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Vitamin C deficiency accelerates bone loss

It has been already known that vitamin C is an antioxidant and it may even be able to cure certain cancers when the vitamin is IV injected in humans (some alternative physicians use vitamin C to treat cancer). But a new study in International Journal of Experimental Pathology suggests that vitamin C can also help maintain bone health.

It was observed that vitamin C deficiency can cause failure of collagen synthesis, which can lead to symptoms of scurvy including spontaneous bone fractures in senescence market protein 30 knockout ((SMP) 30 knockout (KO))mice, according to study authors, J.K. Park of Kyungpook National University in Daegu, Korea and colleagues.

Because spontaneous bone fracture can also be caused by low bone mineral density, the current study was conducted to examine the effects of vitamin C deficiency on the balance between osteoblasts and osteoclasts in mice of concern.

For the study, (SMP) 30 knockout (KO) mice were fed a vitamin C-free diet, and only one group of mice were given water with 1.5g/L of vitamin C, whereas wild-type and KO mice were given normal drinking tap water without vitamin C for 16 weeks.

"After 16 weeks, all femur samples were removed for histopathological examination. The femurs of KO mice showed significantly reduced bone area and decreased number of osteoblasts compared with those of WT mice and KV mice. KO mice also exhibited the lowest level of alkaline phosphatase (ALP) expression in their femurs," the researchers reported.

It was also found that "KO mice showed the most elevated expression of the receptor activator of nuclear factor kappa-B ligand (RANKL). Moreover, KO mice had the strongest peroxisome proliferator-activated receptor (PPAR)-γ expression level in their osteoblasts and the highest number of TUNEL-positive bone marrow cells."

The researchers concluded "vitamin C deficiency plays an important role in spontaneous bone fracture by inhibiting osteoblast differentiation and promoting transition of osteoblasts to adipocytes, and this could in turn be related to the increased PPAR-γ expression."