Calcium in the form of phosphates and carbonates represents a large reservoir of base in our body. In response to an acid load such as the modern diet these salts are released into the systemic circulation to bring about pH homeostasis [
7]. It has been estimated that the quantity of calcium lost in the urine with the modern diet over time could be as high as almost 480

gm over 20 years or almost half the skeletal mass of calcium [
21]. However, urinary losses of calcium are not a direct measure of osteoporosis. There are many regulatory factors that may compensate for the urinary calcium loss. When the arterial pH is in the normal range, a mild reduction of plasma bicarbonate results in a negative calcium balance which could benefit from supplementing bicarbonate in the form of potassium bicarbonate [
22]. It has been found that bicarbonate, which increases the alkali content of a diet, but not potassium may attenuate bone loss in healthy older adults [
23]. The bone minerals that are wasted in the urine may not have complete compensation through intestinal absorption, which is thought to result in osteoporosis. However, adequate vitamin D with a 25(OH)D level of >80

nmol/L may allow for appropriate intestinal absorption of calcium and magnesium and phosphate when needed [
24]. Sadly, most populations are generally deficient in vitamin D especially in northern climates [
25]. In chronic renal failure, correction of metabolic acidosis with bicarbonate significantly improves parathyroid levels and levels of the active form of vitamin D 1,25(OH)2D
3 [
26]. Recently, a study has shown the importance of phosphate in Remer's PRAL formula. According to the formula it would be expected that an increase in phosphate should result in an increase in urinary calcium loss and a negative calcium balance in bone [
27]. It should be noted that supplementation with phosphate in patients with bed rest reduced urinary calcium excretion but did not prevent bone loss [
28]. The most recent systematic review and meta-analysis has shown that calcium balance is maintained and improved with phosphate which is quite contrary to the acid-ash hypothesis [
29]. As well a recent study looking at soda intake (which has a significant amount of phosphate) and osteoporosis in postmenopausal American first nations women did not find a correlation [
30]. It is quite possible that the high acid content according to Remer's classification needs to be looked at again in light of compensatory phosphate intake. There is online information promoting an alkaline diet for bone health as well as a number of books. However, a recent systematic review of the literature looking for evidence supporting the alkaline diet for bone health found no protective role of dietary acid load in osteoporosis [
31].
Another element of the modern diet is the excess of sodium in the diet. There is evidence that in healthy humans the increased sodium in the diet can predict the degree of hyperchloremic metabolic acidosis when consuming a net acid producing diet [
32]. As well, there is evidence that there are adverse effects of sodium chloride in the aging population. A high sodium diet will exacerbate disuse-induced bone and muscle loss during immobilization by increasing bone resorption and protein wasting [
33]. Excess dietary sodium has been shown to result in hypertension and osteoporosis in women [
34,
35]. As well, dietary potassium which is lacking in the modern diet would modulate pressor and hypercalciuric effects of excess of sodium chloride [
36].
Excess dietary protein with high acid renal load may decrease bone density if not buffered by ingestion of supplements or foods that are alkali rich [
37]. However, adequate protein is necessary for prevention of osteoporosis and sarcopenia; therefore, increasing the amount of fruit and vegetables may be necessary rather than reducing protein [
38].