Monthly Archives: April 2014

High-Protein Diets are Not Detrimental to Bone in the Short Term in Women

Abstract

The impact of dietary protein on calcium absorption and kinetic measures of bone turnover in women.

Although high-protein diets induce hypercalciuria in humans, the source of the additional urinary calcium remains unclear. One hypothesis is that the high endogenous acid load of a high-protein diet is partially buffered by bone, leading to increased skeletal resorption and hypercalciuria. We used dual stable calcium isotopes to quantify the effect of a high-protein diet on calcium kinetics in women. The study consisted of 2 wk of a lead-in, well-balanced diet followed by 10 d of an experimental diet containing either moderate (1.0 g/kg) or high (2.1 g/kg) protein. Thirteen healthy women received both levels of protein in random order. Intestinal calcium absorption increased during the high-protein diet in comparison with the moderate (26.2 +/- 1.9% vs. 18.5 +/- 1.6%, P < 0.0001, mean +/- sem) as did urinary calcium (5.23 +/- 0.37 vs. 3.57 +/- 0.35 mmol/d, P < 0.0001, mean +/- sem). The high-protein diet caused a significant reduction in the fraction of urinary calcium of bone origin and a nonsignificant trend toward a reduction in the rate of bone turnover. There were no protein-induced effects on net bone balance. These data directly demonstrate that, at least in the short term, high-protein diets are not detrimental to bone.

Kerstetter JE, O’Brien KO, Caseria DM, Wall DE…
J. Clin. Endocrinol. Metab. Jan 2005
PMID: 15546911

Review: Low Protein Intake and Bones – 2003

Abstract

Low protein intake: the impact on calcium and bone homeostasis in humans.

Increasing dietary protein results in an increase in urinary calcium. Despite over 80 y of research, the source of the additional urinary calcium remains unclear. Because most calcium balance studies found little effect of dietary protein on intestinal calcium absorption, it was assumed that the skeleton was the source of the calcium. The hypothesis was that the high endogenous acid load generated by a protein-rich diet would increase bone resorption and skeletal fracture. However, there are no definitive nutrition intervention studies that show a detrimental effect of a high protein diet on the skeleton and the hypothesis remains unproven. Recent studies from our laboratory demonstrate that dietary protein affects intestinal calcium absorption. We conducted a series of short-term nutrition intervention trials in healthy adults where dietary protein was adjusted to either low, medium or high. The highest protein diet resulted in hypercalciuria with no change in serum parathyroid hormone. Surprisingly, within 4 d, the low protein diet induced secondary hyperparathyroidism that persisted for 2 wk. The secondary hyperparathyroidism induced by the low protein diet was attributed to a reduction in intestinal calcium absorption (as assessed by dual stable calcium isotopes). The long-term consequences of these low protein-induced changes in calcium metabolism are not known, but they could be detrimental to skeletal health. Several recent epidemiological studies demonstrate reduced bone density and increased rates of bone loss in individuals habitually consuming low protein diets. Therefore, studies are needed to determine whether low protein intakes directly affect rates of bone resorption, bone formation or both.

Kerstetter JE, O’Brien KO, Insogna KL
J. Nutr. Mar 2003
PMID: 12612169 | Free Full Text

The subject is complicated with a lot of conflicting data. The full article is great.

When BMD is the primary outcome, most (39–48), but not all (49–53), epidemiological studies show a positive relationship between protein intake and BMD. Stated another way, most of the epidemiological evidence shows that when other known dietary factors are controlled, those individuals who consume low protein diets have lower BMD. Using the National Health and Nutrition Examination Survey (NHANES) III database, we found that in 1882 non-Hispanic white women 50 y old and older, after adjusting for age and body weight, a low protein intake was associated with a significantly lower hip bone mineral density (Fig. 5) (47). Consistent with these data, Hannan and colleagues (46) studied 615 participants in the Framingham Osteoporosis Study over a 4-y period and found that lower levels of protein intake were associated with significantly higher rates of bone loss at the hip and spine. These findings confirm the earlier work of Freudenheim et al. (39), who reported that a low protein intake was associated with greater loss in bone density from the wrist in 35- to 65-y-old women. Most recently, Promislow et al. (48) found a positive association between total dietary protein intake and BMD in elderly men and women participating in the Rancho Bernardino study. Therefore, there is substantial agreement in those studies in which BMD is the primary outcome. Munger et al. (59), reporting data from the Iowa Women’s Health Study, found an increased risk of hip fracture in 55- to 69-y-old women consuming the lowest amounts of protein.

Adequate dietary protein may also help in fracture healing and in preventing bone loss after fracture. Bonjour and colleagues (73) studied the effects of 6 mo of protein supplementation, after osteoporotic hip fracture, in a group of elderly subjects. These patients had self-selected protein intakes that were very low (∼40 g). The administration of additional protein (+20 g) was associated with significant attenuation of proximal femur bone loss in the fractured hip such that, at 1 y, bone loss rates were 50% lower in the protein-supplemented individuals. The correction of poor protein nutrition also improved serum prealbumin and insulin-like growth factor 1 (IGF-1) concentrations and decreased the length of rehabilitation (73).

There is agreement that diets moderate in protein (in the approximate range of 1.0 to 1.5 g protein/kg) are associated with normal calcium metabolism and presumably do not alter skeletal homeostasis. Approximately 30–50% of adults in the United States consume dietary protein that could be considered moderate. At low protein intakes, intestinal calcium absorption is reduced, resulting in increases in serum PTH and calcitriol that persist for at least 2–4 wk. The long-term implications of these findings are unknown; however, recent epidemiological data suggest increased rates of bone loss in individuals consuming such diets. Individuals consuming high protein intakes, particularly from omnivorous sources, develop hypercalciuria that is attributable for the most part to an increase in intestinal calcium absorption. Whether high protein diets result in an increase in bone resorption and higher fracture rates remains uncertain.

 

Potassium Bicarbonate Decreases Resorption and Increases Bone Formation in Postmenopausal Women

Abstract

Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate.

In normal subjects, a low level of metabolic acidosis and positive acid balance (the production of more acid than is excreted) are typically present and correlate in degree with the amount of endogenous acid produced by the metabolism of foods in ordinary diets abundant in protein. Over a lifetime, the counteraction of retained endogenous acid by base mobilized from the skeleton may contribute to the decrease in bone mass that occurs normally with aging.
To test that possibility, we administered potassium bicarbonate to 18 postmenopausal women who were given a constant diet (652 mg [16 mmol] of calcium and 96 g of protein per 60 kg of body weight). The potassium bicarbonate was given orally for 18 days in doses (60 to 120 mmol per day) that nearly completely neutralized the endogenous acid.
During the administration of potassium bicarbonate, the calcium and phosphorus balance became less negative or more positive–that is, less was excreted in comparison with the amount ingested (mean [+/- SD] change in calcium balance, +56 +/- 76 mg [1.4 +/- 1.9 mmol] per day per 60 kg; P = 0.009; change in phosphorus balance, +47 +/- 64 mg [1.5 +/- 2.1 mmol] per day per 60 kg; P = 0.007) because of reductions in urinary calcium and phosphorus excretion. The changes in calcium and phosphorus balance were positively correlated (P < 0.001). Serum osteocalcin concentrations increased from 5.5 +/- 2.8 to 6.1 +/- 2.8 ng per milliliter (P < 0.001), and urinary hydroxyproline excretion decreased from 28.9 +/- 12.3 to 26.7 +/- 10.8 mg per day (220 +/- 94 to 204 +/- 82 mumol per day; P = 0.05). Net renal acid excretion decreased from 70.9 +/- 10.1 to 12.8 +/- 21.8 mmol per day, indicating nearly complete neutralization of endogenous acid.
In postmenopausal women, the oral administration of potassium bicarbonate at a dose sufficient to neutralize endogenous acid improves calcium and phosphorus balance, reduces bone resorption, and increases the rate of bone formation.

Sebastian A, Harris ST, Ottaway JH, Todd KM…
N. Engl. J. Med. Jun 1994
PMID: 8190153 | Free Full Text

Potassium Citrate, but not Chloride, Increases Bone Density in Postmenopausal Women

Abstract

Partial neutralization of the acidogenic Western diet with potassium citrate increases bone mass in postmenopausal women with osteopenia.

Chronic acid loads are an obligate consequence of the high animal/grain protein content of the Western diet. The effect of this diet-induced metabolic acidosis on bone mass is controversial. In a randomized, prospective, controlled, double-blind trial, 161 postmenopausal women (age 58.6 +/- 4.8 yr) with low bone mass (T score -1 to -4) were randomly assigned to 30 mEq of oral potassium (K) citrate (Kcitrate) or 30 mEq of K chloride (KCl) daily. The primary end point was the intergroup difference in mean percentage change in bone mineral density (BMD) at lumbar spine (L2 through L4) after 12 mo. Compared with the women who received KCl, women who received Kcitrate exhibited an intergroup increase in BMD (+/-SE) of 1.87 +/- 0.50% at L2 through L4 (P < 0.001), of 1.39 +/- 0.48% (P < 0.001) at femoral neck, and of 1.98 +/- 0.51% (P < 0.001) at total hip. Significant secondary end point intragroup changes also were found: Kcitrate increased L2 through L4 BMD significantly from baseline at months 3, 9, and 12 and reached a month 12 increase of 0.89 +/- 0.30% (P < 0.05), whereas the KCl arm showed a decreased L2 through L4 BMD by -0.98 +/- 0.38% (P < 0.05), significant only at month 12. Intergroup differences for distal radius and total body were NS. The Kcitrate-treated group demonstrated a sustained and significant reduction in urinary calcium excretion and a significant increase in urinary citrate excretion, with increased citrate excretion indicative of sustained systemic alkalization. Urinary bone resorption marker excretion rates were significantly reduced by Kcitrate, and for deoxypyridinoline, the intergroup difference was significant. Urinary net acid excretion correlated inversely and significantly with the change in BMD in a subset of patients. Large and significant reductions in BP were observed for both K supplements during the entire 12 mo. Bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as citrate, and the effect is independent of reported skeletal effects of K.

Jehle S, Zanetti A, Muser J, Hulter HN…
J. Am. Soc. Nephrol. Nov 2006
PMID: 17035614 | Free Full Text

Despite more than 70 yr of sustained interest in the possibility that chronic metabolic acidosis might decrease bone mass, central questions regarding the effect of acid-base alterations on human bone physiology and pathophysiology remain unanswered (4,27,28). First, does chronic metabolic acidosis of any magnitude decrease bone mass? Second, does the low-grade chronic metabolic acidosis that is induced by the acidogenic Western diet result in osteoporosis? Third, can neutralization of dietary acid result in increased bone mass in normal humans or those with osteopenia?

Indirect support for a possible role of chronic metabolic acidosis to reduce bone mass comes from small, uncontrolled studies in humans with nonazotemic renal disease (distal renal tubular acidosis [29,30]). Chronic dietary acid loads were shown to result in significant and reversible negative calcium balance (6), and experimental increases in animal protein intake or its chief acidogenic constituent, methionine, within the range that is characteristic of the Western diet were shown to cause both negative calcium balance and increased systemic acid load (31,32). Compatible with and strongly supportive of these observations, short-term neutralization of endogenous acid production by oral ingestion of bicarbonate for 7 to 18 d in both postmenopausal women and young healthy adults resulted in calcium retention and—on the basis of analysis of bone markers—in inhibition of bone resorption (13,14).

[…]

This study establishes that bone mass can be increased significantly in postmenopausal women with osteopenia by increasing their daily alkali intake as Kcitrate and that this effect is independent of reported in vitro skeletal effects of co-administered K. The magnitude of the effect is large, and the safety profile was found to be excellent, albeit based on a limited sample size. The results strongly support the thesis that neutralization of the modern Western diet will promote skeletal health. The associated BP effects of the K supplement provide additional incentive to move forward with controlled outcome trials using long-term Kcitrate treatment.

Potassium Citrate or Fruits + Veggies, No Benefit Over 2 Years

Abstract

Effect of potassium citrate supplementation or increased fruit and vegetable intake on bone metabolism in healthy postmenopausal women: a randomized controlled trial.

Alkali provision may explain why fruit and vegetables benefit bone health.
We aimed to determine the effects of alkali-providing potassium citrate (double-blind) and fruit and vegetable intake (single-blind) on bone turnover over 2 y.
We conducted a randomized placebo-controlled trial in 276 postmenopausal women (aged 55-65 y). Women were randomly assigned to 4 groups: high-dose potassium citrate (55.5 mEq/d), low-dose potassium citrate (18.5 mEq/d), placebo, and 300 g additional fruit and vegetables/d (equivalent of 18.5 mEq alkali). Serum and fasted urine for bone markers were collected at baseline and at 3, 6, 12, 18, and 24 mo. An additional urine sample was collected at 4-6 wk. Bone mineral density (BMD) was measured at baseline and 2 y.
Repeated-measures ANOVA showed no difference between groups for urinary free deoxypyridinoline cross-links relative to creatinine (fDPD/Cr), serum N-terminal propeptide of type 1 collagen, or beta C-terminal telopeptide, although, at 4-6 wk, fDPD/Cr was lower in the high-dose potassium citrate group (P = 0.04). Mean +/- SD spine BMD loss in the placebo group (1.8 +/- 3.9%) did not differ significantly from that in the treatment groups (2.1 +/- 3.2%; P = 0.88). Hip BMD loss in the placebo and low-dose potassium citrate groups was 1.3 +/- 2.3% and 2.2 +/- 2.3%, respectively (P = 0.14).
Two-year potassium citrate supplementation does not reduce bone turnover or increase BMD in healthy postmenopausal women, which suggests that alkali provision does not explain any long-term benefit of fruit and vegetable intake on bone.

Macdonald HM, Black AJ, Aucott L, Duthie G…
Am. J. Clin. Nutr. Aug 2008
PMID: 18689384 | Free Full Text

In summary, neither potassium citrate at 18.5 or 55.6 mEq/d nor 300 g self-selected fruit and vegetables/d influenced bone turnover or prevented BMD loss over 2 y in healthy postmenopausal women. Further work is required to investigate whether particular fruit and vegetables are important and how much of each is optimal for bone health.

Potassium Citrate Increases Calcium Levels in Adults

Abstract

Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women.

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 randomized, double-blind, placebo-controlled study, 52 men and women (mean age 65.2 ± 6.2 years) were randomly 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.

Moseley KF, Weaver CM, Appel L, Sebastian A…
J. Bone Miner. Res. Mar 2013
PMID: 22991267

Potassium Citrate Increases Bone Density and Volume in Adults

Abstract

Effect of potassium citrate on bone density, microarchitecture, and fracture risk in healthy older adults without osteoporosis: a randomized controlled trial.

The acid load imposed by a modern diet may play an important role in the pathophysiology of osteoporosis. Our objective was to evaluate the skeletal efficacy and safety and the effect on fracture prediction of K-citrate to neutralize diet-induced acid loads.
We conducted a randomized, double-blind, placebo-controlled trial at a teaching hospital.
Subjects included 201 elderly (>65 yr old) healthy men and women (t-score of -0.6 at lumbar spine).
Intervention was 60 mEq of K-citrate daily or placebo by mouth. All subjects received calcium and vitamin D.
The primary outcome was change in areal bone mineral density (aBMD) at the lumbar spine by dual-energy x-ray absorptiometry after 24 months. Secondary endpoints included changes in volumetric density and microarchitectural parameters by high-resolution peripheral quantitative computed tomography in both radii and both tibiae and fracture risk assessment by FRAX (Switzerland).
K-citrate increased aBMD at lumbar spine from baseline by 1.7 ± 1.5% [95% confidence interval (CI) = 1.0-2.3, P < 0.001] net of placebo after 24 months. High-resolution peripheral quantitative computed tomography-measured trabecular densities increased at nondominant tibia (1.3 ± 1.3%, CI = 0.7-1.9, P < 0.001) and nondominant radius (2.0 ± 2.0%, CI = 1.4-2.7, P < 0.001). At nondominant radius, trabecular bone volume/tissue volume increased by 0.9 ± 0.8%, (CI = 0.1-1.7), trabecular thickness by 1.5 ± 1.6% (CI = 0.7-2.3), and trabecular number by 1.9 ± 1.8% (CI = 0.7-3.1, for all, P < 0.05). K-citrate diminished fracture prediction score by FRAX significantly in both sexes.
Among a group of healthy elderly persons without osteoporosis, treatment with K-citrate for 24 months resulted in a significant increase in aBMD and volumetric BMD at several sites tested, while also improving bone microarchitecture. Based on the effect on fracture prediction, an effect on future fractures by K-citrate is possible.

Jehle S, Hulter HN, Krapf R
J. Clin. Endocrinol. Metab. Jan 2013
PMID: 23162100

Despite the conflicting evidence for the acid load theory, potassium or citrate nonetheless appear to increase bone density. How it does that is debated.

Bicarbonate, but Not Potassium, Decreases Resorption

Abstract

Treatment with potassium bicarbonate lowers calcium excretion and bone resorption in older men and women.

Bicarbonate has been implicated in bone health in older subjects on acid-producing diets in short-term studies.
The objective of this study was to determine the effects of potassium bicarbonate and its components on changes in bone resorption and calcium excretion over 3 months in older men and women. Design, Participants, and Intervention: In this double-blind, controlled trial, 171 men and women age 50 and older were randomized to receive placebo or 67.5 mmol/d of potassium bicarbonate, sodium bicarbonate, or potassium chloride for 3 months. All subjects received calcium (600 mg of calcium as triphosphate) and 525 IU of vitamin D(3) daily.
Twenty-four-hour urinary N-telopeptide and calcium were measured at entry and after 3 months. Changes in these measures were compared across treatment groups in the 162 participants included in the analyses.
Bicarbonate affected the study outcomes, whereas potassium did not; the two bicarbonate groups and the two no bicarbonate groups were therefore combined. Subjects taking bicarbonate had significant reductions in urinary N-telopeptide and calcium excretion, when compared with subjects taking no bicarbonate (both before and after adjustment for baseline laboratory value, sex, and changes in urinary sodium and potassium; P = 0.001 for both, adjusted). Potassium supplementation did not significantly affect N-telopeptide or calcium excretion.
Bicarbonate, but not potassium, had a favorable effect on bone resorption and calcium excretion. This suggests that increasing the alkali content of the diet may attenuate bone loss in healthy older adults.

Dawson-Hughes B, Harris SS, Palermo NJ, Castaneda-Sceppa C…
J. Clin. Endocrinol. Metab. Jan 2009
PMID: 18940881 | Free Full Text

Supplementation with potassium did not significantly alter calcium excretion or markers of bone turnover in this study. This is in contrast to earlier reports of Lemann et al. (19) and Jones et al. (20) who found that increasing potassium intake decreased urinary calcium excretion. The apparently conflicting observation that higher potassium intake is associated with higher BMD in healthy perimenopausal women (21) may result from the fact that potassium-rich diets tend to be alkali-producing, in that they are rich in fruits and vegetables. Treatment with potassium did enhance sodium excretion, as has been documented widely.

In conclusion, we have found that reducing the acidogenicity of the diet into the alkali-producing range with bicarbonate lowers calcium excretion and the bone resorption rate in healthy older men and women consuming rather typical acid-producing American diets. Treatment with 67.5 mmol/d of potassium bicarbonate was safe and well tolerated in this population. Increasing intake of alkali merits further consideration as a safe and low-cost approach to improving skeletal health in older men and women.

Potassium Citrate Reduces Resorption in Postmenopausal Women

Abstract

Effects of potassium citrate supplementation on bone metabolism.

Western diets rich in animal protein result in long-term acid loading that, despite corresponding increases in net renal acid excretion, may induce a chronic state of acidemia. This may have deleterious effects on both the kidney and bone, by increasing the risk of calcium stone in the former and leading to chemical dissolution of mineral alkaline salts in the latter. Whereas supplementation with alkaline citrate has been shown to reduce stone recurrences, its effect on bone turnover has received less attention. The aim of the present study was to evaluate whether potassium citrate favorably affects bone turnover markers in postmenopausal females with low bone density. Thirty women, aged 58 +/- 8.1 years, were enrolled and studied on basal conditions and after a 3-month course of potassium citrate supplementation (0.08-0.1 g/kg b.w. daily). Twenty-two women concluded the study while 8 withdrew. Twenty-four age-matched healthy women were taken as control cases. All were evaluated for electrolyte and acid-base balance-related parameters, bone turnover, markers and renal function. A significant decrease in net acid excretion was observed upon citrate supplementation, and this was paralleled by a significant decrease of urinary deoxypyridinolines, hydroxyproline-to-creatinine ratios, and, to a lesser extent, serum osteocalcin. Percent variations of urine citrate were inversely related to those of deoxypyridinolines and hydroxyproline. No change in these chemistries occurred in the control group. Our results suggest that treatment with an alkaline salt, such as potassium citrate, can reduce bone resorption thereby contrasting the potential adverse effects caused by chronic acidemia of protein-rich diets.

Marangella M, Di Stefano M, Casalis S, Berutti S…
Calcif. Tissue Int. Apr 2004
PMID: 15255069

Review: Potassium and Osteoporosis

Abstract

Potassium and health.

Potassium was identified as a shortfall nutrient by the Dietary Guidelines for Americans 2010 Advisory Committee. The committee concluded that there was a moderate body of evidence of the association between potassium intake and blood pressure reduction in adults, which in turn influences the risk of stroke and coronary heart disease. Evidence is also accumulating of the protective effect of adequate dietary potassium on age-related bone loss and reduction of kidney stones. These benefits depend on organic anions associated with potassium as occurs in foods such as fruits and vegetables, in contrast to similar blood pressure-lowering benefits of potassium chloride. Benefits to blood pressure and bone health may occur at levels below current recommendations for potassium intake, especially from diet, but dose-response trials are needed to confirm this. Nevertheless, intakes considerably above current levels are needed for optimal health, and studies evaluating small increases in fruit and vegetable intake on bone and heart outcomes for short periods have had disappointing results. In modern societies, Western diets have led to a decrease in potassium intake with reduced consumption of fruits and vegetables with a concomitant increase in sodium consumption through increased consumption of processed foods. Consumption of white vegetables is associated with decreased risk of stroke, possibly related to their high potassium content. Potatoes are the highest source of dietary potassium, but the addition of salt should be limited. Low potassium-to-sodium intake ratios are more strongly related to cardiovascular disease risk than either nutrient alone. This relationship deserves further attention for multiple target tissue endpoints.

Weaver CM
Adv Nutr May 2013
PMID: 23674806 | Free Full Text

The full text includes several pages about osteoporosis. This is just the final summary at the end of that section:

In summary, benefits of potassium on bone are seen typically when given as organic salts at relatively high doses of 60 to 90 mmol/d (2400–3600 mg/d). Organic salts of potassium reduce urinary calcium loss and improve calcium balance at these levels. But whether that is related to protection against skeletal buffering of an acidogenic diet is still a topic for debate. Perhaps acid-base balance is not the mechanism in healthy kidneys, but as kidney function declined with age, it may be an important mechanism. The glomerular filtration rate declines by as much as 50% from age 20 to 80 y (68), or perhaps excess acid only affects bone through interaction with receptors on bone cells to stimulate bone turnover, and this process is reduced by the alkaline organic salts of potassium.