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 .
Contrasting effects of potassium citrate and sodium citrate therapies on urinary chemistries and crystallization of stone-forming salts.
Effects of potassium citrate therapy ( 60 mEq/day ) on urinary chemistries and crystallization were compared to those of sodium citrate treatment in five patients with uric acid lithiasis . Both alkali treatments significantly increased urinary pH ( P less than 0.001 ) , from 5.35 + /- 0.18 SD to 6.68 + /- 0.14 for potassium citrate and 6.73 + /- 0.20 for sodium citrate . During potassium citrate therapy , urinary calcium significantly declined from 154 + /- 47 mg/day to 99 + /- 23 mg/day ( P less than 0.01 ) and urinary citrate rose from 398 + /- 119 mg/day to 856 + /- 103 mg/day ( P less than 0.001 ) . The urinary saturation ( activity product ratio ) of calcium oxalate decreased from 3.21-fold to 1.69-fold saturation ( P less than 0.01 ) , and the inhibitor activity against calcium oxalate precipitation ( formation product ratio ) significantly increased . However , sodium citrate therapy did not significantly decrease urinary calcium ( to 139 + /- 24 mg/day ) , although it increased urinary citrate substantially ( to 799 + /- 89 mg/day , P less than 0.01 ) . Urinary environment became supersaturated with respect to brushite ( calcium phosphate ) and monosodium urate . The inhibitor activity against calcium oxalate precipitation was not significantly altered for the whole group ; in two patients , it decreased by more than 30 % . The results indicate that ( 1 ) both alkali therapies are equally effective in preventing uric acid stone formation because of their ability to increase urinary pH , and ( 2 ) potassium citrate may prevent the complication of calcium nephrolithiasis in patients with uric acid stones , whereas sodium citrate may not
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 .