Die Rolle der nahrungsbedingten Säurebelastung für den Knochen

Zusammenfassung

Durch Ernährungseinflüsse auf den Säure-Basen-Status lassen sich nicht nur der Urin pH-Wert und damit das Nierensteinrisiko beeinflussen. Vielmehr hat eine hohe nutritive Säurelast auch Auswirkungen auf präventivmedizinische relevante funktionelle Outcomes wie den Knochenstatus. Klinisch manifeste Azidosen gehen regelmäßig mit überhöhter Kalziumausscheidung, negativer Kalziumbilanz und deutlichem Knochenmineralverlust einher. Auch bei sogenannten milden metabolisch kompensierten Azidoseformen mit Serum-Bikarbonat-Spiegeln und Blut-pH Werten im Normalbereich, wie sie bei hoher Eiweißzufuhr und gleichzeitig sehr geringem Obst- und Gemüseverzehr auftreten können, findet sich gehäuft ein verschlechterter Knochenstatus. Entsprechende Ergebnisse aus prospektiv kontrollierten Beobachtungs- und randomisiert-kontrollierten Interventionsstudien an Erwachsenen werden kurz vorgestellt und bewertet, ebenso wie Langzeitbeobachtungen an gesunden Kindern. Da bei nutritiv hoher Säurebelastung zwar erhöhte renale Kalziumverluste auftreten, die Kalziumbilanz aber nicht per se negativ ist, kann eine verminderte Kalziumverfügbarkeit als Hauptursache für eine reduzierte Knochenmasse unter Ernährung mit hoher Säurelast ausgeschlossen werden. Stattdessen wird die bereits bei milder Azidose oder erhöhter Netto-Säureausscheidung beobachtbare Steigerung der Kortisol-Sekretion als ein wahrscheinlicher Mechanismus für präventivmedizinisch relevante Langzeitbeeinträchtigungen des Skelettsystems diskutiert.

Summary

Nutrition does not only impact via alterations in acid base status on urine pH and the risk of kidney stones. A high dietary acid load also influences preventive-medically relevant functional outcomes, of which one is bone status. Clinical manifest acidoses are regularly paralleled by excess calcium excretion, negative calcium balance, and bone mineral loss. Also, in mild metabolically compensated forms of acidosis with serum bicarbonate and urine pH levels still in the normal range, as can develop with high protein and low fruit and vegetable intakes, an impaired bone status is frequently seen. Corresponding results from prospective controlled observational and randomized controlled interventional studies on bone status in adults are shortly presented as well as long-term observations in healthy children. As renal calcium losses, but not per se negative calcium balances do regularly occur with high dietary acid loads, a reduced availability of calcium is rather not a major cause, responsible for lower bone mass under acidogenic diets. Instead, an alternative endocrine metabolic mechanism is discussed as probable underlying cause for long-term impairment of bone status through habitual high dietary acid intake.

Schlüsselwörter

Ernährung - Potenzielle Renale Säurelast (PRAL) - metabolische Azidose - Kalzium - Knochenstatus - Kinder - ältere Menschen - Glukokortikoide

Keywords

Nutrition - Potential Renal Acid Load (PRAL) - metabolic Acidosis - Calcium - Bone status - Children - Elderly - Glucocorticoids

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