Improved bone strength has been associated with a higher potassium to sodium ratio in the diet. High potassium foods contribute to a higher ratio. Because there are so many factors associated with increased bone strength it is difficult to isolate the interplay between them. Most foods that are high in potassium are also high in bicarbonate or bicarbonate precursors such as citrate. These also are a factor in increased bone strength.
Population studies have shown lower rates of fragility fractures such as hip fractures and have shown increased bone density in one national population that began a national campaign that increased potassium and lowered sodium in the diet. Finland started this campaign in the 1970s and has recently studied the bone mineral density and hip fracture rate in its population, as discussed here (A). It is the only Scandinavian country that has a reduced hip fracture rate and that has shown increased bone mineral density in their population. The other Scandinavian countries have not changed the potassium sodium ratio and remain among the countries with the highest hip fracture rates in the world.
Of course, the improved hip fracture rate may only be associated with, and not be caused by, the change in diet. For the improved hip fracture rate and improved bone density to be caused by this change in diet, basic science studies should agree with the findings. Last post we discussed how studies of the osteoclasts were consistent with increased bone density from high potassium foods. The same is true of the studies on osteoblasts.
Many studies have been done on the cell membrane's ion pores of osteoblasts. These pores control the potassium, sodium and hydrogen ions inside and outside the cell. When they are open they allow passage of the ion.
An example from the many basic science studies on osteoblasts that are consistent with high potassium foods leading to increased bone mineral density is a study from 2009 (1). This study showed that changes in the electrical charge combined with changes in the calcium concentration in the osteoblast cell to lead to changes in the passage of potassium through one of these ion pores in the cell membrane.
This pore allowing potassium into the cell is sensitive to calcium concentration in the cell. Decreased concentration of calcium in the cell opens the pore, allowing passage of potassium. This leads to increased mineralization in the matrix around the osteoblast by causing release of osteocalcin, the main protein for mineralization.
The passage of potassium through the pore also leads to cell proliferation of the osteoblast. More osteoblasts means that more bone can be made and that the bone becomes stronger.
This basic science study, and others, of the osteoblast are consistent with the effect of high potassium foods leading to increased mineralization and increased bone density.
Thus the studies on osteoblasts show a consistency with the high potassium to sodium ratio affecting osteoblasts in a way that will increase bone mineral density. There are other studies showing similar effects with the hydrogen ion and bicarbonate ion interaction, so this is another potential explanation.
Thus the basic science studies do not distinguish whether potassium or bicarbonate is the factor leading to improved bone density. Either is consistent with high potassium foods leading to increased bone mineral density. Future studies may give more insight into which is the more important factor.
Most likely both play a role in increased bone density. With a systems approach it may be possible to distinguish how potassium and bicarbonate interact. But both potassium and bicarbonate precursors are present in high potassium fruits and vegetables. Fruits and vegetables high in potassium are also high in bicarbonate precursors. If you get enough of the plant based high potassium foods you will be getting enough of the factors that prevent osteoporosis.
1. A large-conductance (BK) potassium channel subtype affects both growth and mineralization of human osteoblasts. Henney NC, Li B, Elford C, Reviriego P, Campbell AK, Wann KT, Evans BA. Am J Physiol Cell Physiol. 2009 Dec;297(6):C1397-408. doi: 10.1152/ajpcell.00311.2009. Epub 2009 Sep 23.