This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Because increasing dietary protein increases urine calcium and metabolic acid load and because systemic acidosis favors bone loss, it is thought that higher protein diets increase bone resorption and decrease Bone Mineral Density (BMD). However, most cross-sectional, population-based studies with bone density, or rates of bone loss as the principal outcome, indicate that higher dietary protein intakes are associated with higher (not lower) BMD and slower (not faster) rates of bone loss. Further, increasing dietary protein in subjects consuming low-normal protein diets increases circulating levels of IGF-1 which is known to be important for bone anabolism. Three recent diet-controlled isotopic calcium studies showed no net loss of calcium from bone during high protein diets in humans (1-3). In 1 of these 3 studies, we (1) showed that a high protein diet increased urinary calcium by increasing intestinal calcium absorption. Importantly, during the high protein diet, there was a significant reduction in the fraction of urinary calcium of bone origin and a trend toward a reduction in the rate of bone turnover. None of the 3 isotopic studies found evidence for increased bone loss with increasing dietary protein. In fact, they all suggest the opposite; higher protein diets actually improved calcium retention. These isotopic data lay the groundwork for a long-term protein intervention trial with BMD as the principal outcome variable.
Showing the most recent 10 out of 638 publications
