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CDA attempts to clear confusion over vitamin D and sun exposure

January 06, 2016

Hamrick is looking downstream at leptin-mediated signals in the bone and muscle to better define leptin's role in making both, how signals change with age and which ones respond well to leptin treatment. He thinks he'll find molecules that may be targeted therapeutically and may also be used as frailty biomarkers.

Meanwhile, Hill is focusing on the "microenvironment" of stem cells, primarily the role of SDF-1 as a sort of homing signal for mesenchymal stem cells. "It's like having a standing army somewhere to protect the homeland but you have to call them out periodically to help out in other places and if they can't be replenished at home, eventually it exhausts that army."

As a bonus, if they figure out how to make the cells happier and healthier at home, they will be better backups when needed elsewhere. "Some of the wear and tear we experience as we age is the result of these cells no longer being available to help patch things up," Hill said.

With osteoporosis, the normal balance of bone production by osteoblasts (made by the mesenchymal stem cells) and bone removal by osteoclasts errs on the side of bone loss. Muscle health, which is tied to bone health as well as agility, also suffers, Hamrick said.

Without better options, Isales, who treats osteoporosis, expects patient numbers to continue to grow. "We are living longer and unhealthier," he said. "Our nutrition is generally terrible; we are all eating things we should not be eating." In fact, up to 35 percent of patients over age 60 eat a diet that is protein- and calorie-deficient, according to the National Health and Nutrition Examination Survey of the Centers for Disease Control and Prevention. Osteoporosis also has a strong genetic component. "If your mother had osteoporosis, you are at risk for it no matter how much exercise you get or vitamin D you consume, so genes are an important part of this," Isales said.

Source: Georgia Health Sciences University