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Potassium Intake and the Calcium Economy

Creighton University, Osteoporosis Research Center, Omaha, Nebraska

Address correspondence to: Karen Rafferty, R.D., Creighton University, 601 North 30^th Street, Suite 5766, Omaha, NE 68131. E-mail: karenrd{at}creighton.edu

	ABSTRACT

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Background: Dietary potassium intake (K) lowers urinary calcium (Ca) excretion and, in short-term studies, may improve Ca balance.

Purpose: Our objective was to assess K effects on the Ca economy under steady-state conditions.

Design: 8-day, inpatient metabolic studies of nitrogen, phosphorus, and Ca balance, combined with dual isotopic Ca tracer kinetics studies. Study diet matched to prestudy nutrient intakes.

Subjects: 191 single women studied from 1–5 times at 5-year intervals, for a total of 644 inpatient studies. Median age at time of study: 50.2 yrs; 301 studies were performed postmenopausally without hormone replacement; 343 were either premenopausal or postmenopausal but on estrogen replacement therapy.

Results: Dietary K was highly significantly associated with urinary Ca excretion, with a coefficient of –0.0109 mmol urine Ca/mmol diet K. However, dietary K was negatively correlated with dual-tracer Ca absorption (coefficient for Ca absorption fraction: –0.00094/mmol dietary K), and was not associated with urine Ca after adjustment for Ca absorption.

Conclusion: While a high K diet (i.e., one rich in fruits, vegetables, and dairy products) has multiple health benefits and clearly lowers urine Ca, it does not seem to exert any appreciable net influence on the Ca economy, largely because the reduced calciuria is offset by reduction of intestinal absorption. We note, however, that since the high K intakes in our studies come more from milk and meat than from fruits and vegetables, we cannot exclude a possible balance effect for different food sources of K.

Key words: urine calcium, calcium balance, potassium, calcium absorption, renal net acid excretion

	INTRODUCTION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Of the many factors that might contribute to an increased risk of osteoporosis and osteoporosis-related fractures, nutritional factors are significant because they are modifiable. The benefit of achieving an adequate intake of calcium and vitamin D is well documented. To a lesser extent other dietary components such as fiber, magnesium, vitamin K, sodium, and potassium have also been studied for their effects on bone health.

In the U.S. Food Guide Pyramid, foods are grouped according to similarities in nutrient composition. The major dietary source of both calcium and vitamin D in the U.S. diet is the dairy group—milk and milk products. In studies of the effects of other food and nutrient groups on diet-disease relationships, there is considerable evidence from cancer epidemiology studies of a beneficial effect of fruits and vegetables in reducing cancer risk [1]. Williams et al. showed that frequent consumption of vegetables throughout the year was inversely associated with the risk of Type 2 diabetes [2]. Bazzano et al. reported in the first NHANES epidemiological follow-up study that frequency of fruit and vegetable consumption was inversely associated with stroke incidence, stroke mortality, ischemic heart disease mortality, CVD mortality, and all-cause mortality in the general U.S. population [3]. Nutrition epidemiologic studies in Japan and Finland have shown similar associations [4,5]. And Appel et al. reported that a diet rich in fruits and vegetables has a favorable affect on blood pressure in both normotensive and hypertensive adults [6]. Fruits and vegetables are major sources of diet potassium, and potassium (K) has itself been reported to exert a protective role on bone and the Ca economy. This effect, however, is less clearly established than, for example, K’s role in hypertension.

Because calcium balance is a function of calcium intake, calcium absorption, and calcium excretion, factors influencing each of these functions must be considered for their impact on bone health. Dietary factors which affect the amount of Ca lost in urine are as significant for the calcium economy as dietary factors affecting Ca intake and Ca absorption. For example, in acute, short-term studies ranging from 3 hours’ to 8 weeks’ duration, K (from foods or salts of K as the citrate or bicarbonate) has been reported to reduce urinary Ca losses [6–17] and improve Ca balance [7,11]. Whether these effects would persist is unknown.

This study was undertaken to evaluate the steady state effects of dietary K on urinary Ca excretion and the other components of the Ca economy in healthy women at mid-life, studied on diets to which they had adapted over periods of months or years.

	SUBJECTS AND METHODS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Subjects
Data from our long-running prospective study of mid-life women were evaluated specifically to examine the effect of dietary K on urinary Ca excretion and on Ca balance (and its component fluxes). The participants themselves have been characterized previously [18]. The study was approved by the Creighton University Institutional Review Board and each participant gave written consent. Studies in women with medical conditions affecting the Ca economy or using medications (such as diuretics) that would be predicted to alter K handling were excluded.

Protocol
As previously reported [18], 191 women participated in 8-day, inpatient balance studies approximately every five years over a 25 year period. Each woman contributed from one to five data sets for this analysis. Of the resulting 707 data sets, treated as quasi-independent because multiple visits were 5–15 years apart, 644 met the medical inclusion criteria and had the requisite data for this analysis. All physiological measurements were made while subjects were inpatients, ingesting a constant diet, with full collection of excreta. Diets were calculated and prepared by the unit dietitian to be similar in nutrient composition to usual intakes analyzed from 7-day food records obtained prior to each admission. Dietary K intakes ranged from 1170–4524 mg/d (30–116 mmol/d), mean 2465 mg ± 493 (63.2 mmol/d ± 12.6) with K intakes coming mainly from foods with a counter ion equivalent to bicarbonate (HCO₃^–). The mean K intake in these studies was similar to national data for women (2355 mg/day, interquartile range of 1700–4700), as reported by the CDC National Center for Health Statistics [19].

Analytical Methods
Diet Ca, phosphorus (P), and nitrogen were chemically analyzed by methods previously described [18]. The variable labeled "Ca intake" includes both food and medication Ca. Medication Ca comes mainly from tableting excipients, and was chemically analyzed in each instance, as previously described [20]. Studies involving non-food Ca intakes greater than 300 mg/d were excluded because of uncertain (and often poor) Ca bioavailability of such products over the years during which these data were accumulated [21]. Diet protein was calculated as analyzed diet nitrogen x 6.25. Ca absorption fraction was measured by the double-tracer method, as described previously [22].

For both diet K and meat protein, food table values (ESHA Food Processor Plus, Version 7.4, Salem, Oregon) were applied to the weighed quantities of each food item in the ingested, inpatient diet. The accuracy of this approach for K was validated by regressing food table values for the diets concerned on measured urine K in a subset of 123 balances. Urine K was 92% of estimated diet K (as would be predicted, since fecal K tends to average somewhat less than 10% of intake). r² for the relationship was 0.81. Renal net acid excretion (RNAE) was calculated from the diet variables by the method of Frassetto et al. [23]. Body surface area was calculated using the formula of DuBois & DuBois [24], i.e. SurfArea = 0.20247*(Ht^0.725)*(Wt^0.425).

The physiological model incorporating the various Ca intake and output variables can be succinctly stated as follows:

(1)

where AbsFx = the double isotope absorption fraction [22], Cau = urine calcium (mmol/d), and TIC = total endogenous calcium entering the intestinal tract (digestive secretions plus shed mucosa) (mmol/d). Eq. 1 is a somewhat more complex formulation than the usual expression for an external mineral balance, but all of its components are necessary to represent the relevant fluxes that might be affected by K. The other variables of importance in this analysis are defined or calculated as follows:

(2)

(3)

(4)

where EFC = endogenous fecal Ca (i.e., the unabsorbed, externally measurable component of TIC); Ca_F· = fecal Ca content of the I–V Ca tracer; and Ca_s = serum Ca specific radioactivity (i.e., the fraction of the I–V tracer dose/g Ca).

Statistics
Most of the statistical analyses were performed using SPSS for Windows, Version 11.5 (SPSS, Chicago, IL). Estrogen status (Estat) was coded as 1 for studies in premenopausal women or in postmenopausal women receiving hormone replacement therapy (HRT), and as 0 in postmenopausal women not receiving HRT. SPSS Routine "Frequencies" was used to obtain counts for Estat and the medians and percentiles for the other variables. Stepwise linear regression was used to model the dependencies of the individual components of the Ca economy, with P for entry set to 0.05. Additionally, because of the repeated measures inherent in our design, we reanalyzed the models generated by stepwise multiple regression, using PROC MIXED (SAS, Cary, NC), to be certain that within-subject correlation had not caused spurious associations. Additionally, we developed models based only on first studies for each participant (n = 178), thereby avoiding the bias possibly introduced by multiple measurements in some subjects. Only variables found to be significant predictors with at least two methods were retained in the final models. Finally, in order to show graphically the effect of K intake, we developed, for the two most important external components of the Ca economy (intestinal absorption and urinary loss), new dependent variables consisting of residuals from the models including all the significant predictor variables other than K intake. We then ran simple linear bivariate models regressing these sets of residuals against diet K.

	RESULTS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Table 1 sets forth descriptive statistics for the up to 644 sets of observations on which our analyses are based. Since many of the variables had skewed distributions, values for all are given as medians, with 5^th and 95^th percentiles. Median age at study was 50.2 years; 301 of the studies were conducted in postmenopausal subjects without estrogen replacement (Estat = 0) and 343 in women either premenopausal at study or postmenopausal but receiving estrogen replacement (Estat = 1). Median Ca intake was similar to, but slightly higher than the NHANES-III value for this age range, and K intake, as noted above, was also close to the NHANES-III value. Protein intake was almost exactly 1 g/kg body weight, somewhat above the RDA, but, as with Ca and K, very similar to that reported for mid-life women in NHANES-III. Relative to total energy, protein accounted for 14.7% of calories.

Table 2 sets forth the various multivariate regression models developed to explain the variability in each of the components of Ca balance. Models for each of the dependent variables are discussed briefly below.

View larger version (31K): [in this window] [in a new window]   Fig. 1. The residuals from a linear regression model of urine Ca on diet Ca and Estat, plotted against diet K. The line represents the least squares fit, plus and minus its 95% confidence interval. r2 = 0.0114 (P < 0.005). (Copyright, 2004, Robert P. Heaney. Used with permission.)

View larger version (29K): [in this window] [in a new window]   Fig. 2. The residuals from a linear regression model of AbsFx on log of diet Ca, diet P, Surface area, and Estat, plotted against diet K. The line represents the least squares fit, plus and minus its 95% confidence interval. r2 = 0.0095 (P = 0.003). (Copyright, 2004, Robert P. Heaney. Used with permission.)

Calcium Balance
In order to determine whether the K-associated decrease in urine Ca was reflected in a more positive overall Ca balance, we developed models for Ca balance using nutrient intakes, age, body size variables, and estrogen status (Estat). But the only significant determinants of Ca balance were Estat, age, and Ca intake. The coefficient for K intake actually had a negative sign, but was only marginally significant (P = 0.06). This negative effect reflects the fact that, at prevailing Ca intakes, the effect on absorption fraction produced a numerically slightly greater decrease in absorbed Ca than the Ca-sparing effect on urine Ca loss.

Total Intestinal Calcium
We next investigated the determinants of the Ca entering the digestive stream from endogenous sources (GI secretions plus shed mucosa, termed "TIC"). Diet P, height, and meat protein intake were independent predictors (adjusted R² = 0.259). But, as with balance, the association of K intake with TIC was not significant.

Endogenous Fecal Calcium (EFC)
Although not a direct component of balance as usually formulated, EFC is the measurable component of TIC (which does figure in Eq. 1). Hence we developed models for it as well. In this data set, the significant independent predictors of EFC were diet P, AbsFx, height, meat protein, and diet K (P < 0.001) (adjusted R² = 0.403). The coefficient of the K term was +0.00475 mmol^–1 (P < 0.005), which indicates an increase in EFC loss as K intake rises, consistent with the negative effect, noted above, on Ca absorption fraction.

	DISCUSSION

 
The positive effect of the administration of alkaline salts of K on Ca metabolism has been documented in a large number of studies, involving children, adults of both sexes, blacks and whites, and women of pre- and postmenopausal status [6–17]. These studies show that low K intakes are associated with increased urine Ca excretion and that high K intakes are associated with reduced urine Ca excretion. Table 3 lists the variously reported effect sizes for studies that were based on 24-hr urine Ca measurements, incorporating our own data from this paper in the last row. The weighted average effect size for all studies combined was –0.015 mmol urine Ca/mmol K intake. While our data produce the lowest coefficient of the series, the range of reported values for this effect is nevertheless fairly narrow and consistent across all studies. Thus, insofar as the urinary Ca effect is concerned, one can conclude that acute studies yield much the same answer as studies performed under steady state, equilibrium conditions. At the same time, Figs. 1 and 2 show graphically that, while the K effect is statistically significant, it amounts for only about 1 percent of the variability in the Ca movement concerned.

It has been hypothesized that alkaline salts of K preserve Ca by serving as a buffer for endogenous acid production. It is known that alkaline salts of K reduce net endogenous acid production, and that urinary Ca excretion correlates significantly with net acid excretion [10,11,17,26,27]. Frassetto et al. showed that net acid excretion can be predicted by the quotient of dietary protein to K, and further that net renal acid excretion is predictive of urinary Ca excretion [23].

In this view, dietary K is actually a proxy for bicarbonate [28]. It is difficult to test this hypothesis fully in this data set. Our data permitted calculation only of RNAE, which is a function of protein and K intakes (and may not be the optimal formulation, inasmuch as it postulates that the relationship of K with variables of interest is hyperbolic). Some evidence supporting a role for acid production can be found in the fact that, in our data, RNAE was significantly positively correlated with urine Ca (P < 0.002), as has been reported by others [23]. However, in a multivariate model, K intake displaced RNAE. Similar evidence can also be found in the models for EFC. The best model (see Table 2) incorporates both diet K and meat protein. However, in a stepwise model RNAE enters in preference to either diet K or the protein intake variables, although the fit is somewhat less good with RNAE alone than with the combination of meat protein and K intake. Moreover, the coefficient of the RNAE term is negative, indicating that high RNAE reduces EFC. Although acid production from protein is generally attributed to its S-containing amino acids, there are other net acid precursors in meat that are not found, for example, in dairy protein, and this distinction may be the basis for the seeming preference of the model for meat protein.

Other indices of bone health, namely bone mineral density (BMD) and rate of bone turnover, have been reported to vary directly with fruit and vegetable consumption. A high past intake of fruit was significantly associated with high femoral neck BMD in postmenopausal women [29], and with BMD at the spine and trochanter in premenopausal women [30]. Similarly, alkali-producing dietary components—fruits and vegetables—have been shown in observational studies to contribute to maintenance of BMD in the elderly [31]. In men, K has been shown to correlate positively with BMD of total body and lumbar spine [32] and urinary K is positively associated with BMD in healthy Ca-replete children [33]. Significant reduction in bone turnover by measurement of serum and urine markers of bone resorption and formation in response to K has also been reported [11,17,29,34].

Those individuals who typically have the highest K intakes, and often the highest net alkaline producing diets, are vegans [35]. The acid/alkaline ash characteristic of their diets will vary depending upon the proportion of cereal grains and soy products in the overall diet (with soy being low in net acid production, and various cereal grains, high). But K intake would be high either way. One might speculate therefore that vegans would have stronger or denser bones than omnivores. Yet of the many epidemiological reports relating bone health to animal- or vegetable-based diets, almost all have found either no differences in BMD between vegetarians and nonvegetarians [36–39] or a lower BMD in vegan groups [40–42]. Kohlenberg-Mueller showed positive Ca balance in both vegan and lactovegetarian diets, with no difference in markers of bone resorption in the two groups [43].

Unlike Lemann et al. [7] and Sebastian et al. [11], we did not find an association of K intake with Ca balance. In contrast with these relatively short-term studies using a pure K salt in a small group of subjects, our data have been derived from a larger cohort of women getting their K entirely from food sources, at an intake level matched during study to their usual, self-selected diets (see Table 3). We observed a Ca-sparing effect on urinary loss similar to that reported by Lemann and Sebastian and their colleagues, but found that intestinal absorption was reduced as well. A very similar reciprocal behavior of urine Ca and intestinal absorption with longer term adaptation was reported by Sakhaee et al. in women treated with thiazide diuretics for six months [44]. At the end of the treatment period in their study, urine Ca had declined by 1 mmol, but intestinal absorption efficiency had declined as well—sufficiently, in fact, to negate completely any gain related to the decreased urinary loss. Our failure to find an effect of K intake on urine Ca in models using absorbed Ca as the predictor variable suggests that, at least under equilibrium conditions, absorbed Ca is the driving influence.

Given the inherent noisiness of the balance measurement, failure to find a positive balance might have been due to insufficient power. However, in these studies we used a tracer-based, computed balance, which is inherently more precise [45] than the classical measured balance method used by Lemann and Sebastian and their colleagues. So it is unlikely that we missed a balance effect.

The net effect of the two countervailing associations of K intake with the Ca fluxes involved in balance can be best illustrated with a concrete example. Assume a Ca intake close to the median for our subjects (e.g., 15 mmol/d). Increasing K intake by the amount of K in one 6 ounce (170 g) baked potato (20 mmol K) would result in a reduction in Ca absorption from other foods of 0.282 mmol/d, plus an added 0.096 mmol/d from endogenous Ca entering the digestive stream (TIC), or 0.378 mmol/d in all. At the same time, the extra K would be associated with reduced urinary Ca loss, amounting to 0.218 mmol/d. The calculated net difference is –0.160 mmol/d (6.4 mg/d). In brief, the reduced renal loss is somewhat less than, but numerically close to, the reduced absorption, effectively eliminating any appreciable net balance change.

It may be worth noting in passing that, at the time our data were gathered, the US RDA for K was 2000 mg (51 mmol)/day. At a median consumption of 61.6 mmol K/day in our cohort, the US RDA was exceeded. However, compared with the more recent DRI, in which the recommended daily K intake was increased to 4700 mg (120 mmol)/day [46], our cohort achieved a K intake only 51% of the reference value. Of further interest, at the mean K consumption reported, fruits and vegetables accounted for 44% of the total dietary K, with milk accounting for 10%, and meat, 17% of total dietary K. We looked separately at the dietary sources of K for those subjects whose usual dietary K intake exceeded 3500 mg (90 mmol)/day (N = 11). In this higher K group, fruits and vegetables accounted for 37% of dietary K, but milk and meat accounted for 47%, nearly half the total daily K intake. None of the subjects in the total cohort had a dietary K intake at the current AI of 4700 mg (120 mmol)/day.

	CONCLUSION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
We found that K intake reduced urine Ca excretion, amounting to 0.0109 mmol Ca conserved/mmol ingested K, somewhat lower than, but generally similar in size to, the effect previously reported by others. However, we did not find a Ca balance effect, largely because intestinal Ca absorption was affected in the opposite direction. We suggest that physiological adaptation to dietary input over time accounts for the difference in outcome between this study and results reported in short-term intervention trials. However, in contrast to other studies similarly based on a whole foods model, in which the dietary K source was primarily fruits and vegetables, we need to note that in our cohort, milk and meat were major contributors to K intake. To the extent, therefore, that K may be a proxy for something in fruits and vegetables, our failure to find a balance effect cannot safely be extrapolated to a fruit and vegetable rich diet. Nevertheless, insofar as the effect on urine Ca is concerned, K in our diets exhibited effects similar to those reported for both natural foods and pure K salts in other studies.

	ACKNOWLEDGMENTS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Work supported by Health Future Foundation and NIH (AR07912). The authors acknowledge with gratitude the help of Gleb Haynatzki, Ph.D. and Vera Haynatzka, Ph.D., with the statistical modeling.

Received January 7, 2004. Accepted May 25, 2004.

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TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 

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