For a 50-year old caucasian woman today, the risk of a hip fracture over her remaining lifetime is about 17%. Tomorrow the situation will clearly be worse because the continual increase in life expectancy will cause a 3-fold rise in worldwide fracture incidence over the next 60 years, particularly in women, but also in men. In addition, a secular increase in the incidence of hip fractures in individuals of the same age has been noted in both sexes by several investigators, and the cost of hip fractures is expected to dramatically increase in the next decades. Consequently, preventive strategies are urgently required. A great deal has been learned in recent years about the risk factors for hip fracture, the pathophysiology of this fracture, and the prediction of fracture risk, particularly through bone mass measurements on the hip and biochemical evaluations of parathyroid and vitamin D status. The two main determinants of hip fractures are falls and bone loss leading to an intrinsic femoral fragility. A substantial femoral bone loss continues throughout the old age, with a continuous and exponential increase in the risk of hip fracture, and any reduction or arrest of this loss will induce an important reduction in the incidence of hip fractures. A preventive effect on the risk of hip fracture may be partly achieved by using long term estrogen replacement therapy after menopause, but also by using vitamin D and calcium supplements for a late prevention in elderly people. Vitamin D insufficiency and deficit in calcium intake are very common in elderly people living either in institutions or at home, particularly in Europe where dairy products are not fortified with vitamin D. The cumulative response to this deficit in calcium intake and low vitamin D status is a negative calcium balance which stimulates parathyroid hormone secretion. In 300 residents of nursing homes, we recently found a significant negative correlation between serum 25 OHD and log serum PTH after age-adjustment. In addition, in 446 elderly women living at home in 5 French cities and selected from the voting lists, we also found an age-adjusted relationship between serum 25 OHD and PTH concentrations. This senile secondary hyperparathyroidism is one of the determinants of femoral bone loss and can be reversed by calcium and vitamin D supplements.
We have shown in a 3-year controlled prospective study that the daily use of these supplements (1.2 g of calcium and 800 IU of vitamin D3) given in a large population of 3270 elderly ambulatory women living in nursing homes reduced of 23% (intention-to-treat analysis) the number of hip fractures and other non vertebral fractures.
In parallel, serum perathyroid hormone concentration was reduced of 28% and low serum 25-hydroxyvitamin D concentration returned to normal values. After 18 months of treatment the bone density of the total proximal femoral region had increased 2.7% the vitamin D3-calcium group and decreased 4.6% in the placebo group (p < 0.001). This prevention is safe and can be recommended in people living in institutions. It could be also useful in other elderly subjects particularly at risk because of a low calcium intake, an absence of solar exposure and a previous history of falls. From the data of our study we assessed the economic consequences in terms of medical cost of this prevention. In case of treatment of all women living in nursing homes in France, this would saved FF 150000000 per year, the economic balance of prevention becoming positive as soon as the age of the beginning of the prevention reaches 73.5 years. It is now possible to partly stop bone loss in elderly people and it is never too late to prevent hip fractures with calcium and vitamin D supplements.
Scand J Rheumatol Suppl. 1996;103:75-8; discussion 79-80.
Prevention of hip fractures by correcting calcium and vitamin D insufficiencies in elderly people.