Phosphate rich foods linked to high blood pressure and other health conditions.

phA new cause for high blood pressure was discovered linked to phosphate rich food such as processed cheese, parmesan, cola, baking powder and most processed foods, where phosphate is widely used as a preservative and pH stabilizer.

The consumption of phosphates in large quantities, stimulates the production of the FGF23, a hormone produced in bones, impacting on the cardiovascular system. The study reveals the connection between this hormone, renal disease and cardiovascular disease and that FGF23 controls renal excretion of sodium, thus impacting on blood pressure.

A raised level of FGF23 also increases strain on the heart. Reinhold Erben, the lead study author explains that, “In patients with chronic renal disease, both the phosphate levels and the levels of FGF23 are chronically high”. This often leads to cardiovascular disease.

A second study, published by Erben’s group revealed that FGF23 also controls calcium levels. As with sodium, the calcium is filtered in the kidneys and reabsorbed back into the body. If this reabsorption does not take place, the body loses calcium. Too much FGF23 leads to increased take up of calcium by the kidneys, and results in vascular calcification. Olena Andrukhova, the leading author of both studies, is keen to stress that, “Patients with chronic kidney disease often also suffer from cardiovascular disease. Raised FGF23 levels are partly responsible for this. Our results for the first time are able to explain this connection.”


Olena Andrukhova, Svetlana Slavic, Alina Smorodchenko, Ute Zeitz, Victoria Shalhoub, Beate Lanske, Elena E. Pohl and Reinhold G. Erben. FGF23 Regulates Renal Sodium Handling and Blood Pressure. EMBO Molecular Medicine, May 2014 DOI: 10.1002/emmm.201303716

Olena Andrukhova, Alina Smorodchenko, Monika Egerbacher, Carmen Streicher, Ute Zeitz, Regina Goetz, Victoria Shalhoub, Moosa Mohammadi, Elena E Pohl, Beate Lanske, Reinhold G Erben. FGF23 promotes renal calcium reabsorption through the TRPV5 channel. The EMBO Journal, 2014; DOI: 10.1002/embj.201284188

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