Mammals have complex regulatory mechanism that maintain the pH of tissues, including the blood, within a narrow range of limits. This is required because the enzymes that are contained within these tissues are only able to function within narrow ranges of pH. As the pH falls outside of this range the enzymes become inactive and metabolic pathways cease to function. The blood for example contains buffers that are able to prevent rises in hydrogen ions causing dramatic changes to the pH. A category of acute conditions exist in medicine whereby large and potentially fatal changes to the metabolic regulation of the tissues results in metabolic acidosis or metabolic alkalosis. These conditions are well reported and occur rarely in otherwise healthy individuals. However, diet is now known to cause chronic but less severe decreases in pH, and such chronic cases are thought to be the cause of a number of disease of Western origin, most significantly osteological complains such as osteoporosis.
The renal net acid excretion (NAE) is a measure of the amount of organic acid excreted in the urine, and this can be used as a measure to determine the acidity of the blood. This is because the excretion of hydrogen ions (that are responsible for acidifying the blood) is necessary when the non-metabolizable anions (organic acids including non-metabolisable aromatic and aliphatic acids, as well as chloride, sulphate and phosphate) exceeds the sum of the mineral cations (which includes sodium, potassium, calcium and magnesium). The NAE can in turn be used to estimate the potential renal acid load (PRAL) of a particular diet. However, it is important to take account of the absorption rates of the components of the diet as not all of the acid or base forming components are absorbed. A number of studies have assessed the effectiveness of these estimates and generally they have been shown to correlate well with the actual physiological measured values of both the NAE and PRAL values.
Acid and alkalis are not formed in the intestine directly, but it can have an influence on the acid load through changes to the absorption rates of minerals. In addition, the secretion of large amounts of bicarbonate to the small intestine to buffer anions, can deplete the blood of bicarbonate. Therefore indirectly the small intestine can contribute to the acid load. However, true acid production occurs in the liver, and the metabolism of absorbed food components here determines the likelihood of changes to the blood pH. For example, the oxidation of sulphur containing amino acid to urea and carbon dioxide also yields sulphuric acid. Likewise phosphorus containing food components can be metabolised yielding phosphoric acid as a by product. In contrast, alkali salts of organic acids, such as sodium citrate are metabolised to carbon dioxide and water, and this yields a cation (sodium) along with bicarbonate, thus increasing the buffering capacity of the blood.
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