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The Thyroid Treatment/Osteoporosis Controversy
Does Thyroid Treatment Contribute to Loss of Bone Density?

by Mary Shomon

Osteoporosis is a common condition where the bone becomes thin and fragile, creating an increased risk of fracture. Osteoporosis is usually painless until a fraction takes place, and osteoporosis is a major contributing factor to bone fracture, including hip fractures, which are more common as people age. There are almost 2 million hip fractures annually around the world. While in the U.S., osteoporosis affects an estimated 26 million Americans, and more than 20 million are women, it is vastly undiagnosed. Only 10% of women with osteoporosis are estimated to currently be diagnosed and treated for the condition. Diagnosis, prevention, and treatment of osteoporosis is possible with the use of bone mineral density (BMD) testing and several effective treatments.

The relationship between thyroid disease and osteoporosis is a controversial one. While it's accepted that significant periods of hyperthyroidism have an effect on bone mineral density and can increase the risk of osteoporosis, there is tremendous controversy over whether long-term use of levothyroxine (i.e., Synthroid, Levoxyl) at suppressive or non-suppressive levels increases the risk of osteoporosis.

Thyroid cancer survivors are typically given thyroid hormone at levels that suppress thyroid function and TSH levels almost completely. These would be low or nearly 0.00 TSH levels. Most thyroid cancer patients, however, receive supplemental calcium or calcitonin to reduce any risk of reduced bone density.

Other patients, however, may find that while they feel best in the low end of the TSH range - not suppressed, but at TSH levels in the 1 to 2 range - doctors are reluctant to dose to that level, citing concerns over osteoporosis. Other doctors refuse to consider the use of supplemental T3 thyroid hormone, also citing osteoporosis concerns due to hyperthyroidism induced by the T3.

Whether or not these concerns are valid is a controversy that is not resolved by the research findings, which are contradictory. A search of the medical journal literature shows there is no agreement as to the impact of thyroid hormone treatment on osteoporosis risk.

A study released in June, 2000, at the World Congress on Osteoporosis in Chicago, Illinois, found that taking thyroxine (i.e., Synthroid) does not increase the risk of osteoporosis. The research, presented by Dr. Martin Stenstrom of the University of Gothenburg in Sweden, studied more than 750 women who were taking prescribed thyroid medication for thyroid disease. Over an 18 month period, bone mineral density was measured, and compared to a control group who were not taking thyroid hormone. No differences were noted in bone mineral density between those taking the thyroid hormone, and the control group. An October, 1998 study reported on in the Journal of Gynecological Endocrinology found that levothyroxine suppressive therapy, if carefully carried out and monitored, has no significant effect on bone mass. ( Gynecol Endocrinol 1998 Oct;12(5):333-7, "Bone mineral density in premenopausal women receiving levothyroxine suppressive therapy.").

The highly regarded Journal of Clinical Endocrinology and Metabolism found that even "suppressive," levothyroxine therapy -- prescribing medicine that lowers TSH levels to hyperthyroid levels below normal range -- if carefully carried out and monitored, has no significant effect on bone metabolism or bone mass. ( J Clin Endocrinol Metab 1994 Apr;78(4):818-23, "Carefully monitored levothyroxine suppressive therapy is not associated with bone loss in premenopausal women.")

A major thyroid-related journal, Thyroid, found that long-term levothyroxine therapy using suppressive doses has no significant adverse effects on bone. (Thyroid, 1995 Feb;5(1):13-7, "Suppressive doses of thyroxine do not accelerate age-related bone loss in late postmenopausal women.")

Finally, in 1998, the Journal of Hormonal and Metabolic Research found that there was no difference in bone mineral density between thyroid patients and controls, and that the main factor in bone density and bone turnover is menopausal status. The researchers found that slightly suppressive levothyroxine doses constitute neither an actual risk factor for bone loss nor, consequently, for osteoporotic fractures. (Horm Metab Res 1995 Nov;27(11):503-7, "A slightly suppressive dose of L-thyroxine does not affect bone turnover and bone mineral density in pre- and postmenopausal women with nontoxic goitre.")

On the other hand, there is some research that suggests that the osteoporosis risk may be a legitimate concern.

A May 2000 study in the European Journal of Endocrinology found that long-term treatment with levothyroxine to normal range TSH levels was associated with a slightly increased risk for osteoporotic fracture. (Eur J Endocrinol 2000 May;142(5):445-450, "The effect of long-term, non-suppressive levothyroxine treatment on quantitative ultrasonometry of bone in women.").

And the Journal of Clinical Endocrinology and Metabolism has said that, although controversies exist on the possible adverse effect of T4 on bone mass, most studies reported bone loss in estrogen-deprived postmenopausal women taking suppressive doses of levothyroxine. Levothyroxine- suppressive therapy was associated with bone loss in postmenopausal women, however, it could be prevented by either calcium supplementation or intranasal calcitonin. ( J Clin Endocrinol Metab 1996 Mar;81(3):1232-6, "Prevention of bone loss induced by thyroxine suppressive therapy in postmenopausal women: the effect of calcium and calcitonin.")

While the research is contradictory and sometimes confusing, the predominance of the evidence is pointing toward the conclusion that non-suppressive thyroid replacement does not dramatically increase the risk of osteoporosis, and that a key risk factor seems to be age and menopausal status. It does not seem logical for doctors to refuse to treat to lower-normal TSH level, or to provide supplemental and not excessive T3 treatment - both therapies which may help resolve major hypothyroidism symptoms for some patients- solely on the basis of concerns over osteoporosis. This is particularly true for patients who are pre-menopausal.

The osteoporosis research findings should also raise concern over a smaller subset of doctors who practice according to the belief that patients should be given enough thyroid hormone to reduce TSH to the highest possible TSH level within normal range. These doctors are practicing faulty logic, having heard about the research associating suppressed TSH levels with the osteoporosis risk, so they believe that that if a very low TSH level poses a risk, then why not keep people at the highest possible level within the range, and thereby avoid the risk. Patients have reported doctors who provide only enough levothyroxine to get a patient to the absolutely highest levels within the normal range, and the patients continued to suffer a host of thyroid symptoms.

Unfortunately, this policy does not make much scientific sense. There is no evidence that keeping patients at the high end of normal has any ability to reduce osteoporosis risk compared to medicating patients to mid- or lower-normal range TSH. There is very real evidence, however, that leaving patients even slightly hypothyroid can increase the risk of high cholesterol, clogged arteries, and heart attack. Many patients have also found that they feel best at levels in the low normal -- TSH 1 to 2 -- range, and insufficient treatment dramatically affects quality of life and general wellness.

Comprehensive and definitive research needs to be conducted to decide once and for all whether suppressed, low normal, or even mid-normal TSH levels are "dangerous" or increase the risk of osteoporosis, and whether the use of supplemental T3 has any effect on osteoporosis risk This risk also needs to be assessed in comparison to the many other health risks -- including the very real risk of heart disease, America's number one killer -- that are associated with higher TSH levels or physiologic hypothyroidism.

What Should You Do?

You should discuss your thyroid hormone replacement drug treatment and optimum TSH level with your doctor, to determine what the best possible options are for you. But think twice before you accept "risk of osteoporosis" as a blanket reason why your doctor won't allow your TSH to be in the mid or low-normal range, or why your doctor refuses to consider T3 treatment.

There are some specific things you can do to reduce your risk of osteporosis:

  • Younger thyroid patients should pay particular attention to building bone during the period before age 30. Weight bearing exercise and sufficient calcium intake are the best ways to build bone when younger, and should continue as a way to maintain bone.
  • Consider having a bone density test at 40, and every several years thereafter. This is particularly important for thyroid patients.
  • Hormone replacement therapy, calcium supplementation, and drugs such as Fosamax, can also be discussed with the doctor for use in slowing loss in bone density or as preventatives.

According to research reported on in the June 7 issue of the "Journal of the American Medical Association," calcium supplements may interfere with the absorption of thyroid hormone medications. Taking calcium carbonate supplements at the same time as thyroid hormone can reduce T4 absorption, which results in elevated TSH levels and hypothyroidism. Given that many thyroid patients are women in their 40s and beyond, who take calcium to help prevent osteoporosis, there may be concerns over how to take your calcium? Doctors suggest taking your thyroid hormone first thing in the morning, an hour before breakfast, and take calcium supplements 12 hours later, to help prevent any absorption problems. Also, remember, don't take thyroid hormone medicine wiht calcium-fortified orange or other fruit juices, as the calcium in the juice can cause the same absorption problems.

Osteoporosis: Cures on the Horizon?

More effective treatments for osteoporosis may also be on the horizon. In late June, 2000, the British medical Journal The Lancet rpeorted that women over 60 taking statin" type cholesterol drugs -- brand names such as Zocor, Lipitor, and Pravachol, and generics such as lovastatin and pravastatin, among others. -- for at least a year had half the risk of breaking bones, without any negative side effects, such as increased risk of breast cancer, that can be associated with hormone therapy. Some experts believe that in the next three to five years, statins may replace estrogens as preventatives for osteoporosis.

Another study was presented at the Spring 2000 Endocrine Society meeting, suggesting that an over-the-counter dietary supplement called Promensiltm; can help in preventing osteoporosis. Promensil, manufactured by Novogen, Ltd., is a natural dietary supplement made from plant estrogens (isoflavones) extracted from red clover. Some experts, however, believe that the concentrated isoflavones in Promensil will negatively impact thyroid health in the same way that isoflavones from soy foods and supplements can increase the risk of thyroid problems and aggravate existing thyroid problems. In Australia, where Novogen is based, the company has been under attack for allegedly misleading advertising.

Researchers reported in June 2000 that parathyroid hormone (PTH) treatment can help stimulate the growth of new bone. Research trials have already been conducted, showing the positive impact PTH can have on both bone density and even bone size. The results will be presented to the United States Food and Drug Administration later in 2000, as a step toward getting approval for use of PTH in treating osteoporosis. There are some concerns, however, that PTH may increase the risk of certain types of bone cancer, and the FDA is considering limiting PTH studies to only those with severe osteoporosis, and is considering further investigations of the carcinogenic potential of PTH.

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