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 .
Effects of potassium alkali and calcium supplementation on bone turnover in postmenopausal women.
Potassium citrate may improve calcium balance by conferring an alkali load . Calcium supplementation slows postmenopausal bone loss by inhibiting PTH secretion . This study explores whether combined treatment with potassium citrate and calcium citrate is more effective than either agent alone in inhibiting bone loss . In a crossover study involving 18 postmenopausal women , the following treatments were compared : potassium citrate ( 4.3 g or 40 mmol/d ) , calcium citrate ( 800 mg or 20 mmol/d ) , combined treatment , and placebo . During the last 2 d of each 2-wk phase , serum and 24-h urine were collected for assessment of calcium metabolism , alkali load , and bone turnover markers . Compared with placebo , potassium citrate provided an alkali load and significantly decreased urinary calcium without changing serum PTH ( sPTH ) or bone turnover markers .  Calcium citrate significantly increased absorbed calcium , marginally decreased sPTH , and significantly reduced bone resorption markers . Combined treatment retained key features of potassium citrate and calcium citrate . However , more alkali was delivered than with potassium citrate alone , and absorbed calcium did not differ from calcium citrate alone . Compared with placebo , combined treatment increased urinary calcium , marginally reduced sPTH , provided a clear alkali load , and reduced the bone resorption markers serum type I collagen C-telopeptide and urinary N-telopeptide by 20.4 % ( P < 0.0001 ) and 18.2 % ( P = 0.005 ) , respectively . A significant trend was noted for the decrease in bone resorption markers as treatment changed from placebo to potassium citrate to calcium citrate to combined treatment . In postmenopausal women , combined treatment with potassium citrate and calcium citrate inhibits bone resorption by providing an alkali load and increasing absorbed calcium
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 .