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 .
Renal response to acute acid loadingAn organ physiological approach
Objective : In previous studies of the renal response to acute NH 4 Cl acidosis no correlation was found between systemic acid – base status and the traditionally used quantity , renal net acid excretion ( NAE ) . If NAE is to be considered a physiologically meaningful quantity then this is surprising , as the extracellular acid – base status would be expected to be the key physiological trigger for renal NAE . The object of this study was to investigate the renal response to acute non‐carbonic acid loading using a quantitative organ physiological approach . Material and Methods : Five‐h NH 4 Cl loading studies were performed in 10 healthy men using a r and omized , placebo‐controlled , crossover design . Arterialized capillary blood , serum and urine were collected hourly during the loading studies for the measurement of electrolytes and acid – base status . Concentrations of non‐metabolizable base ( NB ) and acid ( NA ) were calculated from measured concentrations of non‐metabolizable ions according to Kildeberg . Results : In the steady state ( placebo ) the rate of renal excretion of NA ( = −NB ) was close to zero , indicating that the net extrarenal input of NA ( endogeneous production , gastrointestinal absorption , skeletal release , etc . ) was likewise about zero . An inverse correlation was found between blood pH and the rate of renal excretion of NA . Only a small amount of the acid load ( ≈8 % ) was excreted during the 5‐h study period and this was accompanied by massive calciuria , indicating that mobilization of NB from bone contributed substantially to the current net extrarenal NA input . Conclusion : From a physiological point of view , NB can be regarded as the actual substrate for renal acid – base control , and measurement of renal turnover of NB may give a more precise description of renal acid – base metabolism during acid loading than previously described methods
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 .