High dietary acid load (DAL) could be detrimental to KLF10

High dietary acid load (DAL) could be detrimental to KLF10 Etoposide (VP-16) bone mineral density (BMD). from dietary calcium (PRALdiet) and Etoposide (VP-16) diet + supplemental calcium (PRALtotal). Assessments for linear pattern in adjusted mean BMD of the hip and lumbar spine were performed across energy adjusted NEAP and PRAL quartiles. Modification by calcium intake (dietary or total) above or below 800 mg/d was assessed by interaction terms. Overall mean age was 69 ± 0.3y. Among women there was no association between NEAP and BMD. PRALdiet was positively associated with proximal femur BMD (p pattern=0.04). No associations were observed with PRALtotal at any BMD site (P-range: 0.38-0.82). Among men no significant associations were observed of BMD with NEAP or PRAL. However an conversation between PRALdiet and calcium intake was observed with proximal femur BMD (p=0.08). An inverse association between PRALdiet and proximal femur BMD was detected among men <800 mg/d dietary calcium (p=0.02); and no associations ≥800 mg/d (p=0.98). A significant conversation with PRALtotal was not observed. In conclusion when supplemental calcium is considered there is no association between DAL and BMD among adults. Men with low dietary calcium showed an inverse relation with PRAL at the proximal femur; in women no conversation was observed. This study highlights the importance of calcium intakes in counteracting the adverse effect of Etoposide (VP-16) DAL on bone health. Further research should determine the relation between DAL and change in BMD with very low calcium intake. Keywords: dietary acid load BMD NHANES calcium intake dietary protein Introduction Osteoporosis is usually characterized by low bone mass and can lead to increased risk of fracture at the hip spine and wrist (1 2 Hip fractures have debilitating consequences with mortality rates up to 24% one year post-fracture (3) and are a major economic burden (4 5 Due to the inherent loss in quality of life and large medical costs following an osteoporotic fracture prevention of this disease is a public health priority. The acid generating capacity of the western diet (because of its high animal protein content) has been implicated as a potential contributor to bone loss. This hypothesis however remains controversial. Dietary protein is a primary contributor to dietary acid load (DAL) mainly through the metabolism of methionine and cysteine to sulfuric acid (6). Concurrently herb foods also generate base-forming constituents primarily in the form of bicarbonate (7). The calculation of DAL from dietary constituents is usually termed net endogenous acid production (NEAP) and it includes both the acid and the base generating capacity of the entire diet. Data from the third National Health and Nutrition Examination Survey (NHANES) show the average American diet to be acid producing with an NEAP of positive 48 mEq/d (8). Chronic disruption in the extracellular pH such as with higher NEAP may activate compensatory mechanisms to return the acid-base disruption to equilibrium (7). In theory the skeleton could act as a primary buffer system where calcium is released from the bone matrix to counteract the acidic environment generated by higher NEAP. Previous research suggested that chronic acidosis results in augmented osteoclastic bone resorption and decreased osteoblastic bone formation (9). The result of the increased bone resorption was a concurrent increase in urinary calcium Etoposide (VP-16) (10-12). However recent research suggests that greater dietary calcium intake may offset the calciuric effect of protein around the bone matrix (13). Therefore greater NEAP may only be detrimental to bone under conditions of low calcium intake. Therefore the ability of calcium to modify the association between NEAP and bone health warrants further investigation. The current epidemiological literature examining the potential association between DAL and bone are conflicting (14-18) and those measuring long term fracture risk have shown null results (19). However randomized control trials using change in bone mineral density (BMD) as an outcome measure in postmenopausal women have shown that bone loss can be reversed with the addition of a base (either potassium citrate and/or calcium citrate) (20-23). It has yet to be decided whether chronic ingestion of an.