The average American diet, which is high in protein and low in fruits and vegetables, generates a large amount of acid, mainly as sulfates and phosphates. The kidneys respond to this dietary acid challenge with net acid excretion, as well as ammonium and titratable acid excretion. Concurrently, the skeleton supplies buffer by active resorption of bone. Indeed, calciuria is directly related to net acid excretion. Different food proteins differ greatly in their potential acid load, and therefore in their acidogenic effect. A diet high in acid-ash proteins causes excessive calcium loss because of its acidogenic content. The addition of exogenous buffers, as chemical salts or as fruits and vegetables, to a high protein diet results in a less acid urine, a reduction in net acid excretion, reduced ammonium and titratable acid excretion, and decreased calciuria. Bone resorption may be halted, and bone accretion may actually occur. Alkali buffers, whether chemical salts or dietary fruits and vegetables high in potassium, reverse acid-induced obligatory urinary calcium loss. We conclude that excessive dietary protein from foods with high potential renal acid load adversely affects bone, unless buffered by the consumption of alkali-rich foods or supplements.

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Currently, the recommended upper limit for ascorbic acid (AA) intake is 2000 mg/d. However, because AA is endogenously converted to oxalate and appears to increase the absorption of dietary oxalate, supplementation may increase the risk of kidney stones. The effect of AA supplementation on urinary oxalate was studied in a randomized, crossover, controlled design in which subjects consumed a controlled diet in a university metabolic unit. Stoneformers (n = 29; SF) and age- and gender-matched non-stoneformers (n = 19; NSF) consumed 1000 mg AA twice each day with each morning and evening meal for 6 d (treatment A), and no AA for 6 d (treatment N) in random order. After 5 d of adaptation to a low-oxalate diet, participants lived for 24 h in a metabolic unit, during which they were given 136 mg oxalate, including 18 mg 13C2 oxalic acid, 2 h before breakfast; they then consumed a controlled very low-oxalate diet for 24 h. Of the 48 participants, 19 (12 stoneformers, 7 non-stoneformers) were identified as responders, defined by an increase in 24-h total oxalate excretion > 10% after treatment A compared with N. Responders had a greater 24-h Tiselius Risk Index (TRI) with AA supplementation (1.10 +/- 0.66 treatment A vs. 0.76 +/- 0.42 treatment N) because of a 31% increase in the percentage of oxalate absorption (10.5 +/- 3.2% treatment A vs. 8.0 +/- 2.4% treatment N) and a 39% increase in endogenous oxalate synthesis with treatment A than during treatment N (544 +/- 131 A vs. 391 +/- 71 micromol/d N). The 1000 mg AA twice each day increased urinary oxalate and TRI for calcium oxalate kidney stones in 40% of participants, both stoneformers and non-stoneformers.

Oral doses of caffeine increase the urinary excretion of calcium, magnesium, sodium and chloride for at least 3 h after consumption. The hypercalciuric effect can be blocked by adenosine receptor agonists. The effect is proportional to dose per lean body mass and no adaptation to the urinary losses occurs with continuing consumption of caffeine. Uncompensated losses of calcium would be a risk factor for development of osteoporosis. Risks of osteoporosis due to caffeine consumption are reviewed. Comparison of data from epidemiological surveys and animal and human studies suggests that for younger adult women consuming adequate calcium, moderate caffeine intakes may have little or no deleterious effects. Increased urinary and intestinal losses may be compensated for by increased intestinal calcium absorption. However older women do not seem to compensate adequately to maintain their former calcium balance, especially when calcium intakes are below recommendations.