[Anonymous]

#1049244

Greetings: I’ve been doing some lay research recently (no you don’t lay around and research things) on the link between Grave’s disease and osteoporosis, and I think I’ve found something. I’ll try not to make it too complicated, and maybe George and/ or Tu can add something in.

At first glance, the thyroid gland has nothing to do with calcium, bones, or osteoporosis. The thyroid gland produces hormones that affect heart rate, metabolism, etc – the ‘fire’ of the body’s furnace. Calcium levels in the body are strictly controlled by something else, called the parathyroid. There are four parathyroid nodules, located behind the thyroid gland at the base of the neck. Although they are anatomically very close, the two don’t have any obvious relationships with each other.

The parathyroid monitors and controls calcium levels in the body. That’s its job, and that’s all it does. About 99.5% of the body’s calcium is held in the bones, and the rest floats around the bloodstream and other places. Having an imbalance of calcium can have a lot of effects – too little and the body takes calcium from the bones to compensate – too much, and it can have effects on the stomach lining, pancreas, kidneys, etc. Because the kidneys filter blood of impurities, having too much calcium in the blood can lead to deposits and kidney stones. In rare cases one can develop calcium deposits on the back of the heart and other places.

The parathyroid works with other aspects of the body in an intricate relationship. Levels of parathyroid hormone determine how well the wall of the intestines absorb calcium from what you eat, how much calcium is excreted from the kidneys through your urine, and how much calcium is given to or taken from your bones.

Bones are living tissue, and there are two different types of cells involved in bone growth. Osteoclasts chew up old bone, and osteoblasts make new bone. As people age, the rate of the osteoclasts starts to outpace the osteoblasts, so that the body loses slightly more bone than it makes. A number of factors can contribute to this. Having an overactive parathyroid gland is one of them – if the parathyroid is producing too much hormone, the osteoclasts work overtime.

So what does this have to do with the thyroid gland and Grave’s disease? As far as I can tell, nothing. However, aside from T3 and T4, the thyroid gland produces a hormone called calcitonin. Calcitonin in the body has some effect on slowing the action of the osteoclasts and results in less bone loss. Can’t say for sure, and others are welcome to join in here, but if having an overactive thyroid gland lowers the levels of calcitonin, that may be a link.

BTW, since fingernails are essentially calcium, lower levels of calcium in the bloodstream may result in softer nails as calcium is pulled from ‘hard’ tissues.

Me.

[Anonymous]

#1146457

Mike–It looks like we’re both doing similar reseaarch. Your explanation of the parathyroid gland functions is really good. I have been wondering what happened to the calcitonin production in my body when the thyroid was zapped with RAI.

Research indicated that the part of the thyroid that makes calcitonin is very sensitive to radioactivity and is likely to have been destroyed (although sometimes some remains and recouperates). This raises the question of what happens to me when I don’t have this source of calcitonin (CT). My (former) endocrinologist said that CT neither causes nor cures any disease. This drove me to further research. It seems that CT, in slightly different forms, is made in other parts of our bodies because it is vital. However, my internist tested my CT levels and they are low. I don’t know the implications of this. CT was out of style in medical research for a while, but it seems to be coming back. It is, after all, used to treat osteoporosis.

The other thing I worried about is the effect of RAI on the parathyroid glands, since they are basically imbedded in the thyroid. Research showed that they are in fact affected by radioactivity, although it usually takes time (years?) for the effects to show up. The response is for one or more of the parathyroid glands (PT) to become enlarged (an adenoma or hyperplasia) and put out too much hormone. The hormone triggers too much calcium in the blood. This can cause a lot of bad effects on our bodies.

In addition, there is a correlation between hypothyroidism and hyperparathyroidism (too much PT hormone). There may also be a link between ATDs and hyperparathyroidism (a few studies).
Symptoms of hyperparathyroidism include bone and muscle pain, depression, brain fog, digestive problems, and more (not hair loss, I don’t think). A lot of them are like hypothyroid symptoms.

We should all have our intact calcium blood levels checked periodically. We should all have our parathyroid hormone levels checked, too, although that test is expensive and has to be sent to a specialized lab. My calcium levels have been bouncing around the normal range, but my parathyroid levels are quite high. There is debate (between me and the doctors) about the implications of this.

I can dig up the references for this information if you want it, although things aren’t well organized. I also saw some material on hyperthyroidism and leaching of calcium from bones, which I may have saved.

Let me know if you want more information.

Elisa

[Anonymous]

#1146458

This issue of calcitonin has been discussed before. The fact is, however, that too little calcitonin has NOT been shown to cause a problem with calcium retention in humans. It’s one of those theories that makes sense to us laymen, but that has no factual demonstration in real life. According to every endocrinology book I’ve read (and that includes two texts) to research some of these issues, the bottom line is that calcitonin is the one hormone in the human body for which there is no disease condition known for either too much or too little of it. There ARE disease conditions which can be ID’d if you have too much of it, but the corollary ( that having too much of it shows you have this disease) is not true.

Bobbi

[Anonymous]

#1146459

Hi Mike,

You are doing some fine research! Even my new endo checked my parathyroid levels. I still am awaiting his call back on my blood tests.
Both of my children were born with pseudohypoparathyroidism. And yes a lot of what you posted about I have heard before from my children’s endos. My new endo decided for sure to check my parathyroid after I complained (at the end of my visit) about how my calcium deposits that I have in the bend of my right arm sometimes bother me. One had been just big enough to bother me years ago that when I was in he Navy they cut it out! Now that I think back on it I think it was a couple of Air Force Corpmen that did the procedure. Gee, that was back in 1973! I was very grateful to have it removed!

He also asked if I had a bone denisity test done yet. I am still waiting for the health insurance approval. He asked that at the beginning of the visit.

I am so glad that others are taking the time to learn all about this stuff. Research is the key for the doctors to unlock the mysteries of the endrocrine system. In the meantime I am grateful to be able to count my blessings, big and small!

Thank you,
Michele B.

[Anonymous]

#1146460

Bobbi wrote: This issue of calcitonin has been discussed before. The fact is, however, that too little calcitonin has NOT been shown to cause a problem with calcium retention in humans. It’s one of those theories that makes sense to us laymen, but that has no factual demonstration in real life…

The following was written by doctors, not by a lay person like me. You decide:

“Remodeling consists of tearing down small parts of the bones, and then re-forming them. The breaking down portion is termed “resorption” and is performed by large cells within the bones called “osteoclasts”. Osteoclasts live in the central portion of the bone. They are continually removing small (microscopic) portions of bone at the edge of the bone surface. Nearby, bone forming cells called “osteoblasts” begin to fill in the holes left behind. Here is the big problem: remodeling does not seem to be a perfect give and take of bone mass. The osteoblasts are less efficient at making bone than the osteoclasts are at removing it. Although the difference is slight, this is what accounts for the gradual loss of bone density (BMD) as a person ages. Any factor which causes a higher rate of bone remodeling will ultimately lead to a more rapid loss of bone mass and thus more fragile bones….

….Calcitonin is a hormone which is naturally produced in the thyroid. Calcitonin is a powerful inhibitor of osteoclastic activity (the cells which continuously reabsorb bone). When given to patients with osteoporosis, calcitonin produces modest increases in bone mass.

[Anonymous]

#1146461

Mike,
Great summary of the physiology of the parathyroid glands, calicitonin function, and bone production/resorption! When I was first diagnosed, I asked my endocrinologist if there were any long term effects of Graves’ he said that the only thing that had been substantiated was a higher incidence of osteoporosis. I will go to the literature and see if I can find the reference for this study and then read it to see how the authors explain this phenomenon physiologically. My guess is that nobody really knows why. Probably a lot of hand waving. I’ll post what I find.
george.

[Author]

Posts