What are the worst foods for increasing blood pressure when you don't want your high blood pressure raised? It's the phospate-rich foods. Phosphate rich foods include processed cheese, Parmesan, cola, baking powder and most processed foods. Phosphates are widely used in the food industry as preservatives and pH stabilizers. A new study has revealed evidence showing why phosphate rich foods can increase blood pressure and promote vascular calcifications has been discovered by scientists at the Vetmeduni Vienna. The key is the hormone, FGF23 (Fibroblast Growth Factor 23). But you can avoid the foods that quickly calcify your arteries and organs, especially if you have a family history of above average or high blood pressure. Here's why phosphate-rich foods can increase blood pressure and promote calcifications in your arteries.
When the level of FGF23 is raised, as through a high phosphate diet, calcium and sodium accumulate, putting strain on the cardiovascular system. The study appears today in the journal, EMBO Molecular Medicine. Why phosphate rich foods can increase blood pressure and promote vascular calcifications has been discovered by scientists at the Vetmeduni Vienna.
When the level of FGF23 is raised, as through a high phosphate diet, calcium and sodium accumulate, putting strain on the cardiovascular system. The study appears today, May 5, 2014 in the journal, EMBO Molecular Medicine. You can check out the new article, "FGF23 Regulates Renal Sodium Handling and Blood Pressure," just published online today, May 5, 2014, in the journal EMBO Molecular Medicine." Authors are Olena Andrukhova, Svetlana Slavic, Alina Smorodchenko, Ute Zeitz, Victoria Shalhoub, Beate Lanske, Elena E. Pohl and Reinhold G. Erben. You also can check out a few month's older article, "FGF23 promotes renal calcium reabsorption through the TRPV5 channel," published January 17, 2014 in the journal EMBO Molecular Medicine. Authors of the January 17, 2014 article are Olena Andrukhova, Alina Smorodchenko, Monika Egerbacher, Carmen Streicher, Ute Zeitz, Regina Goetz, Victoria Shalhoub, Moosa Mohammadi, Elena E. Pohl, Beate Lanske and Reinhold G. Erben.
When large quantities of phosphates are consumed, production of the FGF23 hormone is stimulated, which has a negative effect on the cardiovascular system. Reinhold Erben, the head of the Unit of Physiology, Pathophysiology and Biophysics at the Vetmeduni Vienna, warns that “our phosphate consumption is relevant for our state of health,” according to the May 5, 2014 news release, "New cause of high blood pressure and heart disease discovered."
More than 500 million people around the world suffer from chronic kidney disease. Clinical studies have shown that these patients often develop cardiovascular diseases such as high blood pressure and vascular calcification. Until now, the connection between renal disease, the accumulation of the hormone FGF23 which is produced in the bones, and cardiovascular disease was unclear.
FGF23 controls renal excretion of sodium, and so the blood pressure
The researchers showed that FGF23 has a so called sodium conserving effect, meaning it controls the reabsorption of filtered sodium in the kidneys. Mice lacking FGF23 excrete higher amounts of sodium in their urine, resulting in low blood pressure. Animals with high FGF23 levels show high levels of sodium in their blood, and in turn, high blood pressure.
A raised level of FGF23 puts increased strain on the heart. Reinhold Erben explains, according to the news release, 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.
FGF23 controls calcium, and therefore vascular calcification
A second study, published by Erben’s group in mid-January in EMBO, showed 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.”
Feedback loop between kidneys and bones
The hormone FGF23 is formed in the bones and controls the excretion of phosphate via the kidneys. When there is too much phosphate present in the body, the FGF23 level rises which leads to the excretion of excess phosphate. If too much phosphate is ingested with food, or if the excretion process via the kidneys does not work correctly, phosphate and FGF23 levels increase. A dangerous spiral begins that can have serious consequences on the overall health.
New critical values of FGF23 in science
The newly discovered functions of the hormone FGF23 were, until recently, attributed to another protein, αKlotho. Several scientific publications had assumed αKlotho to be the crucial factor for calcium conservation in the kidneys. With their newly published work, Erben and his colleagues show for the first time that FGF23 is responsible for this function, and not αKlotho. However, αKlotho is essential for the FGF23 effects, because it acts as a co-receptor for FGF23.
Andrukhova emphasizes that “The focus in science is increasingly shifting from αKlotho to FGF23. The level of FGF23 in kidney patients can even indicate their life expectancy. The inhibition of FGF23 or its pathway could be a possibility to bring cardiovascular disease and vascular calcification under control.”
For more information see, "FGF23 Regulates Renal Sodium Handling and Blood Pressure," by authors: Olena Andrukhova, Svetlana Slavic, Alina Smorodchenko, Ute Zeitz, Victoria Shalhoub, Beate Lanske, Elena E. Pohl and Reinhold G. Erben. The study is published online since May 5, 2014 in the journal EMBO Molecular Medicine. You also can take a look at the website of the University of Veterinary Medicine -- Vienna.