British Journal of Nutrition

  • British Journal of Nutrition / Volume 110 / Issue 07 / October 2013, pp 1168-1177
  • Copyright © The Author 2013 The online version of this article is published within an Open Access environment subject to the conditions of the Creative Commons Attribution licence <http://creativecommons.org/licenses/by/3.0/>.
  • DOI: http://dx.doi.org/10.1017/S0007114513000962 (About DOI), Published online: 04 April 2013
  • OPEN ACCESS

Review Article

Nutritional disturbance in acid–base balance and osteoporosis: a hypothesis that disregards the essential homeostatic role of the kidney

Jean-Philippe Bonjour 

Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, Rue Gabrielle-Perret-Gentil, CH-1211 Geneva 14, Switzerland

Abstract

The nutritional acid load hypothesis of osteoporosis is reviewed from its historical origin to most recent studies with particular attention to the essential but overlooked role of the kidney in acid–base homeostasis. This hypothesis posits that foods associated with an increased urinary acid excretion are deleterious for the skeleton, leading to osteoporosis and enhanced fragility fracture risk. Conversely, foods generating neutral or alkaline urine would favour bone growth and Ca balance, prevent bone loss and reduce osteoporotic fracture risk. This theory currently influences nutrition research, dietary recommendations and the marketing of alkaline salt products or medications meant to optimise bone health and prevent osteoporosis. It stemmed from classic investigations in patients suffering from chronic kidney diseases (CKD) conducted in the 1960s. Accordingly, in CKD, bone mineral mobilisation would serve as a buffer system to acid accumulation. This interpretation was later questioned on both theoretical and experimental grounds. Notwithstanding this questionable role of bone mineral in systemic acid–base equilibrium, not only in CKD but even more in the absence of renal impairment, it is postulated that, in healthy individuals, foods, particularly those containing animal protein, would induce ‘latent’ acidosis and result, in the long run, in osteoporosis. Thus, a questionable interpretation of data from patients with CKD and the subsequent extrapolation to healthy subjects converted a hypothesis into nutritional recommendations for the prevention of osteoporosis. In a historical perspective, the present review dissects out speculation from experimental facts and emphasises the essential role of the renal tubule in systemic acid–base and Ca homeostasis.

(Received August 24 2012)

(Revised February 22 2013)

(Accepted February 22 2013)

(Online publication April 04 2013)

Key Words:

  • Nutrition;
  • Osteoporosis;
  • Acid–base balance;
  • Renal proton regulation;
  • Urinary calcium

Correspondence

Corresponding author: Dr Jean-Philippe Bonjour, fax +41 22 38 29 973, email jean-philippe.bonjour@unige.ch

Footnotes

  Abbreviations: BMD, bone mineral density; NAE, net renal acid excretion; NEAP, net endogenous acid production; OA, urinary organic acids; PRAL, potential renal acid load; SID, strong ion difference; UCa, calciuria

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