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 protein intake and dietary potential renal acid load are associated with bone modeling and remodeling at the proximal radius in healthy children.
BACKGROUND Protein and alkalizing minerals are increasingly described as playing a major role in influencing bone status , not only in the elderly but also in children and adolescents . OBJECTIVE We examined whether the long-term dietary protein intake and diet net acid load are associated with bone status in children . DESIGN In a prospect i ve study design in 229 healthy children and adolescents aged 6 - 18 y , long-term dietary intakes were calculated from 3-d weighed dietary records that were collected yearly over the 4-y period before a one-time bone analysis . Dietary acid load was characterized as potential renal acid load ( PRAL ) by using an algorithm including dietary protein , phosphorus , magnesium , and potassium . Proximal forearm bone variables were measured by peripheral quantitative computed tomography . RESULTS After adjustment for age , sex , and energy intake and control for forearm muscularity , BMI , growth velocity , and pubertal development , we observed that long-term  dietary protein intake  was significantly positively associated with periosteal circumference ( P < 0.01 ) , which reflected bone modeling , and with cortical area ( P < 0.001 ) , bone mineral content ( P < 0.01 ) , and polar strength strain index ( P < 0.0001 ) , which reflected a combination of modeling and remodeling . Children with a higher dietary PRAL had significantly less cortical area ( P < 0.05 ) and bone mineral content ( P < 0.01 ) . Long-term calcium intake had no significant effect on any bone variable . CONCLUSIONS Long-term dietary protein intake appears to act anabolically on diaphyseal bone strength during growth , and this may be negated , at least partly , if dietary PRAL is high , ie , if the intake of alkalizing minerals is low
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 .