Osteologie 2008; 17(02): 55-59
DOI: 10.1055/s-0037-1619850
Ernährung und Knochengesundheit
Schattauer GmbH

Säure-Basen-Gehalt der Nahrung und Knochengesundheit

Acid-base content of diet and bone health
J. Vormann
1   Institut für Prävention und Ernährung, Ismaning/München
› Author Affiliations
Further Information

Publication History

Publication Date:
28 December 2017 (online)

Zusammenfassung

Die Regulation des pH-Werts innerhalb und außerhalb der Zellen ist eine wesentliche Voraussetzung für die Funktionsfähigkeit unseres Organismus. Der Säureüberschuss in unserer Nahrung kann – insbesondere bei altersbedingt nachlassender Nierenfunktion – zur sogenannten latenten Azidose führen. Die übliche westliche Ernährung enthält täglich einen Säureüberschuss von 50–100 mmol, der über die Niere eliminiert werden muss. Ursache ist der hohe Konsum von schwefelhaltigem Protein aus tierischen und Getreideprodukten bei gleichzeitig zu geringem Basenverzehr aus Gemüse, Obst und Salat. Obwohl eine ernährungsinduzierte latente Azidose nicht zu Änderungen des Blut-pH-Werts führt, werden endogene Puffer verbraucht, die insbesondere aus dem Knochen wieder aufgefüllt werden, wodurch langfristig das Osteoporoserisiko steigt. Daten aus physiologischen, epidemiologischen und Interventionsstudien belegen, dass ein ausgeglichener Säure-Basen-Status Knochenparameter verbessert und das Osteoporoserisiko begrenzt. Die nahrungsbedingte Säure-Basen-Zufuhr lässt sich mit neu entwickelten PRAL-Tabellen (potentielle renale Säurelast) berechnen.

Summary

The regulation of pH inside and outside of cells is essential for nearly all processes within our body. The high acidity of our usual diet, combined with declining renal function associated with ageing, leads to so called “latent acidosis”. The usual “western” diet supplies a daily surplus of 50–100 mmol acid that has to be excreted through the kidneys. The high consumption of sulphur containing proteins from animal and grains products with declining intake of base-yielding fruits and vegetables is responsible for this acid load. Although a diet-induced latent acidosis does not produce major changes in blood pH due to buffering this compensation leads necessarily to the consumption of endogenous buffer reserves and, therefore, predominantly to a loss of bone, probably resulting in osteoporosis. Evidence is cumulating from physiological, epidemiological and intervention studies, that normalization of acid-base-status will effectively improve bone parameters, reducing osteoporosis risk. Individual dietary acid-load can be estimated with newly developed PRAL (potential renal acid load) tables.

 
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