DEAR DR. ROACH: I’m 70, Caucasian and slim. I was diagnosed with osteoporosis five years ago. Before that, I took Fosamax for five years. The only things I take are 1,000 mg calcium citrate, 3 mg boron and a multivitamin containing 2,000 IU vitamin D. An X-ray showed three compression fractured vertebra. I read that taking more than 1,000 IU of vitamin D can cause bone mass loss! I started crying thinking that I caused the fractures from taking too much vitamin D. I’ve stopped the multivitamin and just take 500 IU of the vitamin D. I’m outside an hour a day. Do you know of bone mass loss from too much? — V.W.
ANSWER: Low levels of vitamin D are a common and treatable cause of bone loss, which can ultimately lead to fractures. It’s a good idea to check the vitamin D level in people with known osteoporosis. There remains some controversy about the optimum level of vitamin D, but a level between 30 and 50 ng/mL is generally considered safe.
Very high levels of vitamin D can cause calcium to come out of bones, and can cause risk of kidney stones as well as symptoms. However, this is almost unheard of in a dose less than 4,000 units daily. I think it is very unlikely that you were taking too much vitamin D, so there’s no need to blame yourself.
Although people with boron deficiency are at higher risk of bone loss, using boron as part of osteoporosis treatment has never been shown to reduce fracture rates. I don’t recommend boron supplementation. Leafy green vegetables like spinach and kale are good sources in the diet.
DEAR DR. ROACH: If you are an 80-year-old woman who has used Synthroid for decades, could it be the cause of osteoporosis and significant bone loss of the jaw? — D.M.P.
ANSWER: Excess thyroid hormone clearly causes reductions in bone density and increases the risk of fractures. Synthroid, a brand of levothyroxine, is used to replace thyroid hormone in people who can’t make it (called hypothyroidism), especially people who have autoimmune thyroid disease causing a too-low level of thyroid hormone and people who have had surgery on their thyroid gland.
Healthy bone is metabolically active. Bone-absorbing cells (osteoclasts) constantly “eat” away bone, followed by bone-creating cells (osteoblasts), which come in and lay down new bone. One professor I had likened it to road repair: Bones, like roads, sustain damage over time. A repair team needs to dig up the bad road and replace it with new pavement. But the processes must be balanced — too much digging without repaving and the road is full of holes; not enough removal of damaged road and the slapped-down repairs are weak and inefficient.
Without treatment of hypothyroidism, bone absorption is slowed and bone density actually increases. Unfortunately, people with untreated hypothyroidism also are at risk for fracture: Without normal reabsorption of bone balanced with new bone formation, bone can become brittle. The opposite is true in hyperthyroidism: Bone absorption is faster than new bone formation. Too much and too little thyroid both lead to fracture risk, but too much is probably worse.
If the thyroid levels are right where they should be, then there is no increased risk for osteoporosis or fracture. Unfortunately, that doesn’t protect a woman from developing bone loss, and most 80-year-old women will have significant reductions in their bones compared with young women, even with normal thyroid levels.