Review

Role of Dietary Sodium in Osteoporosis

Robert P. Heaney, M.D.

Creighton University, Omaha, Nebraska
Key words: sodium, salt, calcium, calciuria, osteoporosis, calcium requirement

Sodium, in the form of sodium chloride, elevates urinary calcium excretion and, at prevailing calcium
intakes, evokes compensatory responses that may lead to increased bone remodeling and bone loss. The calciuria
is partly due to salt-induced volume expansion, with an increase in GFR, and partly to competition between
sodium and calcium ions in the renal tubule. Potassium intakes in the range of current recommendations actually
reduce or prevent sodium chloride-induced calciuria.
At calcium intakes at or above currently recommended levels, there appear to be no deleterious effects of
prevailing salt intakes on bone or the calcium economy, mainly because adaptive increases in calcium absorption
offset the increased urinary loss. Such compensation is likely to be incomplete at low calcium intakes. Limited
evidence suggests equivalent bone-sparing effects of either salt restriction or augmented calcium intakes. Given
the relative difficulty of the former, and the ancillary benefits of the latter, it would seem that the optimal strategy
to protect the skeleton is to ensure adequate calcium and potassium intakes.

Background recall that “exchangeability” means a bi-directional movement of

The adult human body contains from 90 to 130 g sodium
[1]. Roughly half of that is in bone, and the bulk of the
remainder is in extracellular fluid (ECF), where it plays a
crucial role in determining the osmolality of the milieu interior.
About half of bone sodium is exchangeable with ECF sodium;
by contrast, less than 1% of bone calcium exchanges with ECF
calcium ions. This large difference in exchangeability indicates
that bone sodium is located quite superficially, i.e., on the
surfaces of crystals that are themselves located on microana-
tomic bone surfaces. Bone sodium is not known to play a
critical role in bone material properties or in calcium homeosta-
sis. Its presence in bone is generally attributed to the fact that
it is the principal cation of the ECF that bathes the bone-
forming site during its mineralization. As such, some of the
ECF sodium is simply trapped as ECF water is displaced by
growing calcium phosphate crystals. Probably because of its
superficial location, some bone sodium is mobilized in sys-
temic acidosis, approximately in parallel with the mobilization
of bone carbonate (which is also superficially located). While
some investigators suggest that bone sodium plays a role in total
body sodium homeostasis, the majority view is that bone is at most
a passive participant in ECF sodium homeostasis. It is important to
ions— one ion into bone for each one out. Thus “exchangeability”
is not the same as, and does not connote, “availability”.
The nutritional requirement for sodium has been set most
recently at 1500 mg (65 mmol)/d [2]. This is almost certainly
higher than actual need, as indigenous peoples of the Amazon
basin, for example, ingest less than one-tenth that amount [3].
At the same time, the estimated requirement is substantially
less than the quantities usually ingested in developed nations.
The nations of Europe and North America have median sodium
intakes that range from about 2300 mg (100 mmol)/d on the
low side to about 4300 (187 mmol) on the higher end [3]. East
and Southeast Asian societies have median sodium intakes as
high as 5300 – 6000 mg (230 –260 mmol)/d. Ingested sodium
serves several functions in addition to its essential nutrient role
(i.e., replacing excretory and cutaneous losses that would oth-
erwise threaten intravascular volume). Sodium added to foods
enhances desirable flavors, masks unpleasant flavors, improves
texture, inhibits bacterial action, and controls yeast fermenta-
tion. Often high salt foods do not taste “salty”, as the added salt
is serving other functions. A good example is found in the dry
cereal, Cheerios™, which does not taste salty, but contains
more than twice as much salt per serving as do potato chips,
which do have a distinctly salty taste.

Address reprint requests to: Robert P. Heaney, M.D., John A. Creighton University Professor, Creighton University, 2500 California Plaza, Omaha, Nebraska 68178.
E-mail: rheaney@creighton.edu

Journal of the American College of Nutrition, Vol. 25, No. 3, 271S–276S (2006)
Published by the American College of Nutrition

271S
Dietary Sodium in Osteoporosis
Sodium-Calcium Interactions
While within the skeleton sodium and calcium interactions
are probably of minor importance, a more significant, and
certainly better studied interaction of sodium and calcium oc-
curs at the level of diet, and in the subsequent processing of the
absorbed dietary minerals. As long ago as 1937 Aub et al.
observed that sodium chloride increased urine calcium [4], and
in 1961 Walser showed that sodium and calcium competed for
the same reabsorption mechanism in the proximal renal tubule
[5]. This means that an increase in the filtered load of either
sodium or calcium leads to increased excretion of both ions,
thereby establishing the mechanistic basis by which a sodium
load produces calciuria. However, McCarron et al. [5a] showed
that high salt intakes resulted in volume expansion and an
increase in filtered calcium load, and attributed the sodium-
induced calciuria to that mechanism.
A possible role for sodium intake in the pathogenesis of
osteoporosis was first emphasized by Goulding who, in a series
of animal and human experiments, showed that sodium intake
could affect bone mass in animals, and that the effect required
a functioning parathyroid apparatus [6 –10].
The effects of sodium on the calcium economy are nicely
summarized in several review papers [11–13]. My purpose here
is to bring these reviews up to date by focusing principally on
more recent reports. Numerous studies have found statistically
significant positive and quite consistent correlations between
24-h urine sodium excretion and 24-h urine calcium [4,7–9,14 –
23]. Taken together, the available studies indicate that urine
calcium rises by from 0.5 to 1.5 mmol (20 – 60 mg) for every
100 mmol (2300 mg) sodium ingested. Most reviewers have
used the mid point of that range (i.e., 1.0 mmol/100 mmol) to
characterize the effect. In most studies the calciuric effect of
increased sodium intake has been found in most or all subjects.
However, Ginty et al. [23a] reported a substantial subset of
their subjects who exhibited absolutely no calciuria in response
to sodium loading. By contrast, Evans et al. [23b] reported a
calciuric response in every one of their subjects. The reasons
for these reported differences in individual response are un-
clear, but could possibly reflect differences in volume expan-
sion in response to sodium loading [5a].
Given the fact that contemporary North American sodium
intakes generally fall between 100 and 200 mmol/d (i.e., 2300 –
4600 mg/d), it follows that approximately 1.0 to 2.0 mmol
(40 – 80 mg) of the 24-h total urine calcium excretion is being
pulled out of the body by sodium. Ho et al. [22] concluded that
sodium intake was the principal determinant of urine calcium in
Hong Kong Chinese, and Matkovic et al. [23] came to a similar
conclusion for pubertal girls in the U.S. Itoh and Suyama [14],
in a study of nearly 900 Japanese adults in whom sodium
intakes tend to be much higher than in Europe or North Amer-
ica, found a positive correlation between sodium intake and
urine calcium in both sexes, and across all age groups, even
272S
after adjusting for weight and for dietary intakes of protein,
phosphorus, and calcium.
Thus, on prevailing diets, sodium intake accounts for much
of the obligatory urinary loss of calcium from the body, and it
would be for this reason that sodium intake might play a role in
the pathogenesis of osteoporosis. Clearly, if absorbed calcium
is less than the amount needed to offset this loss (in addition to
what is needed to cover bone building and cutaneous and
digestive juice losses), then bone mass must suffer. Moreover,
the remodeling activity needed to release calcium from bone
would also be elevated. Both low mass and high remodeling are
now recognized as risk factors for osteoporotic fractures [24].
It would be expected that increased urinary calcium loss
following a sodium load would produce a fall in extracellular
fluid calcium ion concentration. Such a fall would, in turn,
produce a rise in parathyroid hormone secretion, with a conse-
quent increase in synthesis of 1,25(OH)2D3, and ultimately in
both calcium absorption efficiency and bone remodeling activ-
ity. The predicted changes have been found in some, but not all
studies [17,25]. Breslau et al. demonstrated that a change in
urine calcium evoked the predicted directional change in serum
PTH in serum 1,25(OH)2D3 concentration, and in calcium
absorption efficiency as well, at least in premenopausal women
[17,19]. But they failed to observe changes in absorption in a
small study involving postmenopausal women. These findings
suggested, at least qualitatively, that premenopausal women
could handle the challenge of contemporary sodium intakes
with less skeletal impact than postmenopausal women and, by
implication, that sodium intakes may be contributing to post-
menopausal osteoporosis.
At least two groups of investigators have found that calcium
absorption efficiency rises with induced calciuria, as from a
sodium load [17,25], and falls with urine calcium, as from the
calcium-sparing effect of thiazides [26]. These changes indicate
that there is an at least directional adjustment for variations in
excretory loss, i.e., intestinal absorption rises when urine loss
increases, and falls when urinary loss is reduced. Breslau et al.
[17] reported that the change in absorption, while occurring in
normal subjects, did not occur in two patients with surgical
hypoparathyroidism, consistent with Goulding’s findings in
rats [6]. By contrast, Meyer et al. [25] did find an increase in
calcium absorption efficiency in two patients with hypopara-
thyroidism following a sodium load, suggesting, at least in
these individuals, that the response was mediated by some
mechanism other than increased PTH secretion. While the
discrepancy between these studies cannot be resolved with
available data, it does appear reasonably certain that, other
effects aside, a sodium load leads to increased PTH secretion
with all of its usual consequences (increased 1,25(OH)2D3
synthesis, increased calcium absorption, increased bone resorp-
tion, and improved renal tubular reabsorption of calcium). But
additional mechanisms may be operative as well.
What is critically important, but not precisely known, is
whether the absorptive compensation is quantitatively adequate
VOL. 25, NO. 3

to offset the high obligatory loss. Ultimately this depends upon
how high the dietary calcium intake may be. At typical calcium
intakes (e.g., about 600 mg (15 mmol)/d), women at mid-life
have a gross absorption efficiency of about 27% [27], and
endogenous fecal calcium (EFC) loss of about 110 mg (2.75
mmol)/d. Computing actual mass transfers, one notes that 27%
of 600 mg is a gross absorption of 162 mg (4 mmol). Against
the offset of EFC loss, that gain translates to net absorption of
52 mg (for a net absorption efficiency of about 9%). A rise in
sodium intake of 100 mmol/d will increase obligatory calcium
loss by about 1 mmol (40 mg)/d. To extract that much addi-
tional calcium from the diet would require a gross absorption
efficiency of 34%, or about a 25% increase in absorption
fraction above the mean for that intake. That may just barely be
possible at this calcium intake.
Closer to the extremes of calcium intake, the results are less
ambiguous. At an intake of about 300 mg (7.5 mmol) Ca/d
(about the 25th percentile for mid-life women), absorption
fraction averages about 37% [27], for a gross absorption of 111
mg (2.8 mmol). To offset an additional 40 mg (1 mmol) urinary
loss would require an increase in absorption efficiency to about
50%—very likely beyond the capacity of most middle-aged
women. By contrast, at an intake of 1200 mg/d (as currently
recommended after age 50), absorption efficiency averages
about 20%, for a gross absorption of 240 mg (6 mmol) and a net
absorption of about 120 mg (3 mmol). To offset an additional
40 mg (1 mmol), urinary loss would require an increased
absorption efficiency to only 23%— clearly feasible.
These quantitative considerations help to make sense of the
several reports indicating that the effects of sodium on various
bone status indicators are dependent upon calcium intake
[28,29]. In brief, if calcium intake is in the range currently
recommended, sodium intakes in the range prevailing in most
of the developed nations has little or no net effect on calcium
balance, since increased urinary calcium losses evoke adaptive
responses that result in improved dietary calcium extraction.
That protection fails when diet calcium is low.
Sodium and Bone
Several groups of investigators have shown that bone re-
modeling, as measured by various remodeling biomarkers, var-
ies inversely with sodium intake [7,9,20,30 –32] and that so-
dium restriction reduces excretion of resorption biomarkers.
This finding is consistent with and follows upon the effect of
sodium loads on increasing PTH secretion and is predictable
inasmuch as the elevation in PTH evoked by excess calcium
losses would inevitably increase bone remodeling. Evans et al.
[31a], in a small study, found the increase in resorption fol-
lowing one week of high sodium intake to be confined to
postmenopausal women, but the confidence limits for the rise
in pre- and postmenopausal women overlapped, and it is not
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION
Dietary Sodium in Osteoporosis
clear that the two groups differed significantly from one an-
other. Nevertheless, the larger rises in calciuria in the post-
menopausal women are consistent with other studies [e.g.,
17,191 indicating more effective compensation pre-menopause.
Often the observed increase in remodeling has been taken to
indicate that sodium increases bone loss, although this does not
necessarily follow, and there are few reports of a direct con-
nection between sodium intake and subnormal bone status in
humans at typical sodium intakes.
The very wide range in national salt intakes demonstrated in
Intersalt [3], most of them in considerable excess of probable
nutritional need, affords an opportunity to test salt’s role in the
pathogenesis of osteoporosis. But little or no association
emerges from such analyses. Finland and the United Kingdom,
with relatively high rates of osteoporosis, have lower salt
intakes than Hungary, Spain, or Malta, for example, with
generally lower rates of osteoporosis. Japan, with one of the
highest salt intakes of a developed nation, has substantially
fewer hip fractures than European Caucasian populations.
However, all such ecologic studies are fraught with difficulty.
Good estimates of true osteoporosis prevalence are not avail-
able for many of the populations studied by Intersalt, and, more
importantly, these populations differ widely in genetic suscep-
tibility to osteoporosis, vitamin D status, and calcium intake,
among other critical variables. Nevertheless, the data available
from Intersalt certainly do not point to a strong pathogenetic
role for salt.
However, there is at least one case report of probably
salt-associated osteoporosis [33]. A 50-year-old postmeno-
pausal woman with adequate hormone replacement therapy had
high turnover osteoporosis with vertebral compression frac-
tures and a urine calcium in excess of 7.5 mmol/d (300 mg).
She was observed in the hospital to be using table salt from a
paper bag, in quantities so large as to make the food on her
plate white, and she reported having done so for the previous 20
years. Therapeutic reduction in salt intake reduced her urinary
calcium loss to below 2.5 mmol (100 mg)/d. Presumably, if salt
is a factor in the pathogenesis of osteoporosis, it is acting by its
calciuric effect, at least in individuals at typical calcium in-
takes, where absorptive adaptation would be insufficient to
compensate for excess losses of the magnitude observed in this
patient.
Whether clinically significant bone loss actually occurs at
more typical salt intakes has been the subject of very few
studies. Greendale et al. found no association between sodium
intake from diet records and bone status 15 years later [34].
Sodium intakes in their subjects averaged about 150 mmol
(3450 mg)/d in men and 112 mmol (2576 mg)/d in women.
However, estimates of sodium intake from diet records corre-
late poorly with actual sodium intake, and thus this negative
finding cannot absolve sodium intake in this connection. Ac-
curate estimates of sodium intake require measurement of 24-h
urine sodium, preferably over a several day interval. This need
273S
Dietary Sodium in Osteoporosis
Fig. 1. Effects of various sodium and potassium salts on urine calcium.
(Copyright Robert P. Heaney, 2003. Used with permission.)
probably explains the scarcity of epidemiological studies test-
ing the association of sodium intake and bone mass.
Dawson-Hughes et al. [15], in a 4-year prospective study,
found the expected correlation between sodium intake (as mea-
sured by urinary sodium) and urinary calcium excretion in
healthy elderly men and women, but no correlation of sodium
intake with bone mineral density at any site, in either sex.
Sodium intakes in their study averaged 156 mmol (3600 mg)/d
in men, and 118 mmol (2700 mg)/d in women, i.e., fairly
typical for North America. In this study the authors reported
that the correlation between urine sodium and urine calcium
was strongest at high calcium intakes, while Nordin [11,12]
reported the opposite. There is no evident explanation for this
discordance. In any event, this failure by Dawson-Hughes, et
al. to find skeletal differences is suggestive of compensation for
the sodium-induced calciuria, as described above.
The principal human study linking high salt intake to bone
loss was by Devine et al. [35], who showed that change in bone
mineral density at the total hip and at an ultradistal ankle site
over a two year period was inversely related to sodium intake
estimated from urine sodium content. But they found no such
effect at the spine, femoral neck, intertrochanteric region, or
radius. From multiple regression models these investigators
calculated that halving the sodium intake of their subjects (from
⫺2000 to ⫺1000 mg/d) would have been predicted to obliter-
ate the hip bone loss. But in the same model, doubling of
calcium intake (i.e., raising it into the currently recommended
range) would have produced approximately the same beneficial
effect, without requiring a reduction in salt intake.
Potassium and Anion Effects
For the most part, when the papers cited in this review speak
of “sodium,” what is meant is “sodium chloride,” i.e. table salt,
the form in which about 90% of contemporary sodium intakes
are ingested. The accompanying anion is usually ignored. This
is probably a mistake. Berkelhammer et al. [36] showed clearly,
in patients receiving total parenteral nutrition (TPN), that sub-
stituting acetate for chloride in TPN solutions reduced urine
calcium losses dramatically. In oral feeding studies, Lutz [37]
showed that substituting sodium bicarbonate for sodium chlo-
ride promptly reduced urine calcium. Similarly, sodium bicar-
bonate loads do not induce an increase in urine calcium, unlike
274S
Fig. 2. Effect of a high salt load, with and without supplemental
potassium citrate, on 24-hr urine calcium excretion in postmenopausal
women. The low salt regimen provided 87 mmol (5 g) salt/d and the
high salt, 225 mmol (13.2 g)/d. The potassium supplement provided 90
mmol (29.2 g) potassium citrate/d. N ⫽ 26 for each of the treatment
groups. The rise in urine calcium on the high salt regimen was highly
statistically significant (P ⬍ 0.005). Plotted from the data of Sellmeyer
et al. [39]. (Copyright Robert P. Heaney, 2003. Used with permission.)
sodium chloride [37,38]. Fig. 1 illustrates, schematically, the
differing effects on urine calcium of various sodium and po-
tassium salts.
These data indicate that the anion is important, at least for
the understanding of what is happening. Nevertheless it re-
mains true that contemporary diet sodium is overwhelmingly in
the form of sodium chloride, and as such is usually hypercal-
ciuric in its effect. Even this statement, however, is not abso-
lute. Oral potassium (as the citrate) completely blocks the
calciuria of a large sodium chloride load (Fig. 2) [39]. It is
believed that both the potassium cation and the bicarbonate
anion (to which citrate is metabolized) work in the distal renal
tubule facilitating reabsorption of the extra calcium not re-
claimed in the proximal tubule because of competition with
sodium for the transport mechanism.
However, just as the undoubted effects of sodium on urine
calcium have not yet been unambiguously shown to have
corresponding effects on bone, so, similarly, amelioration of
those effects by potassium (or bicarbonate) has not been clearly
shown to confer a skeletal benefit, although, in short-term
metabolic experiments, potassium bicarbonate does produce a
positive calcium balance shift [40,41].
Discussion
Summarizing the data available up to the year 2000, much
as has been done for more recent work in this brief review,
Burger et al. [42] concluded that a sodium-osteoporosis link
was still conjectural. Four years later, reviewing the additional
evidence accumulated in the interval, Prentice [43] came to
VOL. 25, NO. 3

essentially the same conclusion, summarizing as follows: “Cur-
rent healthy-eating advice to decrease sodium intake. . .is un-
likely to be detrimental to bone health. . .” Hardly a ringing
indictment of sodium as a cause of osteoporosis.
Based on the multiple regression model of Devine et al.
[35], one might tentatively conclude that contemporary sodium
intakes elevate the calcium requirement—at least for bone
status. However, the two reclamatory strategies suggested by
the Devine model are not equivalent. Higher calcium intakes
(i.e., in the range of currently recommended values) confer
numerous non-skeletal health benefits [44], while the advan-
tages of low sodium intakes, although widely touted, are at best
problematic [45]. Furthermore, from the standpoint of feasibil-
ity, higher calcium intakes are much easier to achieve and
sustain than are reductions in sodium intake of the magnitude
required to offset sodium’s effect on obligatory urinary calcium
excretion [46].
Finally, one must note that, even if sodium’s effect on bone
mass is normally compensated for by adaptive increases in
calcium absorption (or by high calcium intakes), any accom-
panying increase in bone remodeling may constitute a risk
factor for fracture [24]. The reduction in remodeling activity
produced by high calcium intakes provides protection against
that mechanism of fragility. In any event, choosing one or the
other of the options offered by the Devine model would cer-
tainly seem to be more prudent than doing neither.
REFERENCES
1. Maxwell MH, Kleeman CR: “Clinical Disorders of Fluid and
Electrolyte Metabolism.” New York: McGraw-Hill, 1962.
2. Food and Nutrition Board, Institute of Medicine: “Dietary Refer-
ence Intakes for Water, Potassium, Sodium, Chloride, and Sul-
fate.” Washington, DC: National Academies Press, 2004.
3. Intersalt Cooperative Research Group: Intersalt: an international
study of electrolyte excretion and blood pressure. Results for 24
hour urinary sodium and potassium excretion. Br Med J 297:319–
328, 1988.
4. Aub JC, Tibbetts DM, McLean R: The influence of parathyroid
hormone, urea, sodium chloride, fat and of intestinal activity upon
calcium balance. J Nutr 113:635–655, 1937.
5. Walser M: Calcium clearance as a function of sodium clearance in
the dog. Am J Physiol 200:769–773, 1961.
5a. McCarron DA, Rankin LI, Bennett WM, Krutzik S, McClung
MR, Luft FC: Urinary calcium excretion at extremes of sodium
intake in normal man. Am J Nephrol 1:84–90, 1981.
6. Goulding A: Effects of dietary NaCl supplements on parathyroid
function, bone turnover and bone composition in rats taking re-
stricted amounts of calcium. Miner Electrolyte Metab 4:203–208,
1980.
7. Goulding A: Fasting urinary sodium/creatinine in relation to cal-
cium/creatinine and hydroxyproline/creatinine in a general popu-
lation of women. N Z Med J 93:294–297, 1981.
8. Goulding A, Campbell D: Dietary NaCl loads promote calciuria
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION
Dietary Sodium in Osteoporosis
and bone loss in adult oophorectomized rats consuming a low
calcium diet. J Nutr 113:1409–1414, 1983.
9. Goulding A, Lim PE: Effects of varying dietary salt intake on the
fasting excretion of sodium, calcium and hydroxyproline in young
women. N Z Med J 96:853–854, 1983.
10. Goulding A: Osteoporosis: why consuming less sodium chloride
helps to conserve bone. N Z Med J 103:120–122, 1990.
11. Nordin BEC, Need AG, Morris HA, Horowitz M: The nature and
significance of the relationship between urinary sodium and uri-
nary calcium in women. J Nutr 123:1615–1622, 1993.
12. Nordin BEC, Need AG, Morris HA, Horowitz M: Sodium, calcium
and osteoporosis. In: Burckhardt P, Heaney RP, eds. “Nutritional
Aspects of Osteoporosis.” New York, NY: Raven Press (Serono
Symposia Vol. 85), 279–295, 1991.
13. Massey LK, Whiting SJ: Dietary salt, urinary calcium, and bone
loss. J Bone Miner Res 11:731–736, 1996.
14. Itoh R, Suyama Y: Sodium excretion in relation to calcium and
hydroxyproline excretion in a healthy Japanese population. Am J
Clin Nutr 63:735–740, 1996.
15. Dawson-Hughes B, Fowler SE, Dalsky G, Gallagher C: Sodium
excretion influences calcium homeostasis in elderly men and
women. J Nutr 126:2107–2112, 1996.
16. Muldowney FP, Freaney R, Moloney MF: Importance of dietary
sodium in the hypercalciuria syndrome. Kidney Int 22:292–296,
1982.
17. Breslau NA, McGuire JL, Zerwekh JE, Pak CYC: The role of
dietary sodium on renal excretion and intestinal absorption of
calcium and on vitamin D metabolism. J Clin Endocrinol Metab
55:369–373, 1982.
18. Castenmiller JJ, Mensink RP, van der Heijden L, Kouwenhoven T,
Hautvast JG, de Leeuw PW, Schaafsma G: The effect of dietary
sodium on urinary calcium and potassium excretion in normoten-
sive men with different calcium intakes. Am J Clin Nutr 41:52–60,
1985.
19. Breslau NA, Sakhaee K, Pak CYC: Impaired adaptation to salt-
induced urinary calcium losses in postmenopausal osteoporosis.
Trans Assoc Am Physicians 98:107–116, 1985.
20. Need AG, Morris HA, Cleghorn DB, De Nichilo D, Horowitz M,
Nordin BEC: Effect of salt restriction on urine hydroxyproline
excretion in postmenopausal women. Arch Intern Med 151:757–
759, 1991.
20a. Blackwood AM, Sagnella GA, Cook DG, Cappuccio FP: Urinary
calcium excretion, sodium intake and blood pressure in a multi-
ethnic population: results of the Wandsworth Heart and Stroke
Study. J Hum Hypertens 15:229–237, 2001.
20b. Jones G, Beard T, Parameswaran V, Greenaway T, von Witt R: A
population-based study of the relationship between salt intake,
bone resorption and bone mass. Eur J Clin Nutr 51:561–565,
1997.
21. Zemel MB, Gualdoni SM, Walsh MF, Komanicky P, Standley P,
Johnson D, Fitter W, Sowers JR: Effects of sodium and calcium on
calcium metabolism and blood pressure regulation in hypertensive
black adults. J Hypertension 4(Suppl 5):S364–S366, 1986.
22. Ho, SC, Chen YM, Woo JL, Leung SS, Lam TH, Janus ED:
Sodium is the leading dietary factor associated with urinary cal-
cium excretion in Hong Kong Chinese adults. Osteoporos Int
12:723–731, 2001.
23. Matkovic V, Ilich JZ, Andon MB, Hsieh LC, Tzagournis MA,
275S
Dietary Sodium in Osteoporosis
Lagger BJ, Goel PK: Urinary calcium, sodium, and bone mass of
young females. Am J Clin Nutr 62:417–425, 1995.
23a. Ginty F, Flynn A, Cashman KD: The effect of dietary sodium
intake on biochemical markers of bone metabolism in young
women. Br J Nutr 79:343–350, 1998.
23b. Evans CEL, Chughtai AY, Blumsohn A, Giles M, Eastell R: The
effect of dietary sodium on calcium metabolism in premenopausal
and postmenopausal women. Eur J Clin Nutr 51:394–399, 1997.
24. Heaney RP: Is the paradigm shifting? Bone 33:457–465, 2003.
25. Meyer WJ III, Transbol I, Bartter FC, Delea C: Control of calcium
absorption: effect of sodium chloride loading and depletion. Me-
tabolism 25:989–993, 1976.
26. Zerwekh JE, Pak CYC: Selective effects of thiazide therapy on
serum 1␣,25-dihydroxyvitamin D and intestinal calcium absorp-
tion in renal and absorptive hypercalciurias. Metabolism 29:13–17,
1980.
27. Heaney RP, Recker RR, Stegman MR, Moy AJ: Calcium absorp-
tion in women: relationships to calcium intake, estrogen status, and
age. J Bone Miner Res 4:469–475, 1989.
28. Nakamura K, Hori Y, Nashimoto M, Okuda Y, Miyazaki H, Kasai
Y, Yamamoto M: Dietary calcium, sodium, phosphorus, and pro-
tein and bone metabolism in elderly Japanese women: a pilot study
using the duplicate portion sampling method. Nutrition 20:340–
345, 2004.
29. Carbone LD, Bush AJ, Barrow KD, Kang AH: The relationship of
sodium intake to calcium and sodium excretion and bone mineral
density of the hip in postmenopausal African-American and Cau-
casian. J Bone Miner Metab 21:415–420, 2003.
30. McParland BE, Goulding A, Campbell AJ: Dietary salt affects
biochemical markers of resorption and formation of bone in elderly
women. BMJ 299:834–835, 1989.
31. Need AG, Morris HA, Cleghorn DB, DeNichilo DD, Horowitz M,
Nordin BEC: Effect of salt restriction on urine hydroxyproline
excretion in postmenopausal women. Arch Int Med 151:757–759,
1991.
32. Lin PH, Ginty F, Appel LJ, Aickin M, Bohannon A, Garnero P,
Barclay D, Svetkey LP: The DASH diet and sodium reduction
improve markers of bone turnover and calcium metabolism in
adults. J Nutr 133:3130–3136, 2003.
33. Palmieri GMA: Osteoporosis and hypercalciuria secondary to ex-
cessive salt ingestion. J Lab Clin Med 126:503, 1995.
276S
34. Greendale GA, Barrett-Connor E, Edelstein S, Ingles S, Haile R:
Dietary sodium and bone mineral density: results of a 16-year
follow-up study. JAGS 42:1050–1055, 1994.
35. Devine A, Criddle RA, Dick IM, Kerr DA, Prince RL: A longitu-
dinal study of the effect of sodium and calcium intakes on regional
bone density in postmenopausal women. Am J Clin Nutr 62:740–
745, 1995.
36. Berkelhammer CH, Wood RJ, Sitrin MD: Acetate and hypercalci-
uria during total parenteral nutrition. Am J Clin Nutr 48:1482–
1489, 1988.
37. Lutz J: Calcium balance and acid-base status of women as affected
by increased protein intake and by sodium bicarbonate ingestion.
Am J Clin Nutr 39:281–288, 1984.
38. Lemann J Jr, Gray RW, Pleuss JA: Potassium bicarbonate, but not
sodium bicarbonate, reduces urinary calcium excretion and im-
proves calcium balance in healthy men. Kidney Int 35:688–695,
1989.
39. Sellmeyer DE, Schloetter M, Sebastian A: Potassium citrate pre-
vents increased urine calcium excretion and bone resorption in-
duced by a high sodium chloride diet. J Clin Endocrinol Metab
87:2008–2012, 2002.
40. Lemann J Jr, Pleuss JA, Gray RW: Potassium causes calcium
retention in healthy adults. J Nutr 123:1623–1626, 1993.
41. Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC Jr:
Improved mineral balance and skeletal metabolism in postmeno-
pausal women treated with potassium bicarbonate. N Engl J Med
330:1776–1781, 1994.
42. Burger H, Grobbee DE, Drueke T: Osteoporosis and salt intake.
Nutr Metab Cardiovasc Dis 10:46–53, 2000.
43. Prentice A: Diet, nutrition and the prevention of osteoporosis.
Public Health Nutr 7(1A):227–243, 2004.
44. Heaney RP: Ethnicity, bone status, and the calcium requirement.
Nutr Res 22:153–178, 2002.
45. Taubes G: The (political) science of salt. Science 281:898–907,
1998.
46. Hooper L, Bartlett C, Smith GD, Ebrahim S: Systematic review of
long term effects of advice to reduce dietary salt in adults. BMJ
325:628–636, 2002.
Received January 9, 2006.
VOL. 25, NO. 3