Urine calcium excretion rates were consistent with osteoporosis development ; however calcium balance studies did not demonstrate loss of whole body calcium with higher net acid excretion .
No study revealed a biologic mechanism functioning at physiological pH. Finally , r and omized studies did not provide evidence for an adverse role of phosphate , milk , and grain foods in osteoporosis .
Conclusions A causal association between dietary acid load and osteoporotic bone disease is not supported by evidence and there is no evidence that an alkaline diet is protective of bone health
Background Modern diets have been suggested to increase systemic acid load and net acid excretion .
In response , alkaline diets and products are marketed to avoid or counteract this acid , help the body regulate its pH to prevent and cure disease .
The objective of this systematic review was to evaluate causal relationships between dietary acid load and osteoporosis using Hill 's criteria .
Acute effects of calcium sodium citrate supplementation of a test meal on mineral homeostasis, oxalate, and calcium oxalate crystallization in the urine of healthy humans--preliminary results in patients with idiopathic calcium urolithiasis.
Calcium , in the form of regular food supplementation , can improve bone metabolism , but it can also increase the risk for renal calcium stones , and may aggravate pre-existing calcium urolithiasis . To study the first of these two aspects , ten healthy volunteers were given a conventional test meal ( breakfast ; calcium content 28 mg ) with or without two dosages of calcium ( as calcium-sodium citrate , CSC 1 , 680 mg ; CSC 2 1,360 mg ) , taken after an overnight 12 h fast . To study the latter aspect , patients with idiopathic recurrent calcium urolithiasis ( ICU ) received a balanced test meal of fixed composition , containing 1,000 mg calcium either as CSC ( Meal + CSC3 ; n = 6 ) or as calcium gluconate ( Mcal ; n = 8) . In normals , CSC induced a dose-dependent increasing intestinal absorption of calcium , and a decrease in oxalate absorption ; in serum , CSC  increased calcitonin and suppressed parathyroid hormone , but left unchanged the markers of bone turnover , serum osteocalcin and bone alkaline phosphatase . In urine ,  CSC decreased bone resorption markers ( collagen crosslinks ) and phosphaturia increased citrate , created signs of metabolic alkalosis , and inhibited several parameters of CaOx crystallization . In ICU , the CSC3 load failed to promote the crystallization of CaOx and calcium phosphate . It was concluded that CSC supplementation of a meal : ( 1 ) is well tolerated by healthy subjects and ICU patients , renders calcium highly available to bone , and prevents post-pr and ial oxaluria from rising ; and , ( 2 ) is followed by the inhibition of crystallization of renal stone forming calcium-containing substances . Long-term studies aim ed at evaluating the usefulness of CSC in preserving healthy bone , and in the metaphylaxis of renal stones would appear justified
Urine calcium excretion rates were consistent with osteoporosis development ; however calcium balance studies did not demonstrate loss of whole body calcium with higher net acid excretion .
No study revealed a biologic mechanism functioning at physiological pH. Finally , r and omized studies did not provide evidence for an adverse role of phosphate , milk , and grain foods in osteoporosis .
Conclusions A causal association between dietary acid load and osteoporotic bone disease is not supported by evidence and there is no evidence that an alkaline diet is protective of bone health
Background Modern diets have been suggested to increase systemic acid load and net acid excretion .
In response , alkaline diets and products are marketed to avoid or counteract this acid , help the body regulate its pH to prevent and cure disease .
The objective of this systematic review was to evaluate causal relationships between dietary acid load and osteoporosis using Hill 's criteria .