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Dietary Acid-Base Balance, Bone Resorption, and Calcium Excretion

Division of Rheumatology, Tufts-New England Medical Center (R.J.)
Bone Metabolism Laboratory (L.S., S.S.H., B.D.-H.)
Nutrition Services Department, Metabolic Research Unit (H.R.), Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts

Address correspondence to: Bess Dawson-Hughes, M.D., Bone Metabolism Laboratory at the Jean Mayer, USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St. Boston, MA 02111. E-mail: Bess.Dawson-Hughes{at}Tufts.edu

	ABSTRACT

TOP FOOTNOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 
Objective: Metabolic studies reveal that acidogenic diets increase bone resorption acutely. This study was conducted to examine associations between diet-induced changes in net acid excretion (NAE) and changes in serum parathyroid hormone (PTH), bone resorption, and calcium excretion over a longer period of 60 days.

Methods: Forty healthy older men and women were given 0.75 g/kg of protein as meat, 600 mg of calcium, and 400 IU of vitamin D₃ daily and either cereal (acidogenic) or fruit and vegetable (alkalinogenic) foods as substitutes for some of the cereal in their usual diets. Blood and 24-hr urine measurements were made on days 14 (baseline), 44, and 74.

Results: In all subjects, change in renal NAE was correlated with changes in serum PTH (r = 0.358, P = 0.023), urinary N-telopeptide (NTX) (r = 0.367, P = 0.020), and urinary calcium excretion (r_p = 0.381, P = 0.020, after adjustment for diet group, change in PTH, and change in sodium excretion).

Conclusions: Diet changes that increase renal NAE are associated with increases in serum PTH, bone resorption, and calcium excretion over a 60-day period.

Key words: net acid excretion, calcium excretion, N-telopeptide, PTH

	INTRODUCTION

TOP FOOTNOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 
American diets are considered to be a risk factor for osteoporosis and bone fractures in part due to their high potential acid content. The net endogenous acid produced from these diets, measured as urinary net acid excretion, is estimated to be 40–80 mEq/day [1,2]. Protein and cereal grains are metabolized to acidic residues whereas fruits and vegetables have an alkaline residue. Therefore the balance between intakes of these major dietary components will determine the net potential acid load of a diet [3]. An excess acid load is buffered by bone and in the process calcium is released.

Epidemiologic studies have observed that greater intakes of fruits and vegetables are associated with greater bone mineral density (BMD) [4,5] and lower urinary excretion of markers of bone resorption [5] but not with serum osteocalcin [5]. Short-term dietary interventions using metabolic diets have had mixed results. In one study, an acidogenic diet for 4 days lowered urinary and serum pH and increased urinary C-telopeptide and calcium excretion [6]. In a recent 8-week dietary study, however, a higher dietary protein intake increased urinary NAE but did not affect several markers of bone turnover, calcium retention or urinary calcium excretion [7]. Short-term administration of bicarbonate has resulted in decreases in urinary NAE, NTX [8,9], urinary hydroxyproline excretion [10], and urinary calcium excretion [9–11] and in one study, an increase in serum osteocalcin [10]. On the other hand acute ingestion of acid has been associated with increases in urinary NAE, hydroxyproline and calcium excretion [12].

It is important to determine whether the acid/base balance of the diet has a sustained effect on the skeleton. In this pilot study, we examine associations between diet-induced change in renal NAE and changes in serum PTH, markers of bone turnover, and urinary calcium excretion in free-living subjects over a 60-day period.

	MATERIALS AND METHODS

TOP FOOTNOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 
Subjects
Forty healthy men and women, age 50 and older, were enrolled and all subjects completed the study. Telephone prescreening with a short (11 question) food frequency questionnaire was used to identify subjects with usual dietary protein intakes of 0.75 g/kg/day and calcium intakes of 1000 mg/day and a brief medical history questionnaire was used to determine general eligibility. No subjects were taking estrogen, glucocorticoids, insulin or diuretics and none had a history of a disorder known to alter calcium or bone metabolism. Screening evaluation included DXA scans and blood and urine tests. Subjects were excluded if they had a femoral neck Z score <–2.0, 24-hour urine calcium >300 mg, or abnormal hepatic or renal function tests. The study protocol was approved by the Investigation Review Board at Tufts University and written informed consent was obtained from each subject.

Experimental Design And Diets
Subjects were asked to discontinue any usual vitamin D and calcium supplements from one week prior to enrollment to the end of the study. All subjects took one Posture-D tablet (600 mg of elemental calcium and 125 IU vitamin D₃) and a multivitamin (400 IU vitamin D₃) daily throughout the study (day 0–day 74) in order to reduce inter-subject variability in intakes and serum PTH levels. Calcium tri-phosphate was used because it is pH-neutral supplement and wouldn’t affect NAE. On day 14, subjects were randomized to meat plus fruit and vegetable (F+V) food servings or meat plus cereal grain servings. Meat choices were beef (tenderloin, roast and hamburger), chicken and turkey breast, cod fish, pork tenderloin, and canned tuna; fresh fruit and vegetable choices were 100% fruit juices, bananas, blueberries, oranges, raisins, strawberries, broccoli, carrots, cauliflower, green beans, spinach, sweet potatoes, tomatoes, and zucchini; cereal/grain choices were couscous, pasta, rice, Pop Tarts^TM, and granola bars. All food supplements were prepared in the Metabolic Kitchen and portioned in daily amounts. They could be eaten at any time of the day. Blood and urine tests were made on days 14 (prior to the food supplements), 44, and 74 (end of the study).

All subjects were given servings of meat containing 0.75 g of protein/kg/d on days 14–74. Subjects assigned to F+V group were also provided with servings of fruits and vegetables that contained potential alkali in an amount calculated to neutralize the potential acid load (PRAL) of the meat [3]. Subjects assigned to the cereal group received foods that were low in potential alkali content, mainly grain cereals (for example, rice or pasta salad) with small amounts of fat in the form of olive oil for palatability. These foods were isocaloric with the fruit and vegetable substitutes. The cereal and F&V group food substitutes contained 825 ± 190 mg/day (21.1 ± 4.9 mmol/d) and 1583 ± 190 mg/day (40.6 ± 4.9 mmol/d) of potassium, respectively (P < 0.001). The calculated PRAL of the cereal group foods was acidic (mean = 28.6 ± 5.4 mEq/day) and that of the F&V foods was neutral (mean 0.1 ± 0.3 mEq/day; P < 0.001).

There were no significant group differences in age, sex, or body size. During the period that the food supplements were provided (day 14 to day 74), subjects were counseled by a dietitian to decrease the fat, added sugar, and grain content of their usual diets in order to maintain stable weight during the study. Analyses at the end of the study however revealed that there were deletions in other elements of the diet. The 24-hr urinary potassium content in the F/V group on day 74, 70.2 mmol, was below the expected level of 106 mmol (40 mmol from the added foods and 66 mmol in their basal diets), as shown in Table 1. Similarly, expected changes in NAE were not observed. NAE of the F/V group should have remained constant or declined somewhat (as acidogenic cereals in the self-selected diets were replaced with neutral food supplements), and yet it increased from 36.9 to 44.7 mmol/d (Table 1). These results indicate that the design was not fully implemented and that the diet neutralization portion of the experiment is invalid. Not surprisingly, there were no significant diet group differences in serum osteocalcin, calcium, and urinary NAE, NTX, or calcium excretion or in changes in these measures. However there were substantial individual changes in NAE during the study (as shown in the figures). Herein we report associations of baseline NAE and 60-day change in NAE with baseline and change in serum PTH, biochemical markers of bone turnover, and calcium excretion in the group as a whole.

Dietary intake of protein, calcium, phosphorus, magnesium, vitamin D, and total energy over the preceding two months was assessed on the screening visit (representing baseline intake) and on day 74 with Fred Hutchinson Food Frequency Questionnaire [14]. They were self-administered on site and reviewed for completeness by a dietitian. Supplemental calcium was not recorded on this questionnaire.

Biochemical Measurements
Bloods were drawn after an 8-hour fast. Serum 25(OH)D was measured with radioimmunoassay kits from Diasorin (Stillwater, MN), serum PTH and osteocalcin with radioimmunometric assay kits, and serum IGF-1 with radioimmunoassay kits from Nichols Institute Diagnostics (San Juan Capistrano, CA). Urinary N-telopeptide levels were measured with competitive-inhibition enzyme-linked immunoabsorbent assay kits from Ostex International (Seattle, WA). Serum ionized and total calcium concentrations were measured with ion-selective electrodes measurement kit from Medica (Bedford, MA). Urinary sodium, potassium and calcium were measured by direct-current plasma emission spectroscopy with a Spectraspan 6 (Beckman Instruments, Palo Alto, CA). The intra- and inter-assay CVs of the above assays are 2.7 and 6.8% respectively. Urinary nitrogen was measured with a model FP-2000 nitrogen/protein determinator (LECO, St. Joseph, MI). This instrument employs a Dumas combustion method and detection using a thermal conductivity cell. It measures nitrogen with a precision of 15 ppm. Serum cortisol and 24-hour urinary free cortisol were assayed with solid-phase radioimmunoassay kits (Coat-A-Count Cortisol Kit, Diagnostic products Corp., Los Angeles, CA) with intra- and inter-assay CVs of 4.8 and 5.2% respectively. Osteoprotegerin and receptor activator of nuclear factor-kB ligand (RANKL) were measured using enzyme-linked immunosorbent assay from Osteogenic Core Technologies (Torrance, CA) with intra- and inter-assay CVs of 4.5 and 7.4% respectively. Samples from individual subjects were batched except for serum ionized calcium and serum and urinary creatinine analyses. NAE was measured in 24-hr urine collections by a modification of the Jorgensen titration method [15], as described by Chan [16]. Net acid excretion (NAE) = Titratable acid (TA) + Ammonium (NH₄⁺) – Bicarbonate (HCO₃^–). Briefly, TA – HCO₃ was assessed after addition of HCl, boiling the sample, and then titrating the sample to neutral pH. To measure the NH₄⁺, formol was added to the sample to release a H⁺ from NH₄⁺ and the sample was again titrated to neutral pH. All titrations were carried out with a TIM 900 Titration Manager by Radiometer Analytical (Hach Inc, Loveland, CO). The precision of NAE measurements in our laboratory was determined by analyzing aliquots of a single 24-hr urine collection on 15 different days. The aliquots were stored frozen at –20 degrees Celsius for 4 to 9 months and thawed only once. The CV of the NAE measurements was 10.9%. The CV of the TA measurements on the same 15 samples was 5.0%.

Statistical Analysis
Pearson correlations of baseline measurements and of their changes over 60 days in all subjects were performed and their corresponding P-values reported. The partial correlation coefficients were examined after adjusting for potential confounders in ANCOVA models. All results were the mean ± SD. All P-values were two-sided, and P < 0.05 was considered statistically significant. Analyses were conducted with SPSS version 11.5 (SPSS Inc, Chicago).

	RESULTS

TOP FOOTNOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 
The clinical characteristics of the 40 subjects are shown in Table 2. Eighteen men and 22 women participated; their mean age was 63.7 ± 8.4 years.

View larger version (14K): [in this window] [in a new window]   Fig. 1. A. Correlation between 24-hour urinary nitrogen to potassium ratio and 24-hour urinary net acid excretion (mmol/d) on day 14 (baseline) in 40 subjects (r = 0.528, P < 0.001). B. Correlation between change in the 24-hour urinary nitrogen to potassium ratio and change in 24-hour urinary net acid excretion (mmol/d) from day 14 to 74 in 40 subjects (r = 0.453, P = 0.003). Triangles represent subjects given meat and cereal food substitutes and circles represent subjects given meat and fruits and vegetables.

View larger version (12K): [in this window] [in a new window]   Fig. 2. Correlation between change in urinary net acid excretion (mmol/d) and change in serum PTH (pmol/l) from day 14 to 74 in 40 subjects (r = 0.358, P = 0.023). Triangles represent subjects given meat and cereal food substitutes and circles represent subjects given meat and fruits and vegetables.

View larger version (10K): [in this window] [in a new window]   Fig. 3. Correlation between change in 24-hour urinary net acid excretion (mmol/d) and change in 24-hour urinary N-telopeptide (mmol/d) from day 14 to 74 in 40 subjects (r = 0.367, P = 0.020). Triangles represent subjects given meat and cereal food substitutes and circles represent subjects given meat and fruits and vegetables.

Urinary nitrogen excretion and serum IGF-1 were not significantly correlated on Day 14 (r = 0.267, P = 0.095) but the increase in urinary nitrogen excretion during the study was associated with an increase in serum IGF-1 (r = 0.400, P = 0.011). Neither baseline nor change in NAE was associated with baseline or change in serum IGF-1, osteoprotegerin, RANKL, or serum or urinary free cortisol. None of the results was significantly affected by gender.

	DISCUSSION

 
This study reveals that diet-induced changes in renal NAE are associated with changes in indicators of bone health including biochemical markers of bone turnover and calcium excretion and possibly also PTH. The positive but modest association between change in NAE and change in PTH noted in this study has not been observed in previous human studies, including the shorter-term bicarbonate intervention studies [8–11] and an 8-week crossover dietary intervention study [7]. There is also evidence that acidosis directly enhances bone resorption in organ culture [17]. We are not aware that acid affects parathyroid glands in organ culture. Thus our findings may have been due to chance. However, there is evidence that metabolic acidosis acutely stimulates PTH secretion in dogs when the concentrations of calcium and magnesium are clamped, and that during hypocalcemia, metabolic acidosis increases the secretion rate and the half-life of PTH [18]. In a subsequent study, Lopez et al [19] found that acute metabolic alkalosis increased calcium flux to bone and decreased PTH secretion acutely in dogs. In an in vitro study, Bushinsky et al. [17] showed that PTH releases calcium from bone at any pH. The observed association between change in NAE and change in PTH suggests that PTH may in part mediate the bone resorption that accompanies acidogenic diets. This finding will require confirmation in other clinical studies.

In this study, a diet-induced increase in NAE was positively associated with an increase in urinary NTX, suggesting that a dietary acid load stimulates bone resorption over a 60-day period. We know of no indication that an increase in NAE alters the renal handling of NTX. The observed link between change in dietary acid load and change in a marker of bone resorption is in agreement with several [6,9,10] but not all [7] studies. In a 7-day study, Maurer et al noted that when substituting NaHCO₃ and KHCO₃ for NaCl and KCl respectively, urinary NAE and excretion of deoxypyridinoline, pyridinoline and NTX were significantly reduced [9]. Similarly, Sebastian et al [10] found that administration of KHCO₃ decreased NAE and urinary hydroxyproline over 18 days in postmenopausal women. In a 4-day dietary intervention study in 8 young men, consumption of an acidogenic diet caused a 19% increase in urinary C-telopeptide [6]. In contrast, in the only available longer-term diet intervention study, Roughead et al [7] reported no change in urinary NTX after increasing the NAE during an 8-week study in postmenopausal women. Thus our findings are consistent with short-term alkali [9,10] and diet [6] intervention studies, and extend current evidence by suggesting that higher NAE has a sustained association with increased bone resorption over a 60-day period. The lack of association of NAE with serum osteocalcin, a biochemical marker of bone formation, in our study is in contrast to a previous short-term alkali-intervention study [10] but in agreement with a longer-term dietary intervention study [7]. The association of increase in NAE with increase in urinary NTX but not osteocalcin suggests that a more acidic environment may uncouple the bone remodeling process. This has been observed previously in rats [20,21].

In this study, a diet-induced increase in NAE was associated with an increase in urinary calcium excretion and this may have occurred by several mechanisms. The increase in dietary protein may have increased intestinal calcium absorption [22]. The increased NAE may have blocked the renal tubular response to PTH [23]. In addition, calciuria is an expected consequence of enhanced bone resorption. In this study, all subjects started taking the calcium supplements on day one and so were adapted to the higher calcium intakes by the time they began the food substitutions on day 14. The observed increase in urine calcium excretion is in agreement with short-term bicarbonate intervention studies but not with longer-term dietary studies. Lutz [24] found that adding NaHCO₃ to a moderate protein diet for 9 days decreased urinary calcium excretion. Sellmeyer et al. [8] noted that the addition of potassium citrate for 4 weeks in 60 postmenopausal women on high salt diets lowered NAE and urinary calcium excretion compared with the addition the placebo. However, in an 8-week crossover study, Roughead et al. [7] found no change in urinary calcium excretion after increasing renal NAE from 30 to 60 mEq/d by increasing dietary protein intake from 0.94 to 1.62 g/kg/d.

The association between NAE and the urinary nitrogen to potassium ratio is not surprising since nitrogen and potassium have opposing effects on NAE. This same phenomenon was noted in several short-term diet studies with regard to dietary intake of nitrogen (protein) and potassium (F&V). In one study plasma [H⁺] was determined by steady-state rate of endogenous noncarbonic acid production, which negatively correlated with dietary potassium content [25]. Frassetto et al. [26] noted that the dietary protein to potassium ratio accounted for 71% of the variation in renal NAE. Use of the ratio underscores the notion that it is the balance of nutrients in the diet that determines its ultimate pH.

The absence of expected changes in urinary potassium and NAE indicates subject noncompliance that appears to have occurred in the process of deleting foods from their self-selected diets (to some extent, fruits and vegetables rather than grains, added sugar, and fat alone appear to have been deleted). In this study, food substitution was not a successful means of precisely altering the acid-base balance of the diet over a sustained period. This is unfortunate because the alternative, long-term metabolic diet studies, requires access to metabolic research units and is extremely expensive.

In conclusion, a diet-induced increase in NAE is associated with an increase in bone resorption and urinary calcium excretion over a 60-day period in healthy elderly men and women with relatively high protein intakes. This study suggests that changes observed in 7 to 18 day metabolic studies may persist for up to 60 days. This study also raises the possibility that the diet-induced increase in bone resorption may involve PTH-dependent and independent mechanisms.

	ACKNOWLEDGMENTS

TOP FOOTNOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 
We are grateful to the staff of Metabolic Research Unit at Jean Mayer USDA Human Nutrition Research Center on aging at Tufts University for assistance in carrying out this study.

	FOOTNOTES

TOP FOOTNOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 
This material is based on work supported by the National Institute of Health grant No. T32AR07050 and U.S. Department of Agriculture under agreement No. 59-1950-9001. Any opinions, findings, conclusions, or recommendations expressed in this publication are those of the authors, and do not necessarily reflect the view of the National Institute of Health or the U.S. Department of Agriculture.

Received February 8, 2005. Accepted November 17, 2005.

	REFERENCES

TOP FOOTNOTES ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS ACKNOWLEDGMENTS REFERENCES

 

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