly on the skeleton (4–8). Activation of the TSH receptor (TSHR) on the osteoclast prevents the resorption of bone (4). When administered intermittently, TSH stimulates osteoblastic bone formation and, in rodent models, rescues ovariectomy-induced bone loss (5–8). In contrast, absence of the TSHR in the global Tshr–/– mouse causes high-turnover osteoporosis (4). That this osteoporosis is not reversed upon thyroid hormone replacement suggests that absent TSH signaling may have a permissive role in causing this bone loss. Epidemiologic evidence favors strong correlations between low TSH and high bone turnover; low TSH and low bone mineral density (BMD); and low TSH and high fracture risk in hyperthyroid patients (9–23). This raises the question of whether low TSH levels might contribute to the bone loss in hyperthyroidism that has been attributed solely to high thyroid hormone levels.
... Likewise, euthyroid women with serum TSH levels in the lowest tertile of the normal range have a higher incidence of vertebral fractures, independent of thyroid hormone levels (19).
[...pictures as well of the bones and descriptions of how the cells are remodelled badly, even if the mice are given thyroid supplements...]
I am actively trying to assess the risk of Low TSH- like many of you, I want quality of life now, and for me that means suppressing my TSH, which never rises, however little T4 I take. I get very depressed when I lower my dose, stop being able to think, no energy, body can't cope with exercise, bloated, constipated, etc etc
I would like to know your reactions to the above study, and would appreciate if any of you can wade through it!