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The most common imbalance in the acid-base balance in the industrialized countries is mild chronic metabolic acidosis caused by the diet rich in the animal protein. Proteins are metabolized to organic acids. The typical American diet produces after metabolism approximately 100 meq of acid every day (Barzel 1995). This kind of a diet has been proved to cause aciduria and calciuria as a consequence of acidosis and thus a loss of total calcium of the body (Breslau et al. 1988, Schuette et al. 1980, Licata et al. 1981). Cola drinks that contain phosphoric acid are another acidosis-inducing ingredient of diet, especially among young people (Barzel 1995).

Over acidity has been studied by many scientists as you will see here. You can help prevent the negative side effects by eating plenty of green foods and drinking green alkalizing drinks Excessive dietary intake of protein with consequent increase in metabolic acid production result in compensatory mechanisms that lead to progression of kidney stones, bone disease, renal disease and a catabolic state. Chronic metabolic acidosis is a process whereby an excess acid load is placed on the body due to excess acid generation or diminished acid removal by normal homeostatic mechanisms. Excessive meat ingestion and aging are two clinical conditions often associated with chronic metabolic acidosis. The body's homeostatic response to this pathology is very efficient. Therefore, the blood pH is frequently maintained within the "normal" range. However, these homeostatic responses engender pathologic consequences such as nephrolithiasis, bone demineralization, muscle protein breakdown and renal growth.

Bushinsky DA, Smith SB, Gavrilov KL, Gavrilov LF, Li J, Levi-Setti R. Chronic acidosis-induced alteration in bone bicarbonate and phosphate. Am J Physiol Renal Physiol. 2003 Sep;285(3):F532-9. Epub 2003 May 20. PMID: 12759230 [PubMed - indexed for MED

Bushinsky DA, Parker WR, Alexander KM, Krieger NS. Metabolic, but not respiratory, acidosis increases bone PGE(2) levels and calcium release. Am J Physiol Renal Physiol. 2001 Dec;281(6):F1058-66. PMID: 11704556 [PubMed - indexed for MEDLINE]

Acid-base balance has an effect on bone turnover, especially on the rates of bone resorption and calcium mobilization. Bone mineral participates in the defense against acid-base disturbances, especially against metabolic acidosis (Lemann et al. 1966, Green & Kleeman 1991). The role of the bone mineral is important in the acid-base disorders, as no appreciable change in the intestinal calcium absorption occurs (Bichara et al. 1990). In the mammalian body, mainly three hormones regulate the calcium metabolism and the bone turnover. 1,25-dihydroxycholecalciferol (vitamin D derivative) increases calcium absorption from the intestine and, indirectly, from bone. Parathyroid hormone mobilizes calcium from the bone and increases the urinary phosphate excretion. Calcitonin inhibits bone resorption (Ganong 1981). Used as drugs, these hormones are also capable of inducing acid-base disorders. Calcitonin administration (Escanero et al. 1991) and vitamin D excess (Bichara et al. 1990) have been reported to cause metabolic alkalosis.

Dawson-Hughes B. Interaction of dietary calcium and protein in bone health in humans. J Nutr. 2003 Mar;133(3):852S-854S. Review. PMID: 12612168

Krieger NS, Frick KK, Bushinsky DA. Cortisol inhibits acid-induced bone resorption in vitro. J Am Soc Nephrol. 2002 Oct;13(10):2534-9. PMID: 12239242 [PubMed - indexed for MEDLINE]

Kerstetter JE, O'Brien KO, Insogna KL. Low protein intake: the impact on calcium and bone homeostasis in humans. J Nutr. 2003 Mar;133(3):855S-861S. Review. PMID: 12612169

Sakhaee K, Maalouf NM, Abrams SA, Pak CY. Effects of potassium alkali and calcium supplementation on bone turnover in postmenopausal women. J Clin Endocrinol Metab. 2005 Jun;90(6):3528-33. Epub 2005 Mar 8. PMID: 15755853

Marangella M, Di Stefano M, Casalis S, Berutti S, D'Amelio P, Isaia GC. Effects of potassium citrate supplementation on bone metabolism. Calcif Tissue Int. 2004 Apr;74(4):330-5. PMID: 15255069 [PubMed - indexed for MEDLINE]

Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC Jr. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med. 1994 Jun 23;330(25):1776-81. PMID: 8190153 [PubMed - indexed for MEDL

Frassetto L, Morris RC Jr, Sebastian A. Long-term persistence of the urine calcium-lowering effect of potassium bicarbonate in postmenopausal women. J Clin Endocrinol Metab. 2005 Feb;90(2):831-4. Epub 2004 Nov 30. PMID: 15572425 [PubMed - indexed for M

Frassetto L, Morris RC Jr, Sebastian A. Potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women. J Clin Endocrinol Metab. 1997 Jan;82(1):254-9. PMID: 8989270 [PubMed - indexed for MEDLINE]

Morris RC, Schmidlin O, Tanaka M, Forman A, Frassetto L, Sebastian A. Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications. Semin Nephrol. 1999 Sep;19(5):487-93. Review.

Frassetto LA, Nash E, Morris RC Jr, Sebastian A. Comparative effects of potassium chloride and bicarbonate on thiazide-induced reduction in urinary calcium excretion. Kidney Int. 2000 Aug;58(2):748-52. PMID: 10916098 [PubMed - indexed for MEDLINE]

Bushinsky DA, Krieger NS, Geisser DI, Grossman EB, Coe FL. Effects of pH on bone calcium and proton fluxes in vitro. Am J Physiol. 1983 Aug;245(2):F204-9. PMID: 6881337 [PubMed - indexed for MEDLINE]

Frick KK, LaPlante K, Bushinsky DA. RANK ligand and TNF-alpha mediate acid-induced bone calcium efflux in vitro. Am J Physiol Renal Physiol. 2005 Nov;289(5):F1005-11. Epub 2005 Jun 21. PMID: 15972386 [PubMed - indexed for MEDLINE