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Old 10-19-2004, 12:08 PM   #1
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Calcitonin

I was on another thyroid board and someone mentioned that Armour has Calcitonin in it. Calcitonin is good for the bones and our thyroids naturally produce it right? So for those that have osteoperosis taking Armour would help with our bone density, right? I just want to make sure that I understand this so next time I see my doctor I can give him this information, because he didn't want to let me try Armour and once I got some he refused to increase it because I have osteoperosis.

Any additional information would be helpful. Thanks!

 
Old 10-19-2004, 04:11 PM   #2
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Re: Calcitonin

Calcitonin is produced by the Parathyroids, not the thyroid gland. Granted, Armour DOES contain some calcitonin, most likely from the thyroid gland's proximity to the parathyroids, it is not measured or regulated in Armour, so taking it for the calcitionin content is not a good enough reason, and it won't likely convince your doctor.

However, there ARE studies that show that hyPOthyroidism can cause bone loss, too, and the studies done to supposedly "prove" that thyroid meds can cause osteoporosis were all done on one med: You guessed it, it was $ynthroid.

There are other studies that have been done that would show your doctor that treating a thyroid problem properly can help to improve bone density, and that a lack of agressiveness in treating hypo can lead to bone LOSS. Basically, your doctor's fears are not well founded.

Dr. Dommisse's paper that I have posted excerpts from on here occasionally touches on that and also cites references on where he got his info. It might be a good place to start.
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Old 10-19-2004, 04:13 PM   #3
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Re: Calcitonin

Thanks Danny for the info.

 
Old 10-19-2004, 04:24 PM   #4
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Re: Calcitonin

Here are the three places in his paper that he talks about osteoporosis. The bold emphasis is mine.

Dommisse on Osteoporosis:

In the introduction of his paper:
By placing more emphasis on the accurate measures of the actual thyroid hormones, the serum free-T4 and free-T3 levels, than on the 3rd-generation TSH, I have, since early 1989, been optimizing the thyroid function of all my hypothyroid patients, many of them former patients of endocrinologists who use the TSH as the ‘holy grail’ of thyroid diagnosis. This is how I have come to know that, in most instances, the patient is right and the endocrinologists are wrong: The patient is usually being undertreated (because of an unfounded fear of osteoporosis) and incorrectly treated, with T4 only.
...
Many physicians regard hypothyroidism as far more common than is generally acknowledged. This article will detail how patients who are being treated are actually undertreated, because of excessive reliance on the ultrasensitive serum TSH level for monitoring, and the use of a single thyroid hormone, thyroxine (T4), in its treatment. Additionally, there are excessive fears of precipitating or aggravating osteoporosis. Evidence for this is equivocal and shared by concerns of both natural and iatrogenic hypo- and hyperthyroidism causing it (Adlin et al, 1991; Ross, 1991b; Franklyn et al, 1994; Hart, 1995; Uzzan et al, 1996; Bauer et al, 1997) (and, presumably, undertreatment of either being a risk factor as well). The conservative American College of Physicians has recently found enough evidence of the widespread nature of hypothyroidism to recommend that, and since women are 9 times more likely than men to become hypothyroid, women over 50 years of age should be screened for it once every 5 years (Helfand & Redfern, 1998). In an editorial rebuttal, renowned thyroidologist David Cooper argues for a more aggressive approach to case-finding, and treatment of milder degrees of hypothyroidism (Cooper, 1998) and cites powerful support (Surks & Ocampo, 1996; Arem & Escalante, 1996), including the American Thyroid Association (Singer et al, 1995).

In his Myths section:
(9) "Keeping both the FT4 and FT3 levels at the high ends of their normal ranges will cause osteoporosis": This concern was merited 30-50 years ago, when much-higher doses of thyroid hormone were used in the treatment of most cases of hypothyroidism. One of us (JVD) has not observed this complication in over eleven years of this more-aggressive treatment (unpublished data). In fact, his treatment_optimized hypothyroid osteoporotic patients' bone density scans not only don't deteriorate from one year to the next but almost-invariably improve, without the use of elindronate, calcitonin or any other drugs. This means that, for there to be 'overtreatment' of hypothyroidism, it has to be more substantial than is currently thought. Concurrent correction of other factors, such as deficiencies of vitamins, minerals, other hormones, and amino-acids, seems to maintain and extend bone density, even in the presence of optimal or 'aggressive' treatment of hypothyroidism.
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Last edited by Meep; 10-19-2004 at 04:25 PM.

 
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