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Dear Sir:
I expected a number of adverse comments about my recent article in the Journal (1). After all, high-calcium diets have been promoted by the dairy industry, the nutrition establishment, and much of the medical profession for 80 y or more. The dairy interests have a large stake in this and cannot be expected to be unbiased.
It is not useful to reiterate all of the arguments presented in my original paper (1). Whatever the strengths and weaknesses of the epidemiologic studies within the United States may be, they provide little or no support for high-calcium diets (2,3). Increases in calcium retention from balance trials and increases in bone mineral, however measured, are usually interpreted as beneficial (4). Yet the calcium retentions reported in many trials are obviously unreal, and most balance trials are interpreted to yield false retentions (5). It remains to be shown that modest increases in bone mineral actually reduce the fracture rate. Wilkin (6) argues that bone density is not a good predictor of hip fracture and that "some 85% of the contribution to the rise in fracture rate with age is unrelated to bone density." He also states that the data on the antiresorptive drug risedronate show that the risk of fracture had fallen well before bone density peaked and that such trials suggest that "antiresorptive drugs can halve the risk of fracture . . . without restoring significant bone density." He adds that "high turnover of bone seems to be intrinsically unstable, whereas low bone density need be weak only if its low mineral content results from chronically high bone turnover."
Many factors do or have been suggested to modify the risk of osteoporosis and fractures, including sex, genetics, stature, exercise, obesity, and intakes of vitamin D, vitamin A, calcium, fluoride, sodium, potassium, protein, fruit, and vegetables. Ironically, if high calcium intakes are beneficial, supplements may be more helpful than dairy products because high animal protein intakes increase urinary calcium excretion. Most epidemiologic studies in the United States have failed to identify any of the above dietary factors as serious risk factors, although the data on vitamin D appear rather convincing in some situations, and, given the limitations of such studies, I find the data on fruit and vegetables most interesting.
Although more quantitative data on fracture rates in various parts of the world are welcome, we know that populations around the world that use few dairy products and have relatively low calcium intakes develop reasonably well and are obviously not falling apart from fractures. On the other hand, fracture rates are obviously high in the countries that consume the Western-type diet. The evidence that the administration of the hydroxymethylglutaryl-CoA reductase inhibitors (the statins, widely used to reduce serum cholesterol concentrations) also reduce fracture rates is substantial, although the results of any controlled trials are not yet available (7). The statins block the mevalonate pathway, which clearly suggests that dietary practices that promote high cholesterol concentrations also induce a mechanism that makes bone fragile in the elderly. Perhaps this unknown mechanism stimulates bone turnover, as suggested by Wilkin (6), also via the mevalonate pathway, and is also blocked by the statins. Research devoted to this possibility, rather than to the oft-repeated studies of the effects of calcium, should be rewarding.
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