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 .
Acid-base status affects renal magnesium losses in healthy, elderly persons.
Magnesium and calcium deficiency in humans is related to a number of pathological phenomena such as arrhythmia , osteoporosis , migraine , and fatal myocardial infa rct ion . Clinical ly established metabolic acidosis induces renal losses of calcium . In normal subjects , even moderate increases in net endogenous acid production ( NEAP ) impair renal calcium reabsorption but no information is available whether this also influences renal magnesium h and ling . The aim of the study was to examine the relation between NEAP and renal magnesium excretion in healthy , free-living , elderly subjects . The subjects ( age 64 + /- 4.7 y , n = 85 ) were r and omly selected from the population register in Gothenburg ( Sweden ) .  Magnesium , calcium , and potassium  were measured in 24-h urine sample s and NEAP was quantified as renal net acid excretion ( NAE ) . NAE was positively correlated with excretions of magnesium ( R(2 ) = 0.27 , P < 0.0001 ) and calcium ( R(2 ) = 0.30 , P < 0.0001 ) but not potassium . When 24-h urinary magnesium excretion was adjusted for 24-h urinary potassium excretion , a biomarker for dietary potassium intake , the association between magnesium excretion and NAE remained significant ( R(2 ) = 0.21 , P < 0.0001 ) . The significant association between potassium-adjusted magnesiuria and NAE suggests that the acid-base status affects renal magnesium losses , irrespectively of magnesium intake . Magnesium deficiency could thus , apart from an insufficient intake , partly be caused by the acid load in the body
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 .