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17 September 2006

Lifetime high calcium intake increases osteoporotic fracture risk in old age

Thijs R. Klompmaker,
Groove Union Coop. U.A., van Hogendorpstraat 4, 1051 BP Amsterdam, Noord Holland, The Netherlands


Caloric restriction prolongs life span. Calcium restriction may preserve bone health.

In osteoporosis, bone mineral density (BMD) has significantly decreased, due to a lack of osteoblast bone formation. Traditional osteoporosis prevention is aimed at maximizing BMD, but the lifetime effects of continuously maintaining a high BMD on eventual bone health in old age, have not been studied. Strikingly, in countries with a high mean BMD, fracture rates in the elderly are significantly higher than in countries with a low mean BMD. Studies show that this is not based on genetic differences. Also, in primary hyperparathyroidism, on the brink of osteoporosis, BMD levels may be significantly higher than normal.

Maybe, BMD does not represent long term bone health, but merely momentary bone strength. And maybe, maintaining a high BMD might actually wear out bone health.

Since osteoporosis particularly occurs in the elderly, and because in osteoporotic bone less osteoblasts are available, the underlying process may have to do with ageing of osteoblastic cells.

In healthy subjects, osteoblastic bone cells respond to the influx of calcium by composing a matrix upon which calcium precipitates. In the process of creating this matrix, 50–70% of the involved osteoblasts die. The greater the influx of calcium, the greater osteoblast activity, and the greater osteoblast apoptosis rate. An increased osteoblast apoptosis rate leads to a decrease in the age-related osteoblast replicative capacity (ARORC). In comparison to healthy bone, in osteoporotic bone the decrease in the replicative capacity of osteoblastic cells is greater. Due to the eventual resulting lack of osteoblast activity, micro-fractures cannot be repaired. Continuously maintaining a high BMD comes with continuously high bone remodeling rates, which regionally exhaust the ARORC, eventually leading to irreparable microfractures.

Regarding long time influences on bone health, adequate estrogen levels are known to be protective against osteoporosis. This is generally attributed to its inhibiting influence on osteoclast activity. Instead, its net effects on osteoblast metabolism may be the key to osteoporosis prevention. Adequate estrogen levels inhibit osteoblast activity, calcium apposition and osteoblast apoptosis rate, preserving the ARORC.


Regarding osteoporosis prevention, ARORC better than BMD represents bone health. Regarding ARORC, adequate estrogen levels are protective, opposing the similar effects of hyperparathyroidism and a high calcium diet.

Tests need to be performed in mice to assess the lifetime effects of a high versus a low calcium diet, on eventual bone fracture toughness.