Low urine pH and acid excretion do not predict bone fractures or the loss of bone mineral density: a prospective cohort study Renal response to acute acid loadingAn organ physiological approach Dietary acid load, kidney function, osteoporosis, and risk of fractures in elderly men and women Established dietary estimates of net acid production do not predict measured net acid excretion in patients with Type 2 diabetes on Paleolithic–Hunter–Gatherer-type diets Comparative effects of potassium chloride and bicarbonate on thiazide-induced reduction in urinary calcium excretion. Acid-base status affects renal magnesium losses in healthy, elderly persons. Neutralization of Western diet inhibits bone resorption independently of K intake and reduces cortisol secretion in humans. Proteins, dietary acid load, and calcium and risk of postmenopausal fractures in the E3N French women prospective study. Dietary Acid Load and Incident Chronic Kidney Disease: Results from the ARIC Study A diet high in meat protein and potential renal acid load increases fractional calcium absorption and urinary calcium excretion without affecting markers of bone resorption or formation in postmenopausal women. Dietary acid load and risk of hypertension: the Rotterdam Study. Dietary acid load is associated with lower bone mineral density in men with low intake of dietary calcium. A comparison of the effects of feeding sulfur amino acids and protein on urine calcium in man. Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women. The influence of a high dietary intake of purine-rich animal protein on urinary urate excretion and supersaturation in renal stone disease. Quality of diet and potential renal acid load as risk factors for reduced bone density in elderly women. Lower body negative pressure treadmill exercise as a countermeasure for bed rest-induced bone loss in female identical twins. Effect of cranberry juice consumption on urinary stone risk factors. The effects of a low-sodium base-producing diet including red meat compared with a high-carbohydrate, low-fat diet on bone turnover markers in women aged 45-75 years. Whole-body vibration can reduce calciuria induced by high protein intakes and may counteract bone resorption: A preliminary study Potassium bicarbonate attenuates the urinary nitrogen excretion that accompanies an increase in dietary protein and may promote calcium absorption. Plant-Based Diet, Serum Fatty Acid Profile, and Free Radicals in Postmenopausal Women: The Diet and Androgens (DIANA) Randomized Trial More acidic dietary acid-base load is associated with reduced calcaneal broadband ultrasound attenuation in women but not in men: results from the EPIC-Norfolk cohort study.
Background The acid-ash hypothesis , the alkaline diet , and related products are marketed to the general public . Websites , lay literature , and direct mail marketing encourage people to measure their urine pH to assess their health status and their risk of osteoporosis . The objectives of this study were to determine whether 1 ) low urine pH , or 2 ) acid excretion in urine [ sulfate + chloride + 1.8x phosphate + organic acids ] minus [ sodium + potassium + 2x calcium + 2x magnesium mEq ] in fasting morning urine predict : a ) fragility fractures ; and b ) five-year change of bone mineral density ( BMD ) in adults . Methods Design : Cohort study : the prospect i ve population -based Canadian Multicentre Osteoporosis Study .  Multiple logistic regression was used to examine associations between acid excretion ( urine pH and urine acid excretion ) in fasting morning with the incidence of fractures ( 6804 person years ) . Multiple linear regression was used to examine associations between acid excretion with changes in BMD over 5-years at three sites : lumbar spine , femoral neck , and total hip ( n = 651 ) . Potential confounders controlled included : age , gender , family history of osteoporosis , physical activity , smoking , calcium intake , vitamin D status , estrogen status , medications , renal function , urine creatinine , body mass index , and change of body mass index . Results There were no associations between either urine pH or acid excretion and either the incidence of fractures or change of BMD after adjustment for confounders . Conclusion Urine pH and urine acid excretion do not predict osteoporosis risk 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 Summary Because kidney dysfunction reduces the ability to excrete dietary acid excess , we hypothesized that underlying kidney function may have confounded the mixed studies linking dietary acid load with the risk of osteoporosis and fractures in the community . In a relatively large survey of elderly men and women , we report that dietary acid load did neither associate with DEXA-estimated bone mineral density nor with fracture risk . Underlying kidney function did not modify these null findings . Our results do not support the dietary acid-base hypothesis of bone loss . Introduction Impaired renal function reduces the ability to excrete dietary acid excess . We here investigate the association between dietary acid load and bone mineral density ( BMD ) , osteoporosis , and fracture risk by renal function status . Methods An observational study was conducted in 861 community-dwelling 70-year-old men and women ( 49 % men ) with complete dietary data from the Prospect i ve Investigation of the Vasculature in Uppsala Seniors ( PIVUS ) . The exposure was dietary acid load as estimated from 7-day food records by the net endogenous acid production ( NEAP ) and potential renal acid load ( PRAL ) algorithms . Renal function assessed by cystatin C estimated glomerular filtration rate was reduced in 21 % of the individuals . Study outcomes were BMD and osteoporosis state ( assessed by DEXA ) and time to fracture ( median follow-up of 9.2 years ) . Results In cross-section , dietary acid load had no significant associations with BMD or with the diagnosis of osteoporosis . During follow-up , 131 fractures were vali date d. Neither NEAP ( adjusted hazard ratios ( HR ) ( 95 % confidence interval ( CI ) ) , 1.01 ( 0.85–1.21 ) , per 1 SD increment ) nor PRAL ( adjusted HR ( 95 % CI ) , 1.07 ( 0.88–1.30 ) , per 1 SD increment ) associated with fracture risk . Further multivariate adjustment for kidney function or stratification by the presence of kidney disease did not modify these null associations . Conclusions The hypothesis that dietary acid load associates with reduced BMD or increased fracture risk was not supported by this study in community-dwelling elderly individuals . Renal function did not influence on this null finding Background / objectives : Formulas developed to estimate diet-dependent net acid excretion ( NAE ) generally agree with measured values for typical Western diets . Whether they can also appropriately predict NAE for ‘ Paleolithic-type ’ ( Paleo ) diets — which contain very high amounts of fruits and vegetables ( F&V ) and concurrent high amounts of protein is unknown . Here , we compare measured NAEs with established NAE estimates in subjects with Type 2 diabetes (T2D).Subjects/ methods : Thirteen subjects with well-controlled T2D were r and omized to either a Paleo or American Diabetes Association ( ADA ) diet for 14 days . Twenty-four hour urine collection s were performed at baseline and end of the diet period , and analyzed for titratable acid , bicarbonate and ammonium to calculate measured NAE . Three formulas for estimating NAE from dietary intake were used ; two ( NAE_diet R or L ) that include dietary mineral intake and sulfate- and organic acid ( OA ) production , and one that is empirically derived ( NAE_diet F ) only considering potassium and protein intake . Results : Measured NAE on the Paleo diet was significantly lower than on the ADA-diet ( + 31±22 vs 112±52 mEq/day , P=0.002 ) . Although all formula estimates showed similar and reasonable correlations ( r=0.52–0.76 ) with measured NAE , each one underestimated measured values . The formula with the best correlation did not contain an estimate of dietary OA production . Conclusions : Paleo-diets are lower in NAE than typical Western diets . However , commonly used formulas clearly underestimate NAE , especially for diets with very high F&V ( as the Paleo diet ) , and in subjects with T2D . This may be due to an inappropriate estimation of proton loads stemming from OAs , underlining the necessity for improved measures of OA-related proton sources BACKGROUND The chronic low- grade metabolic acidosis that occurs in various renal disorders and in normal people , and that is related both to dietary net acid load and age-related renal functional decline , may contribute to osteoporosis by increasing urine calcium excretion . Administration of potassium ( K ) alkali salts neutralizes acid and lowers urine calcium excretion . Urine calcium excretion also can be reduced by the administration of thiazide diuretics , which are often given with supplemental K to avoid hypokalemia . We determined whether the K alkali salt potassium bicarbonate ( KHCO3 ) and the thiazide diuretic hydrochlorothiazide ( HCTZ ) combined is more effective in reducing urinary calcium than KHCO3 alone or HCTZ combined with the conventionally coadministered nonalkalinizing K salt potassium chloride ( KCl ) . METHODS Thirty-one healthy men and women aged 50 or greater were recruited for a four-week , double-blind , r and omized study . After a baseline period of 10 days with three 24-hour urine and arterialized blood collection s , subjects were r and omized to receive either HCTZ ( 50 mg ) plus potassium ( 60 mmol daily ) as either the chloride or bicarbonate salt . Another 19 women received potassium bicarbonate ( 60 mmol ) alone . After two weeks , triplicate collection s of 24-hour urines and arterialized bloods were repeated . RESULTS Urinary calcium excretion decreased significantly in all groups . KHCO3 alone and HCTZ + KCl induced similar decreases ( -0.70 + /- 0.60 vs. -0.80 + /- 1 . 0 mmol/day , respectively ) . Compared with those treatments , the combination of HCTZ + KHCO3 induced more than a twofold greater decrease in urinary calcium excretion ( -1.8 + /- 1.2 mmol/day , P < 0 . 05 ) . Both HCTZ + KHCO3 and KHCO3 alone reduced net acid excretion significantly ( P < 0.05 ) to values of less than zero . CONCLUSIONS KHCO3 was superior to KCl as an adjunct to HCTZ , inducing a twofold greater reduction in urine calcium excretion , and completely neutralizing endogenous acid production so as to correct the pre-existing mild metabolic acidosis that an acid-producing diet usually induces in older people . Accordingly , for reducing urine calcium excretion in stone disease and osteoporosis , the combination of HCTZ + KHCO3 may be preferable to that of HCTZ + KCl 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 A  Western-type diet  is associated with osteoporosis and calcium nephrolithiasis . On the basis of observations that calcium retention and inhibition of bone resorption result from alkali administration , it is assumed that the acid load inherent in this diet is responsible for increased bone resorption and calcium loss from bone . However , it is not known whether the dietary acid load acts directly or indirectly ( i.e. , via endocrine changes ) on bone metabolism . It is also unclear whether alkali administration affects bone resorption/calcium balance directly or whether alkali-induced calcium retention is dependent on the cation ( i.e. , potassium ) supplied with administered base . The effects of neutralization of dietary acid load ( equimolar amounts of NaHCO(3 ) and KHCO(3 ) substituted for NaCl and KCl ) in nine healthy subjects ( 6 men , 3 women ) under metabolic balance conditions on calcium balance , bone markers , and endocrine systems relevant to bone [ glucocorticoid secretion , IGF-1 , parathyroid hormone (PTH)/1,25(OH)(2 ) vitamin D and thyroid hormones ] were studied . Neutralization for 7 days induced a significant cumulative calcium retention ( 10.7 + /- 0.4 mmol ) and significantly reduced the urinary excretion of deoxypyridinoline , pyridinoline , and n-telopeptide . Mean daily plasma cortisol decreased from 264 + /- 45 to 232 + /- 43 nmol/l ( P = 0.032 ) , and urinary excretion of tetrahydrocortisol ( THF ) decreased from 2,410 + /- 210 to 2,098 + /- 190 microg/24 h ( P = 0.027 ) . No significant effect was found on free IGF-1 , PTH/1,25(OH)(2 ) vitamin D , or thyroid hormones . An acidogenic Western diet results in mild metabolic acidosis in association with a state of cortisol excess , altered divalent ion metabolism , and increased bone resorptive indices . Acidosis-induced increases in cortisol secretion and plasma concentration may play a role in mild acidosis-induced alterations in bone metabolism and possibly in osteoporosis associated with an acidogenic Western diet Excess dietary proteins and " acid ash " diets have been suspected to increase the risk of osteoporosis , but experimental and epidemiological evidence is mixed . We aim ed to determine whether the association between protein intake and the overall acid-base equilibrium of the diet ( as renal net acid excretion [ RNAE ] estimate ) and fracture risk vary according to calcium intake . During an average of 8.37 + /- 1.73 yr of follow-up , 2408 women reported a fracture ( excluding high-impact trauma ) among 36,217 postmenopausal women from the E3N prospect i ve study . We used Cox regression models to study the interaction between calcium and , respectively , proteins and RNAE , from the 1993 dietary question naire for fracture risk determination , adjusting for potential confounders . There was no overall association between fracture risk and total protein or RNAE . However , in the lowest quartile of calcium ( < 400 mg/1000 kcal ) , high protein intake was associated with a significant increased fracture risk ( RR = 1.51 for highest versus lowest quartile ; 95 % CI , 1.17 - 1.94 ) . An increasing fracture risk with increasing animal protein intake was also observed ( trend , p < 0.0001 ) . A similar pattern of interaction for fracture risk was observed between RNAE and calcium . In this Western population of postmenopausal women with normal to high protein intake and fairly high calcium intake , there was no overall association between total protein or RNAE and fracture risk . However , there was some evidence that high protein-high acid ash diets were associated with an increased risk of fracture when calcium intake was low ( < 400 mg/1000 kcal ) Background : Higher dietary acid load can result in metabolic acidosis and is associated with faster kidney disease progression in patients with chronic kidney disease ( CKD ) . However , the relationship between dietary acid load and incident CKD has not been evaluated . Methods : We conducted prospect i ve analyses of the Atherosclerosis Risk in Communities study participants without CKD at baseline ( 1987 - 1989 , n = 15,055 ) .  Dietary acid load was estimated using the equation for potential renal acid load by Remer and Manz , incorporating dietary intake data from a food frequency question naire . Incident CKD was assessed from baseline through 2010 and defined as estimated glomerular filtration rate ( eGFR ) < 60 ml/min/1.73 m2 accompanied by 25 % eGFR decline , CKD-related hospitalization or death or end-stage renal disease identified by linkage to the US Renal Data System registry . Results : In the overall study population , 55 % were female , 26 % were African-American and mean age at baseline was 54 years . During a median follow-up of 21 years , there were 2,351 ( 15.6 % ) incident CKD cases . After adjusting for demographics ( age , sex , race-center ) , established risk factors ( diabetes status , hypertension status , overweight/obese status , smoking status , education level , physical activity ) , caloric intake and baseline eGFR , higher dietary acid load were associated with higher risk of incident CKD ( hazard ratio [ HR ] for quartile 4 vs. 1 : 1.13 , 95 % CI 1.01 - 1.28 , p for trend = 0.02 ; HR per interquartile range increase : 1.06 , 95 % CI 1.00 - 1.11 , p = 0.04 ) . Conclusion : Dietary acid load is associated with incident CKD in a population -based sample . These data suggest a potential avenue for CKD risk reduction through diet Our objective in this study was to determine the effects of a high-protein and high-potential renal acid load ( PRAL ) diet on calcium ( Ca ) absorption and retention and markers of bone metabolism . In a r and omized crossover design , 16 postmenopausal women consumed 2 diets : 1 with low protein and low PRAL ( LPLP ; total protein : 61 g/d ; PRAL : -48 mEq/d ) and 1 with high protein and high PRAL ( HPHP ; total protein : 118 g/d ; PRAL : 33 mEq/d ) for 7 wk each separated by a 1-wk break . Ca absorption was measured by whole body scintillation counting of radio-labeled (47)Ca . Compared with the LPLP diet , the HPHP diet increased participants ' serum IGF-I concentrations ( P < 0.0001 ) , decreased serum intact PTH concentrations ( P < 0.001 ) , and increased fractional (47)Ca absorption ( mean ± pooled SD : 22.3 vs. 26.5 ± 5.4 % ; P < 0.05 ) and urinary Ca excretion ( 156 vs. 203 ± 63 mg/d ; P = 0.005 ) . The net difference between the amount of Ca absorbed and excreted in urine did not differ between 2 diet periods ( 55 vs. 28 ± 51 mg/d ) . The dietary treatments did not affect other markers of bone metabolism . In summary , a diet high in protein and PRAL  increases the fractional absorption of dietary Ca , which partially compensates for increased urinary Ca , in postmenopausal women . The increased IGF-I and decreased PTH concentrations in serum , with no change in biomarkers of bone resorption or formation , indicate a high-protein diet has no adverse effects on bone health BACKGROUND Mild metabolic acidosis , which can be caused by diet , may result in elevated blood pressure ( BP ) . DESIGN The analyses included 2241 participants aged ≥55 y who were free of hypertension at baseline ( 1990 - 1993 ) and who had complete dietary and BP data .  Dietary data were obtained from a 170-item food-frequency question naire . We used 2 measures to characterize dietary acid load : ( 1 )  potential renal acid load ( PRAL ) by using an algorithm including protein , phosphorus , potassium , calcium , and magnesium , and ( 2 ) estimated  net endogenous acid production ( NEAP ) based on protein and potassium . HRs for 6-y incidence of hypertension were obtained in tertiles of PRAL and NEAP with adjustment for age , sex , BMI , smoking , education , and intakes of alcohol , fiber , and total energy . RESULTS We identified 1113 incident cases of hypertension during 8707 person-years of follow-up .  The median dietary acid load ranged from -14.6 to 19.9 mEq/d across categories of PRAL . Hypertension risk was not significantly associated with dietary acid load . The multivariate HRs ( 95 % CIs ) in consecutive tertiles of PRAL were 1.00 ( reference ) , 1.01 ( 0.87 , 1.17 ) , and 1.02 ( 0.88 , 1.18 ) ( P trend = 0.83 ) . The median dietary acid loads were 30.4 , 36.7 , and 43.7 mEq/d , respectively , in consecutive tertiles of NEAP . Corresponding HRs for NEAP were 1.00 ( reference ) , 0.92 ( 0.80 , 1.07 ) , and 0.94 ( 0.81 , 1.10 ) ( P-trend = 0.46 ) . CONCLUSION The findings from this prospect i ve cohort study provided no evidence of an association between dietary acid load and risk of hypertension in older adults High dietary acid load ( DAL ) may be detrimental to bone mineral density ( BMD ) . The objectives of the study were to : ( 1 ) evaluate the cross-sectional relation between DAL and BMD ; and ( 2 ) determine whether calcium intake modifies this association . Men ( n = 1218 ) and women ( n = 907 ) aged ≥60 years were included from the National Health and Nutrition Examination Survey 2005 - 2008 .  Nutrient intake from 2 , 24-hour recalls was used to calculate net endogenous acid production ( NEAP ) and potential renal acid load  ( PRAL ) ( mEq/d ) . PRAL was calculated from dietary calcium ( PRALdiet ) and diet + supplemental calcium ( PRALtotal ) . Tests for linear trend 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 ± 0.3 years . Among women , there was no association between NEAP and BMD  . PRALdiet was positively associated with proximal femur BMD ( p trend = 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 between BMD and NEAP or PRAL . However , an interaction 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 with < 800 mg/d dietary calcium ( p = 0.02 ) ; no associations were found among men with ≥800 mg/d ( p = 0.98 ) . A significant interaction 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 interaction was observed . This study highlights the importance of calcium intake in counteracting the adverse effect of DAL on bone health . Further research should determine the relation between DAL and change in BMD with very low calcium intake It has been suggested that the sulfur amino acids in protein are responsible for the calciuria observed after protein ingestion . This hypothesis was tested by feeding meals containing either 15 g protein ( control ) , 45 g protein ( high protein ) , or 15 g protein plus sulfur amino acids equivalent to those in the high protein diet . Compared to the control , the high protein diet caused an increase in urinary calcium and sulfate and a decrease in the renal reabsorption of calcium . In contrast , the sulfur amino acid supplement had no effect on calcium excretion or reabsorption . Net acid excretion was unaffected by dietary treatment The dietary acid load created by the typical Western diet may adversely impact the skeleton by disrupting calcium metabolism . Whether neutralizing dietary acid with alkaline potassium salts results in sustained improvements in calcium balance remains controversial . In this r and omized , double-blind , placebo-controlled study , 52 men and women ( mean age 65.2 ± 6.2 years ) were r and omly assigned to potassium citrate 60 mmol/d , 90 mmol/d , or placebo daily with measurements of bone turnover markers , net acid excretion , and calcium metabolism , including intestinal fractional calcium absorption and calcium balance , obtained at baseline and at 6 months . At 6 months , net acid excretion was significantly lower in both treatment groups compared to placebo and it was negative , meaning subjects ' dietary acid was completely neutralized ( -11.3 mmol/d on 60 mmol/d ; -29.5 mmol/d on 90 mmol/d , p < 0.001 compared to placebo ) . At 6 months , 24-hour urine calcium was significantly reduced in persons taking potassium citrate 60 mmol/d ( -46 ± 15.9 mg/d ) and 90 mmol/d ( -59 ± 31.6 mg/d ) compared with placebo ( p < 0.01 ) . Fractional calcium absorption was not changed by potassium citrate supplementation . Net calcium balance was significantly improved in participants taking potassium citrate 90 mmol/d compared to placebo ( 142 ± 80 mg/d on 90 mmol/d versus -80 ± 54 mg/d on placebo ; p = 0.02 ) . Calcium balance was also improved on potassium citrate 60 mmol/d , but this did not reach statistical significance ( p = 0.18 ) . Serum C-telopeptide decreased significantly in both potassium citrate groups compared to placebo ( -34.6 ± 39.1 ng/L on 90 mmol/d , p = 0.05 ; -71.6 ± 40.7 ng/L on 60 mmol/d , p = 0.02 ) whereas bone-specific alkaline phosphatase did not change . Intact parathyroid hormone was significantly decreased in the 90 mmol/d group ( p = 0.01 ) . Readily available , safe , and easily administered in an oral form , potassium citrate has the potential to improve skeletal health . Longer-term trials with definitive outcomes such as bone density and fracture are needed 1 . Eight recurrent renal stone-forming patients were housed in a metabolic ward and fed on a low ( LPD ) and a high ( HPD ) animal protein diet , which were isoenergetic . Metabolic studies were made after 2 weeks on each diet . 2 . There was a 90 % increase in urinary urate on HPD compared with LPD , whereas serum urate did not change consistently . 3 . The urinary acid excretion increased by 200 % , including a 100 % increase in ammonium ion excretion . A fall in urine pH by 0.9 unit was also seen . 4 . The calculated ion activities of the urines revealed a profound increase in the uric acid supersaturation , from undersaturation to supersaturation , and in some cases even surpassing the formation product ratio . The ammonium urate supersaturation also increased . The sodium urate supersaturation was unchanged , despite an induced natriuresis . 5 . The risk of forming uric acid or ammonium urate crystals or stones in the urine was increased on a high protein diet , whereas the risk of forming sodium urate crystals was no greater than on a low protein diet . 6 . As uric acid and ammonium urate crystals under certain conditions may adsorb a macromolecular fraction of the human urine , which inhibits calcium oxalate crystal growth , it is proposed that this mechanism , along with a decrease in urine pH , may also interfere with the inhibitory activity of calcium oxalate crystal growth and aggregation BACKGROUND Bone mineral density ( BMD ) may be influenced by the general dietary pattern and the potential renal acid load ( PRAL ) . METHODS We compared the dietary intake ( estimated using the European Prospect i ve Investigation into Cancer and nutrition question naire ) of 497 community-living women ( 60 years of age and older ) grouped according to tertiles of baseline total , trabecular and cortical BMD estimated using tibial peripheral quantitative computed tomography ( pQCT ) , and of BMD variation over 6 years . RESULTS None of the nutrients taken into account nor PRAL was associated with total BMD , with the exception that the intake of polyunsaturated fatty acids ( PUFA ) was slightly higher among women with the highest total BMD . Similar results were found for trabecular BMD . Cortical BMD was associated with serum 25-OH vitamin D ( 38.8 , 43.2 , and 49.5 nmol/L in the first , second , and third tertiles , respectively ; P=0.042 ) . In the longitudinal analysis , a lower BMI was associated with greater loss of total BMD , while lower serum 25-OH vitamin D at baseline was associated with smaller loss of cortical BMD . CONCLUSIONS We found no relationship between dietary acid load and BMD . We also confirmed the role of well-recognized risk factor for osteoporosis Supine weight-bearing exercise within lower body negative pressure ( LBNP ) alleviates some of the skeletal deconditioning induced by simulated weightlessness in men . We examined this potential beneficial effect in women . Because dietary acid load affected the degree of bone resorption in men during bed rest , we also investigated this variable in women . Subjects were 7 pairs of female identical twins assigned at r and om to 2 groups , sedentary bed rest ( control ) or bed rest with supine treadmill exercise within LBNP .  Dietary intake was controlled and monitored . Urinary calcium and markers of bone resorption were measured before bed rest and on bed rest days 5/6 , 12/13 , 19/20 , and 26/27 . Bone mineral content was assessed by dual-energy X-ray absorptiometry before and after bed rest . Data were analyzed by repeated- measures two-way analysis of variance . Pearson correlation coefficients were used to define the relationships between diet and markers of bone metabolism and to estimate heritability of markers . During bed rest , all markers of bone resorption and urinary calcium and phosphorus increased ( P<0.001 ) ; parathyroid hormone ( P=0.06 ) , bone-specific alkaline phosphatase ( P=0.06 ) , and 1,25-dihydroxyvitamin D ( P=0.09 ) tended to decrease . LBNP exercise tended to mitigate bone density loss . The ratio of dietary animal protein to potassium was positively correlated with urinary calcium excretion for all weeks of bed rest in the control group , but only during weeks 1 and 3 in the exercise group . Pre-bed rest data suggested that many markers of bone metabolism have strong genetic determinants . Treadmill exercise within LBNP had less of a protective effect on bone resorption during bed rest in women than previously published results had shown for its effect in men , but the same trends were observed for both sexes . Dietary acid load of these female subjects was significantly correlated with calcium excretion but not with other bone resorption markers PURPOSE We evaluated the effect of cranberry juice on urinary stone risk factors . MATERIAL S AND METHODS A total of 12 normal subjects and 12 calcium oxalate stone formers underwent 2 , 7-day phases of study in r and om order while on a controlled metabolic diet . Subjects ingested 1 l of cranberry juice ( CBJ ) daily in 1 phase and 1 l of deionized water in the other phase . On the last 2 days of each phase 2 , 24-hour urine collection s and blood sample s were obtained for stone risk factors and serum chemistries . RESULTS No significant differences were found between normal subjects and stone formers in response to CBJ and , therefore , the groups were combined . CBJ significantly increased urinary calcium ( from 154 to 177 mg per day , p = 0.0008 ) and urinary oxalate ( from 26.4 to 29.2 mg per day , p = 0.04 ) , thereby increasing urinary saturation of calcium oxalate by 18 % . Urinary citrate was unchanged and urinary magnesium increased slightly . Urinary pH decreased ( from 5.97 to 5.67 , p = 0.0005 ) , and urinary ammonium , titratable acidity and net acid excretion increased during CBJ ingestion . Urinary uric acid decreased ( from 544 to 442 mg per day , p < 0.0001 ) as did serum uric acid . Thus , the urinary saturation of brushite and monosodium urate was reduced by CBJ but the amount of undissociated uric acid increased . CONCLUSIONS CBJ exerts a mixed effect on urinary stone forming propensity . It reduces urinary pH likely by providing an acid load and decreases urinary uric acid perhaps by retarding urate synthesis . Overall CBJ increases the risk of calcium oxalate and uric acid stone formation but decreases the risk of brushite stones A r and omised , parallel- design dietary intervention study was conducted in women ( aged 45 - 75 years ) with prehypertension or stage 1 hypertension . The aim was to compare the effects on bone turnover of a low-Na base-producing ( LNAB ) Dietary Approaches to Stop Hypertension (DASH)-type diet ( including six serves lean red meat/week ) with a high-carbohydrate low-fat ( HCLF ) diet with a higher acid load ( both > 800 mg dietary Ca/d ) . Fasting serum bone markers ( baseline and week 14 ) and 24 h urinary electrolyte excretion ( baseline , weeks 4 , 8 , 12 and 14 ) were measured . After the intervention period , the LNAB group ( n 46 ) had a fall of 26 ( sem 6 ) % ( P < 0.0001 ) in urinary Na , an increase in K excretion ( 6.8 ( sem 3.6 ) mmol/d ; P = 0.07 ) and , compared with the HCLF group ( n 49 ) , a greater reduction in urinary Ca excretion by 0.7 ( sem 0.3 ) mmol/d . Serum 25-hydroxyvitamin D , intact parathyroid hormone and osteocalcin did not change , and both groups had a similar increase of 23 ( sem 5 ) % ( P < 0.0001 ) in C-terminal telopeptide of type I collagen . The HCLF group had an 11 ( sem 4 ) % increase ( P = 0.003 ) in N-terminal propeptide , type I procollagen , which could indicate an increased rate of bone turnover . The fall in urinary Ca with the lower-Na lower-acid load diet is likely to have long-term beneficial effects on bone . As bone resorption was not different between the two dietary patterns with relatively high Ca intake , the effect on bone health of a dietary pattern with a lower acid load warrants further study on a lower Ca intake Abstract Excess protein intake can adversely affect the bone via an increase in calcium excretion , while suitable mechanical loading promotes osteogenesis . We therefore investigated whether vibration exposure could alleviate the bone mineral losses associated with a metabolic acidosis . Ten healthy individuals aged 22 – 29 years ( median = 25 ) underwent three 5-day study periods while monitoring their dietary intake . The study consisted of recording the participants ' usual dietary intake for 5 consecutive days . Participants were then r and omly divided into two groups , one of which received a protein supplement ( 2 g · kg−1 body mass · day−1 ; n = 5 ) and the other whole-body low-magnitude ( 3.5 g ) , low-frequency ( 30 Hz ) mechanical vibration ( WBV ) delivered through a specially design ed vibrating plate for 10 min each day ( n = 5 ) . Finally , for the third treatment period , all participants consumed the protein supplement added to their normal diet and were exposed to WBV exercise for 10 min per day . Daily urine sample s were collected throughout the experimental periods to determine the excretion of calcium , phosphate , titratable acid , urea , and C-telopeptide . As expected , when the participants underwent the high protein intake , there was an increase in urinary excretion rates of calcium ( P < 0.001 ) , phosphate ( P < 0.003 ) , urea ( P < 0.001 ) , titratable acid ( P < 0.001 ) , and C-telopeptide ( P < 0.05 ) compared with baseline values . However , high protein intake coupled with vibration stimulation result ed in a significant reduction in urinary calcium ( P = 0.006 ) , phosphate excretion ( P = 0.021 ) , and C-telopeptide ( P < 0.05 ) compared with protein intake alone , but did not affect titratable acid and urea output . The participants showed no effect of WBV exercise alone on urinary excretion of calcium , phosphate , urea , titratable acid , or C-telopeptide . The results indicate that vibration stimulation can moderate the increase in bone resorption and reduction in bone formation caused by a metabolic acidosis CONTEXT Protein is an essential component of muscle and bone . However , the acidic byproducts of protein metabolism may have a negative impact on the musculoskeletal system , particularly in older individuals with declining renal function . OBJECTIVE We sought to determine whether adding an alkaline salt , potassium bicarbonate ( KHCO3 ) , allows protein to have a more favorable net impact on intermediary indices of muscle and bone conservation than it does in the usual acidic environment . DESIGN We conducted a 41-d r and omized , placebo-controlled , double-blind study of KHCO3 or placebo with a 16-d phase-in and two successive 10-d metabolic diets containing low ( 0.5 g/kg ) or high ( 1.5 g/kg ) protein in r and om order with a 5-d washout between diets . SETTING The study was conducted in a metabolic research unit . PARTICIPANTS Nineteen healthy subjects ages 54 - 82 yr participated . INTERVENTION KHCO3 ( up to 90 mmol/d ) or placebo was administered for 41 d. MAIN OUTCOME MEASURES We measured 24-h urinary nitrogen excretion , IGF-I , 24-h urinary calcium excretion , and fractional calcium absorption . RESULTS KHCO3 reduced the rise in urinary nitrogen excretion that accompanied an increase in protein intake ( P = 0.015 ) and was associated with higher IGF-I levels on the low-protein diet ( P = 0.027 ) with a similar trend on the high-protein diet ( P = 0.050 ) . KHCO3 was also associated with higher fractional calcium absorption on the low-protein diet ( P = 0.041 ) with a similar trend on the high-protein diet ( P = 0.064 ) . CONCLUSIONS In older adults , KHCO3 attenuates the protein-induced rise in urinary nitrogen excretion , and this may be mediated by IGF-I. KHCO3 may also promote calcium absorption independent of the dietary protein content High calorie and fat consumption and the production of free radicals are two major mechanistic pathways between diet and disease . In this study we evaluated the effect of a plant-based diet poor in animal fat and rich in ( n-3 ) fatty acids on fatty acids of serum phospholipids and on the production of reactive oxygen metabolites ( ROMs ) .  One hundred and four healthy female postmenopausal volunteers were recruited and r and omized to a dietary intervention or a control group . Dietary intervention included a program of food education and biweekly common meals for 18 weeks . When the intervention and control groups were compared , it was seen that dietary intervention result ed in a significant reduction of saturated fatty acids ( -1.5 % ) and a significant increase in ( n-3 ) fatty acids ( + 20.6 % ) , in particular docosahexaenoic acid ( + 24.8 % ) . We observed that arachidonic acid decreased ( –7.7 % ) , while ( n-6 ) fatty acids did not , and the (n-3)/(n-6 ) polyunsaturated ratio increased significantly ( + 24.1 % ) . As expected , ROMs decreased significantly in the intervention group ( -6 % ) . The results indicated that a plant-based diet can improve the serum fatty acid profile and decrease ROMs production . These results suggest that a plant-based diet may reduce the body 's exposure to oxidative stress BACKGROUND Dietary patterns that promote mild metabolic acidosis may have a negative effect on  bone density .  OBJECTIVE We investigated the relation between a measure of  dietary acid-base load , potential renal acid load ( PRAL ) , and calcaneal broadb and ultrasound attenuation ( BUA ) after adjustment for confounders and also compared the results with different estimates of acid-base load . DESIGN A cross-sectional study was conducted in 14 563 men and women aged 42 - 82 y living in Norfolk , United Kingdom , in which measures of calcaneal BUA  and dietary PRAL were estimated by using the European Prospect i ve Investigation into Cancer and Nutrition Norfolk ( EPIC-Norfolk ) food-frequency question naire . RESULTS A more acidic dietary intake ( high PRAL ) was significantly associated with lower calcaneal BUA in women but not in men ; there was a difference of approximately 2 % in BUA between the highest and lowest quintiles of PRAL , independent of age , body mass index , smoking habit , physical activity , diagnosed osteoporosis , and history of fracture , and ( in women ) hormone replacement therapy . No relation was observed between history of fracture or incident fracture and PRAL . Those with the greatest PRAL had higher intakes of meat , fish , eggs , and cereal and cereal products and lower intakes of fruit and vegetables , tea , and coffee . CONCLUSION PRAL was inversely associated with bone ultrasound measures in women , but the magnitude of the association was relatively small compared with other known risk factors . Further longitudinal studies are required to establish whether , in the long term , these small effects are important in overall fracture risk in population
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 .