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 .
Long-term persistence of the urine calcium-lowering effect of potassium bicarbonate in postmenopausal women.
Potassium bicarbonate ( KBC ) potently reduces urine calcium excretion in adult humans , including patients with hypertension or calcium urolithiasis , and postmenopausal women . In the latter , who have substantial risk of calcium deficiency , it remains unknown whether the observed short-term urine calcium-lowering effect of KBC persists over years . We studied 170 postmenopausal women r and omized to KBC 30 , 60 , or 90 mmol/d ( KBC treatment ) , or placebo , for up to 36 months . Each received a multivitamin with 400 IU vitamin D , and calcium carbonate as needed to produce a total dietary calcium intake of at least 30 mmol daily . Daily urine calcium excretion ( UCaV ) did not differ among groups at baseline ( all-groups mean + /- SD , 155 + /- 83 mg/d ) . From 1 - 36 months of KBC treatment , adjusting UCaV for creatinine ( Cr ) excretion , each dose of KBC reduced UCaV ( P < 0.01 ) with a dose-dependent trend ( P = 0.05 ) . The reduced UCaV/Cr persisted throughout the KBC treatment period ( up to 36 months ) in all KBC , and the greatest reductions occurred in the subjects with greatest baseline UCaV/Cr ( Delta UCaV/Cr vs. baseline UCaV/Cr ; P < 0.001 ) . Twenty-eight percent of the subjects had high baseline calciuria ( UCaV/Cr > 200 mg Ca/1000 mg Cr ) . With baseline UCaV/Cr of 250 mg/1000 mg Cr , KBC 60 mmol decreased UCaV/Cr by 55.8 mg/1000 mg Cr , a potential daily calcium retention that over a 36-month period would accumulate up to 55,845 mg of calcium , nearly 5 % of bone calcium content . KBC treatment induced a dose-dependent decrease in UCaV/Cr that persisted up to 36 months , with the greatest decreases occurring in those women with the greatest baseline UCaV , nearly a third of whom had high baseline calciuria . Thus , one can preselect postmenopausal women most likely to have the urine calcium-lowering effect of KBC and predict their potential bone calcium increase
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 .