The sources of acids (and alkalis) are from the diet and metabolism. The major potential source of acid is CO2 ('volatile acid'; eqn ) generated by oxidative metabolism; a total of 12-20 mol of CO2 are produced daily. Other metabolic products include lactic acid, other organic acids, and urea, the synthesis of which produces H+. Because of its role in the metabolism of lactic acid and in the synthesis of urea, the liver plays a major role in acid-base home-ostasis that is often not appreciated.
Volatile acid (CO2) is excreted by the lungs, whereas the breakdown of sulfur and phosphorus-containing compounds are 'fixed' acids, requiring excretion by the kidney. For example, cysteine or methionine metabolism leads to the production of sulfuric and phosphoric acid (H2SO4, H3PO4), while the metabolism of other amino acids (lysine, argi-nine, and histidine) leads to the production of hydrochloric acid (HCl). In contrast, organic acids (e.g., lactate, fatty acids) may be completely metabolized to CO2 and H2O and thus excreted by the lungs. In addition, the absorption of dietary phosphate and the fecal loss of bicarbonate represent an additional acid load. In total, the net acid load of fixed acid is approximately 1 mmol kg-1 day-1 and may be increased by a high protein intake or reduced by a strict vegetarian diet.
There is surprisingly little information on the direct contributions of individual foods to the acid burden. However, this source of dietary acid is of increasing importance in view of current popular weight reduction diets (e.g., the Atkins diet). The major acids contained in food are citric acid (in fruit, fruit juices), acetic acid (as a preservative, pickles, vinegar), lactic acid (yogurt, fermented foods), malic acid (fruit), oxalic acid (vegetables that contain smaller amounts of citric and malic acids), and tartaric acid (wine). Oxalic acid precipitates in the gut to form calcium salts, which are excreted in the stool and little is absorbed. The other acids are absorbed but quickly metabolized and present an acid burden in the form of CO2. The largest source of fixed acid comes from the metabolism of amino acids (particularly those from animal proteins - see above). The significance of this source of acid is readily demonstrated in patients consuming a high-protein diet (particularly one rich in animal protein) who have increased urinary acid excretion. Based on studies on the relationship between diet, renal excretion of acid, and urine pH it is theoretically feasible to quantify urinary acid excretion for individual foods. However, because of daily variation in diet (and therefore absence of a metabolic steady state) and inherent variation in the composition of foodstuffs, it has not been possible to date to estimate accurately the effects of diet on renal acid-base metabolism in circumstances reflective of normal dietary intake.
Alkalis are often prescribed to compensate for metabolic acidosis (see below) and in the past were often used to neutralize gastric acidity. Milk and milk products are also alkaline but seldom cause any disturbance, unless consumed in great excess. Excessive consumption of milk or alkali is now rarely seen.
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