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The Journal of Clinical Endocrinology & Metabolism 90(7):3824 –3829
Copyright © 2005 by The Endocrine Society
doi: 10.1210/jc.2004-2205
Effects of Calcium Supplementation on Body Weight and
Blood Pressure in Normal Older Women: A Randomized
Controlled Trial
Ian R. Reid, Anne Horne, Barbara Mason, Ruth Ames, Usha Bava, and Gregory D. Gamble
Department of Medicine, University of Auckland, Auckland 1020, New Zealand
Context: Epidemiological data suggest that high calcium intakes are
associated with decreased body weight and blood pressure. However,
there is little evidence from randomized trials that addresses these
important issues.
Objective: The objective of this study was to assess the long-term
effects of calcium on body weight and blood pressure.
Design: This is a substudy of an ongoing, double-blind, randomized,
controlled trial of calcium supplementation. End points were assessed
at 30 months.
Setting: This study was performed at a university medical center.
Participants: Normal postmenopausal women (mean age, 74 yr;
mean weight, 67 kg; mean blood pressure, 134/70 mm Hg at baseline)
participated in this study.
Intervention: Study subjects were treated with calcium (1 g/d; n ⫽
732) and placebo (n ⫽ 739).
H
IGH INTAKES OF calcium, either in the diet or as
supplements, are now widely recognized as having
beneficial effects on bone mass (1, 2) and, possibly, fracture
incidence (3). However, other health benefits may result from
high calcium intakes, including decreased body weight.
Many epidemiological studies have identified inverse relationships between adiposity and calcium intake (4 –13). For
example, Lin et al. (11) found that calcium intake in young
women (as a ratio to caloric intake) was inversely related to
weight and fat gain over a period of 2 yr. In preschool
children, Carruth and Skinner (4) found that calcium was
inversely related to fat mass, and McCarron (12) found an
inverse relationship between calcium intake and body
weight in the National Health and Nutrition Examination
Survey I. More recently, Zemel et al. (5) reported a similar
result from National Health and Nutrition Examination Survey III, in that the relative risk of being in the highest quartile
for adiposity was 0.16 for those in the highest quartile for
calcium intake (compared with those in the lowest quartile).
This hypothesis has recently been given a major boost by
the work of Davies et al. (13). They reevaluated five previFirst Published Online April 12, 2005
Abbreviations: BMI, Body mass index; DXA, dual energy x-ray
absorptiometry.
JCEM is published monthly by The Endocrine Society (http://www.
endo-society.org), the foremost professional society serving the endocrine community.
Main Outcome Measures: Body weight and blood pressure were the
main outcome measures.
Results: Weight decreased by 368 ⫾ 132 g (mean ⫾ SE) with calcium
treatment and by 369 ⫾ 134 g with placebo (P ⫽ 0.93). Fat and lean
masses did not show an effect of calcium. Blood pressure showed
transient reductions of 1–2 mm Hg at 6 months in the calcium group,
resulting in a significant between-group difference only for systolic
pressure (P ⫽ 0.048). At 30 months, the change from baseline in
systolic pressure was 0.0 ⫾ 0.9 mm Hg in the calcium group and 2.4 ⫾
0.9 mm Hg in the placebo group (P ⫽ 0.14). For diastolic pressures,
the changes were ⫺0.2 ⫾ 0.4 and 0.8 ⫾ 0.4 mm Hg, respectively (P ⫽
0.13). In those with baseline calcium intakes less than 600 mg/d, the
treatment effect was greater and did persist.
Conclusions: Calcium supplementation of 1 g/d does not produce
biologically significant effects on body weight, and its hypotensive
effect is small and transient in most women. (J Clin Endocrinol
Metab 90: 3824 –3829, 2005)
ously published studies in 780 women, aged 20 – 80 yr. Their
observational data showed significant negative associations
between calcium intake and weight; a 1000-mg difference in
calcium intake was associated with an 8-kg difference in
body weight. Calcium intake explained 3% of the variance
in body weight. In a randomized, controlled trial, they found
that calcium supplementation was associated with a negative
effect on body weight of 346 g/yr over 4 yr (P ⬍ 0.025). They
concluded that calcium intake might play an important role
in weight regulation.
With the recognition of obesity as one of the principal
health problems of affluent countries, the possibility that a
safe and inexpensive nutrient such as calcium might play a
role in weight control is a pivotal issue that needs to be
adequately assessed. Despite the epidemiological and clinical data pointing toward an important role of calcium intake
in the regulation of body weight, there is no authoritative
clinical study addressing this question (14). We are currently
conducting a randomized, controlled trial of calcium supplementation in the prevention of fractures. All subjects have
reached 30 months, the first follow-up visit at which body
composition is measured. We have used these data to assess
the long-term effects of calcium supplementation on body
weight. In addition, we have reassessed the effects of this
intervention on blood pressure, because there is also an inconsistent body of evidence suggesting that this is a potential
benefit of the use of calcium.
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Reid et al. • Calcium Effects on Weight and Blood Pressure
J Clin Endocrinol Metab, July 2005, 90(7):3824 –3829
Subjects and Methods
This is a substudy of a randomized controlled trial of calcium supplementation in normal postmenopausal women, designed to assess the
effects of calcium on fracture incidence.
3825
subsequent ones. Therefore, the mean of the second and third readings
has been used in all analyses.
The study was approved by the local ethics committee, and each
subject gave written, informed consent.
Subjects
Statistics
The entry criteria for the study required that subjects be more than
5 yr postmenopausal and more than 55 yr of age. Women receiving
therapy for osteoporosis or taking calcium supplements were ineligible,
as were those with any other major ongoing disease, including serum
creatinine greater than 1.8 mg/dl (0.2 mmol/liter), untreated hypo- or
hyperthyroidism, liver disease, serum 25-hydroxyvitamin D below 10
␮g/liter (25 nmol/liter), malignancy, or metabolic bone disease. None
of the subjects had been regular users of hormone replacement therapy,
anabolic steroids, glucocorticoids, or bisphosphonates in the previous 1
yr. Lumbar spine bone density (Lunar Expert, Lunar Corp., Madison,
WI) was not below the age-appropriate normal range (i.e. z-score greater
than ⫺2).
Women were recruited by advertisement and by mail-outs using
electoral rolls; 2421 women responded to these invitations, of whom 641
did not meet the inclusion criteria, and 309 decided not to participate.
Some 1471 women meeting the selection criteria for the study were
randomized to calcium (n ⫽ 732) or placebo (n ⫽ 739). Their baseline
characteristics are shown in Table 1.
Continuous normally distributed variables were analyzed using a
mixed models approach to repeated measures (Proc Mixed, version 8.12,
SAS Institute, Cary, NC). This approach ensures that all available data
can be included in the analysis even when some subjects have missing
data. A variety of preplanned models were run: an intention to treat
analysis, with and without imputation (maximum likelihood) of missing
values, and with and without adjustment for compliance; a per protocol
analysis; and an analysis of the change in blood pressure, excluding
those taking blood pressure-lowering medication. The intention to treat
analysis was prespecified as the primary analysis. Significant main and
interaction effects were explored using the method of Tukey to preserve
the overall 5% significance level. All tests were two-tailed.
A sample size of 600 in each group provides a power of 80% to detect
differences (at the 5% significance level) of at least 16% of 1 sd. This
equates to 520 g for a change in body weight, 3.4 mm Hg for a change
in systolic blood pressure, and 1.5 mm Hg for a change in diastolic blood
pressure.
Results
Protocol
Treatments were allocated randomly using a minimization algorithm
balancing for current thiazide use, age, and the occurrence of fractures
resulting from minimal trauma after the age of 40 yr. Subjects received
1 g elemental calcium daily as citrate (Citracal, Mission Pharmacal, San
Antonio TX) or an identical placebo. They were asked to take two tablets
(each containing 200 mg elemental calcium) before breakfast and three
tablets in the evening. Dietary calcium intake was assessed using a
validated food frequency questionnaire (15). Compliance was assessed
by tablet counts and was calculated from the number of tablets taken as
a percentage of the number that should have been taken.
Measurements
Body weight was measured at each visit using electronic scales with
subjects wearing light indoor clothing without shoes. No assessment of
the variation in clothing weight between visits was made. At baseline
and 30 months, total body scans using a Lunar Expert instrument (GELunar, software version 1.7, Lunar Corp.) were carried out. This is a
fan-beam, dual energy x-ray absorptiometry (DXA) scanner.
Blood pressure was measured using a Dinamap automatic monitor
(Johnson & Johnson, Tampa, FL) at each visit. Measurements were made
after the woman had been sitting for 5 min. Three recordings were made
3 min apart, as programmed automatically by the device. Analysis of the
data showed that the first recording was significantly higher than the
TABLE 1. Characteristics of study subjects at baseline
Characteristic
Placebo
Calcium
n
739
732
Age (yr)
74.3 (4.3)
74.2 (4.2)
Years since menopause
25.0 (6.3)
24.6 (6.4)
Weight (kg)
67.1 (11.8)
66.9 (11.5)
Height (cm)
159.2 (5.9)
158.9 (5.6)
26.4 (4.2)
26.5 (4.3)
BMI (kg/m2)
Calcium intake (mg/d)
853 (381)
861 (390)
Systolic blood pressure (mm Hg) 133.9 (22.9) 134.9 (22.6)
Diastolic blood pressure (mm Hg)
69.6 (10.0)
70.1 (10.7)
Serum 25-hydroxyvitamin D
20.8 (7.8)
20.6 (7.6)
(␮g/liter)b
Current smokers (%)
2.6
3.4
Data are mean (SD).
a
Between-groups comparisons.
b
Multiply by 2.5 to obtain nmol/liter.
Pa
0.83
0.27
0.25
0.80
0.65
0.67
0.38
0.40
0.69
0.34
The treatment groups were comparable in all indices at
baseline (Table 1). Body weights ranged from 40 –142 kg.
Body mass index (BMI) was distributed as follows: less than
20 kg/m2, 3.7%; 20 –25 kg/m2, 36.6%; 25–30 kg/m2, 41.5%;
and greater than 30 kg/m2, 18.2%, with a similar pattern in
both groups (P ⫽ 0.27). Median alcohol intake was less than
one drink per week (P ⫽ 0.63 between-groups). Body weight
measurements were available in 1204 subjects at 30 months
(82% of the initial cohort), of whom 992 were still taking
study medication. The mean compliance over the study period for the 1204 subjects was 78% in the calcium group and
80% in those receiving placebo (P ⫽ 0.26). The reasons for
women not having weight measured at 30 months were as
follows: 92 remained part of the study, but were only interviewed by telephone at that visit; for three, weight was not
recorded at that visit; two were terminally ill; 17 had died;
and 153 had withdrawn from the study, mostly for personal
reasons or because of other medical problems.
Body weight
At baseline, body weight and BMI were unrelated to dietary calcium intake (r ⫽ ⫺0.01 and r ⫽ ⫺0.04, respectively).
If this analysis was repeated by comparing BMI across quintiles of dietary calcium intake or by comparing calcium intake across quintiles of BMI, similarly negative results were
found (P ⫽ 0.70 and P ⫽ 0.36, respectively).
Changes in body weight for the intention to treat population are shown in Fig. 1. At 30 months, body weight
(mean ⫾ se) decreased by 368 ⫾ 132 g in the calcium group
and by 369 ⫾ 134 g in those taking placebo. Each of these
changes was significant within the respective group, but the
changes over time were not different between groups (P ⫽
0.93 for time-treatment interaction, by ANOVA). The change
in BMI over the duration of the study was ⫹0.01 ⫾ 0.05
kg/m2 for the calcium group and ⫹0.02 ⫾ 0.05 kg/m2 for the
placebo group. These changes were not significantly different (P ⫽ 0.83). When these analyses were repeated using data
3826
J Clin Endocrinol Metab, July 2005, 90(7):3824 –3829
Reid et al. • Calcium Effects on Weight and Blood Pressure
FIG. 1. Changes in body weight in normal postmenopausal women
randomized to receive calcium (1 g/d) or placebo for 30 months. Data
are the mean ⫾ SE. There was no significant difference between
groups (P ⫽ 0.93).
from subjects still taking study medication and with greater
than 80% compliance, the changes in body weight were essentially the same (calcium group, ⫺291 ⫾ 160 g, n ⫽ 411;
placebo group, ⫺331 ⫾ 160 g, n ⫽ 429; between-groups
comparison, P ⫽ 0.86).
The effect of calcium supplementation on weight was also
analyzed in relation to the baseline dietary calcium intake.
When dietary calcium at baseline was incorporated into the
ANOVA as a continuous variable, it was unrelated to the
change in weight (P ⫽ 0.93). Similarly, if subjects were categorized as having a baseline calcium intake of more or less
that 800 mg/d, there was no significant interaction of intake
with the treatment effect (P ⫽ 0.27), and the same was true
if 600 mg/d was used as the cut-point (P ⫽ 0.38). However,
if the analysis was restricted to those with calcium intakes
less than 600 mg/d at baseline, a trend toward greater weight
loss in those taking calcium (⫺749 ⫾ 262 g, compared with
⫺261 ⫾ 268 g in the placebo group at 30 months) was apparent, but this between-group difference was not significant
(P ⫽ 0.19). In the group with calcium intake greater than 600
mg/d, the opposite trend in weight change was apparent (i.e.
the calcium group tended to have a more positive weight
change).
Measurement of body composition by DXA allowed the
effects of calcium supplementation on fat mass and lean mass
to be assessed separately (Fig. 2). Fat mass did not change
significantly in either group (calcium group, ⫹163 ⫾ 146 g;
placebo group, ⫹113 ⫾ 145 g), and there was no difference
between groups (P ⫽ 0.81). In contrast, there was a significant
loss of lean mass in both groups (calcium, ⫺709 ⫾ 62 g;
placebo, ⫺667 ⫾ 61 g), but no significant difference between
the treatments (P ⫽ 0.63).
Blood pressure
Changes in mean systolic and diastolic pressures over the
course of the study are shown in Fig. 3. In the entire cohort,
both systolic and diastolic pressures tended to rise throughout the study (P ⬍ 0.001). In the calcium group, there were
transient reductions in both pressures at 6 months, resulting
in a significant between-group difference for systolic blood
pressure (P ⫽ 0.048), but not for diastolic blood pressure (P ⫽
0.37, time-treatment interaction, by ANOVA). At 30 months,
the change from baseline in systolic pressure was 0.0 ⫾ 0.9
FIG. 2. Changes in fat mass and lean mass (determined by DXA) in
normal postmenopausal women randomized to receive calcium (1 g/d)
or placebo for 30 months. Data are the mean ⫾ SE. There was no
significant difference between groups (Pfat ⫽ 0.81; Plean⫽ 0.63).
mm Hg in the calcium group and 2.4 ⫾ 0.9 mm Hg in the
placebo group (P ⫽ 0.14). For diastolic pressures, the changes
were ⫺0.2 ⫾ 0.4 and 0.8 ⫾ 0.4 mm Hg, respectively (P ⫽ 0.13).
These analyses were repeated in the 1303 subjects who did
not take diuretics or blood pressure-lowering medication
during the study. Similar trends were seen; the changes over
time remained significant, but those between groups did not
reach statistical significance (Pdiastolic ⫽ 0.76; Psystolic ⫽ 0.22).
Dietary calcium at baseline was unrelated to the changes in
blood pressure (Pdiastolic ⫽ 0.39; Psystolic ⫽ 0.13). However,
analyzing separately those with baseline calcium intakes of
more or less than 600 mg suggested that the changes in blood
pressure were larger and more sustained in subjects with low
dietary calcium intakes (Fig. 4). In this group at 30 months,
the systolic pressure was 4.9 ⫾ 2.6 mm Hg lower in the
calcium group (P ⫽ 0.06), and the diastolic pressure was
2.2 ⫾ 1.1 mm Hg lower (P ⫽ 0.05) than that in the placebo
group.
Discussion
The present data indicate that calcium supplementation in
postmenopausal women with dietary calcium intakes on the
order of 800 mg/d causes no significant change in body
weight. This study is very much larger than any other randomized, controlled trial that has addressed this question,
and it has adequate power to detect a biologically significant
effect on weight. We did not formally assess the variation in
clothing weight between visits, but this minor contribution
to measurement variability is accounted for in the power
Reid et al. • Calcium Effects on Weight and Blood Pressure
J Clin Endocrinol Metab, July 2005, 90(7):3824 –3829
3827
FIG. 3. Changes in systolic (SBP, upper panel) and diastolic (DBP,
lower panel) blood pressures in normal postmenopausal women randomized to receive calcium (1 g/d) or placebo for 30 months. Data are
the mean ⫾ SE. For systolic blood pressure, there was a significant
decrease at 6 months with calcium supplementation and a significant
treatment effect overall (P ⫽ 0.048), but there was no treatment effect
on diastolic blood pressure (P ⫽ 0.37).
calculation. Despite the positive findings from the report by
Davies et al. (13), discussed above, other randomized, controlled trials assessing the effects of calcium intake on weight
loss in humans have produced inconsistent results. Zemel et
al. (16) studied 41 obese women receiving energy-deficit diets, randomly assigned to a low calcium intake, a calciumsupplemented diet, or a dairy-supplemented diet. Weight
losses (mean ⫾ se) over 24 wk in the 32 study completers
were 6.60 ⫾ 2.58, 8.58 ⫾ 1.60, and 11.07 ⫾ 1.63 kg, respectively, the low and high calcium groups were not different
on post hoc testing. Jensen et al. (17) found that a 1000-mg
calcium supplement made no difference to weight changes
over a 3-month period in a randomized controlled trial of 62
obese women given low energy diets. In a randomized, controlled trial of calcium supplementation (2, 18), we found that
weight gain was 300 g less in the calcium-supplemented
group, although this was not statistically significant (our
unpublished observations). Shapses et al. (19) also reanalyzed three calcium intervention studies comprising 100
women and found no effect of calcium supplementation on
weight loss over 25 wk. Fujita et al. (20) reanalyzed a randomized, controlled trial and reported no effect of calcium
supplementation on body weight. However, there was a
blunting of the increase in fat mass in those taking an algal
calcium preparation, but not in those taking calcium carbonate. All of these studies are small and are underpowered to
detect small effects on weight that may still be of biological
FIG. 4. Changes in diastolic blood pressure (DBP) in women randomized to receive calcium (1 g/d) or placebo, according to their baseline dietary calcium intake. Data are the mean ⫾ SE. There was no
treatment effect in those subjects with high baseline intakes, but
there was a treatment effect in those with intakes below 600 mg/d (P ⫽
0.05; n ⫽ 301).
significance. However, taken together with the present
study, they suggest that calcium supplementation holds little
promise as a strategy for weight control. In some ways this
negative result is not surprising, because calcium supplements have been used for many decades, and a large number
of clinical trials of their effects on the skeleton have already
been carried out. If they were to have a substantial effect on
body weight, it is likely that it would have been noted some
time ago.
In addition to the clinical and epidemiological data already
reviewed, there are data from animal studies that suggest an
effect of calcium on weight. Stern et al. (21, 22) reported lower
weight gain in rats on a high-calcium diet, and Metz et al. (23,
24) reported similar findings. Papakonstantinou et al. (25)
reported that rats fed a high calcium diet that was also
supplemented with milk protein had 29% less carcass fat.
This was contradicted by similar studies in lean and obese
mice and rats reported by Zhang and Tordoff (26). They
found no effect of calcium consumption on energy intake,
3828
J Clin Endocrinol Metab, July 2005, 90(7):3824 –3829
body weight, or carcass fat content, except in a single study
in which they postulated that the high calcium content of the
diet had made it unpalatable, decreasing food intake. This
explanation might apply to other animal studies also. Zemel
et al. (5, 27) have reported studies in mice overexpressing the
agouti gene. They found that dietary calcium supplementation produced a dose-related diminution in weight gain and
fat mass. In these studies, high calcium intakes were found
to be associated with reduced adipocyte fatty acid synthase
activity and increases in lipolysis (28). Zemel (29) hypothesized that a high calcium intake suppresses PTH and 1,25dihydroxyvitamin D, which leads to reductions in the intracellular concentration of calcium in adipocytes. These
changes would be expected to decrease lipogenesis and increase lipolysis. High calcium intakes could also cause
weight loss, because they bind to fatty acids and bile acids
in the gut, leading to fat malabsorption (30 –33). Although all
of these mechanisms may be operative in humans, the results
of the present study suggest that they are not sufficiently
powerful to predominate over the many other factors that
impact on appetite, digestion, and energy expenditure.
A second, potentially important health benefit from a high
calcium intake is a reduction in blood pressure. A relationship between calcium intake and blood pressure has been
reported from observational studies in a variety of populations (34 –39), typically showing a decrease in both systolic
and diastolic blood pressures of about 0.4 mm Hg for each
increase of 100 mg in daily calcium intake (39). Numerous
randomized controlled trials of calcium supplementation
have been performed, meta-analyses of which show a significant reduction of systolic pressures by about 1 mm Hg
without any significant change in diastolic pressures (40 –
42). The present study is by far the largest to address this
important question, and its duration is one of the longest; a
recent meta-analysis included 42 studies (42) with a median
duration of 8 wk and a median of 53 subjects. Thus, the
present study of 3000 person-years substantially exceeds the
sum of the total clinical trial experience to date in this area.
Few previous studies have included significant numbers of
postmenopausal women, the group that most uses calcium.
The present results are very similar to those of the metaanalyses, showing a small effect on systolic blood pressure,
but no change in diastolic blood pressure. The greater duration of the present study gives important new information
relating to the time course of the antihypertensive effect of
calcium supplementation, which is greatest at 6 months, but
minimal thereafter. This is completely consistent with the
published data; all studies that have found a beneficial effect
of calcium on blood pressure have been less than 6 months
in duration. This suggests that the hypotensive effect of calcium is real, but transient. The post hoc analyses in those with
a baseline calcium intake less than 600 mg/d, however, do
suggest that in these individuals the effects are larger and
more persistent. The Griffith’s meta-analysis (42) suggested
that dietary calcium might have a greater impact than supplements on blood pressure, but this trend was not statistically significant. With these caveats, we conclude that the
therapeutic value of calcium in managing hypertension is
likely to be small and insufficient to justify its routine use in
hypertensive subjects receiving average calcium intakes.
Reid et al. • Calcium Effects on Weight and Blood Pressure
The effects of calcium supplementation on blood pressure
are probably contributed to by the natriuretic effect of calcium (43) and by its effects on PTH and 1,25-dihydroxyvitamin D (44, 45); both of these hormones have pressor effects
in vascular smooth muscle cells (46). Calcium supplementation may also increase concentrations of the vasodilator,
calcitonin gene-related hormone (47), and have effects on the
renin-angiotensin system (48).
On the basis of the present study, it is unlikely that changes
in calcium intake will produce clinically relevant effects on
body weight in postmenopausal women. Whether the same
is true in children, young adults, and men will require additional investigation, but there seems to be little reason to
hypothesize that these effects would be substantially different in those other groups. This finding should not be seen as
a reason to diminish enthusiasm for recommending calcium
supplementation. Its well-established beneficial effects on
bone and the possibility that it may also improve circulating
lipid profiles are both compelling reasons for endorsing its
use in postmenopausal women.
Acknowledgments
We are grateful to Mission Pharmacal (San Antonio, TX) for the
supply of calcium citrate tablets and placebo.
Received November 10, 2004. Accepted April 6, 2005.
Address all correspondence and requests for reprints to: Dr. Ian Reid,
Department of Medicine, University of Auckland, Private Bag 92019,
Auckland 1020, New Zealand. E-mail: [email protected].
This work was supported by the Health Research Council of New
Zealand.
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