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When a high dietary protein intake is consumed, there is an increase in urea excretion, which suggests that amino acid oxidation is increased.[18] High levels of protein intake increase the activity of branched-chain ketoacid dehydrogenase.[18] As a result, oxidation is facilitated, and the amino group of the amino acid is excreted to the liver.[18] This process suggests that excess protein consumption results in protein oxidation and that the protein is excreted.[18] The body is unable to store excess protein.[18][23] Protein is digested into amino acids, which enter the bloodstream. Excess amino acids are converted to other usable molecules by the liver in a process called deamination. Deamination converts nitrogen from the amino acid into ammonia, which is converted by the liver into urea in the urea cycle. Excretion of urea is performed by the kidneys. These organs can normally cope with any extra workload, but, if kidney disease occurs, a decrease in protein will often be prescribed.[24] When there is excess protein intake, amino acids can be converted to glucose or ketones, in addition to being oxidized for fuel.[25] When food protein intake is periodically high or low, the body tries to keep protein levels at an equilibrium by using the "labile protein reserve", which serves as a short-term protein store to be used for emergencies or daily variations in protein intake.[4] However, that reserve is not utilized as longer-term storage for future needs.[4]

Many researchers have also found that excessive intake of protein increases calcium excretion in urine.[4] It has been thought that this occurs to maintain the pH imbalance from the oxidation of sulfur amino acids.[4] Also, it is inconclusive whether bone resorption contributes to bone loss and osteoporosis.[4] However, it is also found that a regular intake of calcium would be able to stabilize this loss.[4]

Another issue arising from over-consumption of protein is a higher risk of kidney stone formation from calcium in the renal circulatory system.[4] It has been found that high animal protein intake in healthy individuals increases the probability of forming kidney stones by 250 percent.[citation needed]

An epidemiological study from 2006 has found no relationship between total protein intake and blood pressure; it did, however, find an inverse relationship between vegetable protein intake and blood pressure.[26]

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How animal protein exerts its effect on calcium excretion is not fully understood. A rise in glomerular filtration rate in response to protein has been suggested as one factor (128) but this is unlikely to be important in the steady state. The major mechanisms are thought to be the effect of the acid load contained in animal proteins and the complexing of calcium in the renal tubules by sulphate and phosphate ions released by protein metabolism (133,134). Urinary calcium is significantly related to urinary phosphate (as well as to urinary sodium), particularly in subjects on restricted calcium intakes or in the fasting state, and most of the phosphorus in the urine of people on Western-style diets comes from animal protein in the diet (63). Similar considerations apply to urinary sulphate but it is probably less important than the phosphate ion because the association constant for calcium sulphate is lower than that for calcium phosphate (135). The empirical observation that each 1 g of protein results in 1 mg of calcium in the urine agrees very well with the phosphorus content of animal protein (about 1 percent by weight) and the observed relationship between calcium and phosphate in the urine (63).

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Abstract

The modern Western-type diet is deficient in fruits and vegetables and contains excessive animal products, generating the accumulation of non-metabolizable anions and a lifespan state of overlooked metabolic acidosis, whose magnitude increases progressively with aging due to the physiological decline in kidney function. In response to this state of diet-derived metabolic acidosis, the kidney implements compensating mechanisms aimed to restore the acid-base balance, such as the removal of the non-metabolizable anions, the conservation of citrate, and the enhancement of kidney ammoniagenesis and urinary excretion of ammonium ions. These adaptive processes lower the urine pH and induce an extensive change in urine composition, including hypocitraturia, hypercalciuria, and nitrogen and phosphate wasting. Low urine pH predisposes to uric acid stone formation. Hypocitraturia and hypercalciuria are risk factors for calcium stone disease. Even a very mild degree of metabolic acidosis induces skeletal muscle resistance to the insulin action and dietary acid load may be an important variable in predicting the metabolic abnormalities and the cardiovascular risk of the general population, the overweight and obese persons, and other patient populations including diabetes and chronic kidney failure. High dietary acid load is more likely to result in diabetes and systemic hypertension and may increase the cardiovascular risk. Results of recent observational studies confirm an association between insulin resistance and metabolic acidosis markers, including low serum bicarbonate, high serum anion gap, hypocitraturia, and low urine pH.

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Bones contain more calcium reserves than any other organ. Calcium is 'withdrawn' from the bone bank when blood levels drop bellow normal, to sustain metabolic needs. When blood calcium levels rise, the excess calcium is 'deposited' in the bone bank. The dynamic transaction of calcium deposits and withdrawals; and process of saving calcium reserves in the bone locker go on regular-basis.

A complex group of hormones ensure an adequate supply of bone minerals to support a variety of physiological functions.

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In response to its dual role of deposits-withdrawals of calcium and phosphorous; performing repair services to mantain a functional skeleton, bone is constantly on the run to remodel itself. Old bone breaks down and new bone formed on a regular basis. In fact, the skeletal tissue is replaced several times during life.


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Accordingly, the "bone mineral overdraft" sets off the clinical condition - the osteoporosis.

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PTH is released in response to low extracellular concentrations of free calcium and tightly regulates blood calcium levels within 8.8 and 10.2 mg/dL

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Regulation of serum calcium

It enhances the release of calcium from the large reservoir contained in the bones.[7] Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH. Stimulation is indirect since osteoclasts do not have a receptor for PTH; rather, PTH binds to osteoblasts, the cells responsible for creating bone. Binding stimulates osteoblasts to increase their expression of RANKL and inhibits their expression of Osteoprotegerin (OPG). OPG binds to RANKL and blocks it from interacting with RANK, a receptor for RANKL. The binding of RANKL to RANK (facilitated by the decreased amount of OPG available for binding the excess RANKL) stimulates these osteoclast precursors to fuse, forming new osteoclasts, which ultimately enhances bone resorption.

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Animal protein tends to leach calcium from the bones, leading to its excretion in the urine. Animal proteins are high in sulfur-containing amino acids, especially cystine and methionine. Sulfur is converted to sulfate, which tends to acidify the blood. During the process of neutralizing this acid, bone dissolves into the bloodstream and filters through the kidneys into the urine. Meats and eggs contain two to five times more of these sulfur-containing amino acids than are found in plant foods.3

International comparisons show a strong positive relationship between animal protein intake and fracture rates. Such comparisons generally do not take other lifestyle factors, such as exercise, into account. Nonetheless, their findings are supported by clinical studies showing that high protein intakes aggravate calcium losses. A 1994 report in the American Journal of Clinical Nutrition showed that when animal proteins were eliminated from the diet, calcium losses were cut in half.4 Patients can easily get adequate protein from grains, beans, vegetables, and fruits.