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Re: and how to inhibit it.... Raybakes » raybakes

Posted by tealady on December 1, 2004, at 18:46:32

In reply to Re: and how to inhibit it.... Raybakes » tealady, posted by raybakes on December 1, 2004, at 17:24:09

> and this abstract shows some good data...
>
> as a risk factor for fractures in women in asia, low calcium intake was a risk factor of 2, use of sedatives was a risk factor of 2.5, high alcohol 2.9, low excercise in youth 7.2, and thyroid drugs 7.1
>
>
> 'Risk factors for hip fracture in Asian men and women: the Asian osteoporosis study.'
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11277276
>
> there may be confounding factors between different societies but medication, alcohol and low excercise appear to be large risk factors.
>
> Ray

Hi Ray,

Re Thyroid meds:

it appearas that IL-6 is probably the issue here again
Osteoporotic cytokines and bone metabolism on rats with induced hyperthyroidism; changes as a result of reversal to euthyroidism
Hyperthyroidism is characterized by increased bone turnover and resorptive activity. Raised levels of serum osteoporotic cytokines, such as interleukin (IL) -1beta, IL-6 and tumor necrosis factor (TNF)-alpha have been demonstrated previously in hyperthyroidism. These elevations are controversial and it is difficult to differentiate the contribution of thyroid hormones to the elevation of cytokines from that of the autoimmune inflammation in Graves' disease (GD) and follicular cell damage in thyroiditis. Therefore, we investigated the effect of thyroid hormones on serum IL-1beta, IL-6, TNF-alpha levels and bone metabolism on L-thyroxine induced hyperthyroid rats and changes in cytokine levels and bone metabolism on the same rats after reversal to euthyroidism. Rats were treated with L-thyroxine for 5 weeks (0.4 mg/ 100 g food). Plasma T3, T4, TSH and serum IL-1beta, IL-6, TNFalpha, Calcium (Ca), phosphorous (P), parathyroid hormone (PTH), alkaline phosphatase (ALP), bone alkaline phosphatase (B-ALP) levels were measured and differential leucocyte counts were made initially, at the 5th week of the experiment (hyperthyroid state) and 5 weeks after quitting the administration of L-thyroxine (euthyroid state). Significant rises in serum IL-1beta, IL-6 and TNFalpha were noted in hyperthyroidism (P < 0.001). In euthyroid state, IL-15, IL-6 and TNFalpha decreased significantly, but IL-beta and TNFalpha were significantly higher than the baseline values (P < 0.05) while IL-6 levels turned back to the baseline values. Plasma T3 and T4 levels were significantly correlated with serum cytokines in hyperthyroid state while there was no correlation in euthyroid states. Ca and P levels did not differ significantly while PTH levels declined significantly in the hyperthyroid state (P < 0.05). After the reversal to the euthyroidism, there was no significant change in Ca, P and PTH levels. ALP and B-ALP increased significantly in hyperthyroidism (P < 0.001, P < 0.01) and they did not decrease in euthyroid state. The lymphocyte number and ratio in differentials increased significantly in the hyperthyroid state (P < 0.001). In euthyroidism they decreased significantly (P < 0.001) but it was significantly higher than the baseline value (P < 0.05). Our findings showed that the deleterious effect on bone metabolism in hyperthyroidism might be mediated by cytokines and the increased bone turnover in hyperthyroidism failed to decrease despite euthyroidism


my comment - It's a pity they did not also retest at 12 weeks after reversal to eurothyroidism....as this is when they say that typically the hypothalmic/piuitary feedback are usually normalised
--------------------------------

This is one of my many "look into sometime " articles.
I'm on thyroid meds too..but so far have kept levels much the same(Z=-1.1 to Z=-1.2 over 3 years) ..with a lot of hard work..pretty disappointing actually.

also
-------------------
Interleukin-6 production and secretion by human parathyroids
Clin Exp Immunol. 2004 Apr;136(1):145-56.
PMID: 15030526 [PubMed - indexed for MEDLINE]

Parathyroid hormone (PTH) stimulates osteoblasts to produce the proinflammatory cytokine interleukin-6 (IL-6), causing bone resorption
________________________________
so it looks to me like IL-6 may "possibly" be the thing that causes the bone resorption..and thyroid hormones(T3 , T4) increase IL-6 if thyroid hormone levels are allowed to get too high as in hyperthyoid.
-----------
Jan


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