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 .
Potassium citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet.
The amount of sodium chloride in the diet of industrialized nations far exceeds physiological requirements . The impact of abundant dietary salt on skeletal health has yet to be established , but is potentially detrimental through increased urinary calcium losses . We examined the effect of increased dietary sodium chloride on urine calcium excretion and bone turnover markers in postmenopausal women and , further , whether potassium citrate attenuates the effects of increased dietary salt . Postmenopausal women ( n = 60 ) were adapted to a low-salt ( 87 mmol/d sodium ) diet for 3 wk , then r and omized to a high-salt ( 225 mmol/d sodium ) diet plus potassium citrate ( 90 mmol/d ) or a high-salt diet plus placebo for 4 wk . Urine calcium , urine N-telopeptide , urine cAMP , serum osteocalcin , and fasting serum PTH were measured at the end of the low- and high-salt diets . On the high salt plus placebo diet , urine calcium increased 42 + /- 12 mg/d ( mean + /- SEM ) , but decreased 8 + /- 14 mg/d in the high salt plus potassium citrate group ( P = 0.008 , potassium citrate vs. placebo , unpaired t test ) . N-telopeptide increased 6.4 + /- 1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0 + /- 1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus potassium citrate group ( P < 0.05 , potassium citrate vs. placebo , unpaired t test ) . Osteocalcin , PTH , and cAMP were not significantly altered . The addition of oral potassium citrate to a high-salt diet prevented the increased excretion of urine calcium and the bone resorption marker caused by a high salt intake . Increased intake of dietary sources of potassium alkaline salts , namely fruit and vegetables , may be beneficial for postmenopausal women at risk for osteoporosis , particularly those consuming a diet generous in sodium chloride
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 .