The role of dietary protein in the pathogenesis of osteoporosis
It has long been known that systemic acidosis brings about depletion of the skeleton via negative calcium balance. In vivo, acidosis can occur systemically due to renal, bronchial or gastrointestinal disease, diabetes, severe (anaerobic) exercise, excessive protein intake, ageing, or menopause. The oxidation of proteins containing sulphur and phosphorus ultimately yields H+ residues corresponding to sulphuric and phosphoric acids, which must be excreted via the kidneys. The average Western diet has been estimated to generate an inorganic H+ residue of about 0.1 mol/day, which is equivalent to about 8 ml of concentrated hydrochloric acid. Recent data indicate that excess acid generated from high protein intakes increases calcium excretion and bone resorption, assessed as urinary pyridinoline and deoxypyridinoline. However, epidemiological studies have also found a signifi cant positive relationship between protein intake and bone mass or density. Similarly, isotopic studies in humans have also demonstrated greater calcium retention and absorption by individuals consuming high-protein diets, particularly when the calcium content of the diet was limiting. High-protein intake may positively impact bone health by several
mechanisms, including calcium absorption, stimulation of the secretion of insulin-like growth factor-1, and enhancement of lean body mass. The perception that high intake of dietary protein brings about a large enough shift in systemic pH to increase
osteoclastic bone resorption seems weak..