NEW CAUSE OF HIGH BLOOD PRESSURE
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. 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.
Over 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 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
stresses 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."
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