There has been controversy for many years about how far nutrition can influence the acid-base balance. Manifest acidosis (shift of the pH level towards acidity) or alkalosis (shift of the pH level towards an excess of alkali) cannot be created by the consumption of particular foodstuffs. However, the pathobiochemical effects of acidosis or alkalosis in the case of diabetes mellitus, hyperuricaemia, gout or restricted kidney function are undisputed. Because the pH level is kept constant, the determination of the intra- and extra-cellular buffer capacity and of the acid excretion is of decisive importance, when assessing the acid-base balance.

Apart from manifest respiratory or metabolic acidosis (indicated by a fall in the blood pH), which is treated by an infusion of solutions containing bicarbonate, cases of latent acidosis occur particularly frequently. In the case of latent or chronic metabolic acidosis, the blood pH has been shifted slightly towards acidity, within the normal range, but, above all, the blood buffer capacity is clearly reduced. In this case, the buffer capacity can be improved by the supply of alkaline minerals (salts of strong bases with weak acids).


Diets and periods of fasting can also stimulate excess acid in the organism. The catabolic state of the metabolism during fasting increases the gain of energy from fatty acids. At the same time, disruptive ketones are increasingly formed and must be disposed of.

A lack of physical activity leads to a lack of oxygen through insufficient muscular circulation, activating anaerobic metabolism with lactic acid as its end product.

Finally, chronic diseases of the lungs, kidneys or liver can impede the natural excretion of excess acids.

Compensation of a latent acidosis

The maintenance of the pH in the extra and intra-cellular environment has a high priority, to guarantee the structure and function of proteins, the stability of cell membranes and the distribution of electrolytes (charged particles) between extra and intra-cellular areas. For this reason, the organism has several possibilities of eliminating acids that could disrupt this natural balance when latent acidosis is present.

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Increased Renal Proton Excretion

During the whole passage of primary urine through the kidneys, proton excretion is actively increased at several points. At the same time, the release of bicarbonate as a base component is restricted. In the case of latent acidosis, citrate, the anion of citric acid, is increasingly removed from the urine, increasing the risk of kidney stones (calcium deposits), because citrate can bind calcium, thus preventing the formation of stones. Modified according to Alpern R.J. and Sakhaee K., 1997.

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Increased Excretion of Nitrogenous Bases (Ammonia)

In the case of latent acidosis, an important adjustment is the increased excretion of ammonium ions (NH3 + H+ <-> NH4+), which are created by the rising acid concentration in the urine and cannot diffuse like ammonia (NH3). The organism loses ammonia, which is formed by the breakdown of nitrogenous amino acids (mainly glutamate), through this. Finally, the breakdown of amino acids leads to the breakdown of muscle protein, which is noticeable to a greater extent in older patients with latent acidosis. In age, latent acidosis, with the consequence of an increased breakdown of protein in the muscles, is more likely to occur, because acid elimination through the kidneys is also reduced through a reduction in the number of kidney tubules. Modified according to Alpern R.J. and Sakhaee K., 1997.

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Increased Base Release from the Bones

In the case of latent acidosis, there is a removal of minerals from the surface of the bones through physico-chemical processes. By the activation of osteoclasts the processes breaking down the bones are intensified; bone restorative processes are, however, suppressed. A negative calcium balance arises because calcium absorption in the kidneys is further decreased by the latent acidosis thus increasing urinary calcium concentration. This increases the risk of kidney stones, because urinary citrate concentration is additionally reduced by acidosis. Modified according to Alpern R.J. and Sakhaee K., 1997.

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Increased Phosphate Excretion

Apart from calcium, phosphate is released from the bones and passed to the blood. Additional protons can be linked to the primary phosphate (HPO42-) and excretion of secondary phosphate (H2PO4-) is accordingly increased. Secondary phosphate represents the main proportion of the acids in the urine that can be measured by titration and is in the second position in the elimination of renal protons in quantity. Modified according to Alpern R.J. and Sakhaee K., 1997.

Possible Consequences of Non-Compensated Latent Acidosis

In the case of experimental acidosis induced orally, the result is a general reduction of buffer capacity – firstly to that of the blood and, with further acidic stress, to that of the intra-cellular spaces and the bone surface. If acid is supplied over a longer period, buffering is performed by releasing minerals from bone (Lemann et al., 1966). This observation has led to the hypothesis that a significant cause of osteoporosis (weakening of the bones) is a high acid strain associated with diet (Wachman und Bernstein, 1968).

In the case of latent acidosis, the connective tissue also suffers. When the buffer capacity is falling, the acid formed in the cells is stored in the musculature and in the connective tissue.

The collagen tissue consists of proteoglycan, whose portion of glucosaminoglycan is, for example, strongly charged with many sulphur residues. If these charges are neutralized by protons, the capacity of the proteoglycan to absorb water is reduced. The consequence is a loss of elasticity that has a deleterious effect on the functioning of cartilage tissue, tendons and ligaments. In the case of mechanical strain, the wearing of the cartilage tissue in particular will be further promoted.

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