Men's Osteoporosis Support GroupShort-term high dietary calcium intake during bedrest has no effect on markers of bone turnover in healthy men Nutrition. 2009 Sep 16. [Epub ahead of print]. Short-term high dietary calcium intake during bedrest has no effect on markers of bone turnover in healthy men. Baecker N and others. PMID: 19765953. This is an interesting study performed on healthy young men in a metabolic lab where they could have highly controlled conditions and monitor the effects of increased calcium intake on various markers of serum and skeletal status. The participants were in either study A with 9 males of average age 23.6 years taking 1,000 mg of calcium daily or study B with 8 males of average age 25.5 years taking 2,000 mg calcium daily. Both studies lasted 14 days with 7 days of bedrest and 7 days ambulatory monitoring. The effect of the calcium supplements was tested via analysis of serum calcium, parathyroid hormone, C-terminal peptides of collagen to test markers of bone resorption and bone alkaline phosphatase to test markers of bone formation. The results showed no effect on serum calcium in either study A or B. The markers of bone formation also were unchanged for either study. However, markers of bone resorption were increased during the bedrest phases. And urinary calcium excretion was greater during bedrest than during the ambulatory phase for both studies. The authors concluded, "Doubling calcium intake to 2000mg/d does not prevent increased bone resorption induced by bedrest." Editor's comments. There is a tendency to assume that increasing the intake of calcium, either from diet or supplements, will solve all the issues that individuals with osteoporosis have. Rather the laws of cause and effect demand analysis of the issues to see exactly what is responsible for whatever effect that is present. In this study the effect is lost calcium in the urine during the bedrest phase of the study. Why does that occur? The lack of physical activity from bedrest, or as would occur during zero-gravity space flight, leads the body to increase bone resorption which releases calcium and the collagen that make up bone into the blood supply where they are filtered and flushed out of the system via the kidneys in the urine. In a low-gravity environment or one of reduced exercise, there is reduced need for heavy, dense bones that exists in the higher gravity and/or exercise conditions. So the body senses whether current exercise and gravity environments require more or less bone mineral density and either bone formation or resorption occur, as needed, to add or subtract from the skeleton to meet the current needs. As long as calcium intake meets the minimal requirement to allow the normal bone formation/resorption to occur, adding more will have no effect on markers of bone formation or resorption, or on serum parathyroid and calcium levels. Once analysis shows the cause of the increased urine calcium levels is bedrest, the way to decrease the urine calcium is to stop the bedrest and increase the exercise. It would be logical to do similar studies on newly diagnosed osteoporosis/osteopenia individuals. Biochemical markers should show increased bone resorption and either normal or decreased bone formation. If this is caused by low calcium intake, one would expect that when calcium was added to the diet the makers of bone resorption should decrease and return to more normal levels. Rather than do this, the shotgun approach is used and everyone is assumed to be ingesting inadequate calcium, so supplements are given.
|