How Far Should Salt Intake Be Reduced?

How Far Should Salt Intake Be Reduced?
Feng J. He, Graham A. MacGregor
Abstract—The current public health recommendations are to reduce salt intake from 9 to 12 g/d to 5 to 6 g/d. However,
these values are based on what is feasible rather than the maximum effect of salt reduction. In a meta-analysis of
longer-term trials, we looked at the dose response between salt reduction and fall in blood pressure and compared this
with 2 well-controlled studies of 3 different salt intakes. All 3 studies demonstrated a consistent dose response to salt
reduction within the range of 12 to 3 g/d. A reduction of 3 g/d predicts a fall in blood pressure of 3.6 to 5.6/1.9 to
3.2 mm Hg (systolic/diastolic) in hypertensives and 1.8 to 3.5/0.8 to 1.8 mm Hg in normotensives. The effect would be
doubled with a 6 g/d reduction and tripled with a 9 g/d reduction. A conservative estimate indicates that a reduction of
3 g/d would reduce strokes by 13% and ischemic heart disease (IHD) by 10%. The effects would be almost doubled with
a 6 g/d reduction and tripled with a 9 g/d reduction. Reducing salt intake by 9 g/d (eg, from 12 to 3 g/d) would reduce
strokes by approximately one third and IHD by one quarter, and this would prevent 20 500 stroke deaths and 31 400
IHD deaths a year in the United Kingdom. The current recommendations to reduce salt intake from 9 to 12 g/d to 5 to
6 g/d will have a major effect on blood pressure and cardiovascular disease but are not ideal. A further reduction to 3
g/d will have a much greater effect and should now become the long-term target for population salt intake worldwide.
(Hypertension. 2003;42:1093-1099.)
Key Words: sodium, dietary blood pressure dose response cardiovascular diseases
High blood pressure is the most important risk factor for
cardiovascular disease.1 A recent World Health Organization
report states that elevated blood pressure alone causes
50% of cardiovascular disease worldwide.1 A more recent
article in The Lancet demonstrates that nonpersonal health
interventions, including government action to stimulate a
reduction in the salt (sodium chloride) content of processed
foods, are cost-effective ways to limit cardiovascular disease
and could avert 21 million disability-adjusted life years per
year worldwide.2 A recent meta-analysis of 1 million adults in
61 prospective studies demonstrates that the relation between
blood pressure and cardiovascular risk is much stronger than
previously estimated.3 Much evidence from epidemiologic,4
migration,5 intervention,6 genetic,7 and animal8 studies suggests
that salt intake plays an important role in regulating
blood pressure. Several meta-analyses of randomized, salt
reduction trials have been published in the last few years.9–12
However, most of the previous meta-analyses included trials
of very short duration (eg, 5 days) and included trials with a
short-term salt loading followed by salt deprivation (eg, from
20 to less than 1 g/d) for only a few days.9,11 These short-term
salt loading and salt depletion experiments are not appropriate
for helping to inform public health policy, which is for a
more modest reduction in salt intake over a more prolonged
period of time. A more recent meta-analysis by Hooper et al12
is an important attempt to look at whether long-term salt
reduction (ie, 6 months) in randomized trials causes a fall in
blood pressure. However, most trials included in this metaanalysis
only achieved a very small reduction in salt intake,
and on average, salt intake was reduced by only 2 g/d. It is
therefore not surprising that there was only a small, but still
highly significant, fall in blood pressure. Furthermore, an
important point as to whether there is a dose response to salt
reduction has been overlooked in this meta-analysis.
Salt intake in many countries is between 9 and 12 g/d. The
current World Health Organization recommendations for
adults are to reduce salt intake to 5 g/d or less,13 and the UK14
and US recommendations15 are 6 g/d or less. However, these
recommendations are based on what is feasible and not on
what might have been the maximum impact on blood pressure
and cardiovascular disease. Recent evidence suggests
that these levels, although they might be feasible, are too
high.
Studies in experimental animals have shown a clear dose
response between salt intake and blood pressure: the higher
the salt intake, the higher the blood pressure.16 A recent study
in chimpanzees, the animal species closest to humans with
98.4% genetic identity, demonstrated a dose response when
salt was increased from their usual intake of 0.5 g/d to 5, 10,
and 15 g/d.8 In humans, it is difficult to conduct such trials,
particularly to keep individuals on a low-salt diet long term
because of the widespread presence of salt in nearly all
processed, restaurant, canteen, and fast foods. However, 2
well-controlled trials have studied 3 salt intakes (ie, from
Received June 23, 2003; first decision July 15, 2003; revision accepted October 10, 2003.
From the Blood Pressure Unit, St George’s Hospital Medical School, London, England.
Correspondence to Prof G.A. MacGregor, Blood Pressure Unit, St George’s Hospital Medical School, Cranmer Terrace, London, SW17 0RE, UK.
E-mail g.macgregor@sghms.ac.uk
© 2003 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org DOI: 10.1161/01.HYP.0000102864.05174.E8
1093
11.2, 6.4, to 2.9 g/d in 1 trial17 and from 8.3, 6.2, to 3.8 g/d
in the other18), and both showed a clear dose response to salt
reduction.
To study this dose-response relation further, we reanalyzed
a recent meta-analysis of randomized, longer-term, salt reduction
trials19 and looked at the dose-response relation and
compared this with the 2 well-controlled studies of 3 salt
intakes to try to determine the optimal salt intake that would
have the maximum impact on blood pressure, strokes, and
ischemic heart disease (IHD).
Methods
The methods of the meta-analysis were reported in detail elsewhere19
and are summarized here. The inclusion criteria were as follows:
1. Random allocation to either a reduced salt intake or usual salt
intake (ie, control).
2. No concomitant interventions in either group.
3. Net reduction in 24-hour urinary sodium 40 mmol (2.4 g of salt
per day). Net reduction in 24-hour urinary sodium was calculated
as UNa (Post) UNa (Pre) for crossover trials, where UNa (Post)
designates urinary sodium on the reduced salt intake and UNa
(Pre) designates urinary sodium on the usual salt intake. In parallel
trials, the net change in urinary sodium was calculated as {[UNa
(Post) UNa (Pre)]reduced salt group} {[UNa (Post) UNa (Pre)]control
group}.
4. Duration of salt reduction must have been for 4 or more weeks.
5. Study participants were not children or pregnant.
Mean effect sizes were calculated by weighting each trial by the
inverse of the variance. Weighted linear regression was used to
examine the dose-response relation between the change in 24-hour
urinary sodium and the change in blood pressure.20 From the
regression line, we calculated the predicted falls in blood pressure
with a reduction of 3, 6, and 9 g/d in salt intake.
Results
Trials in Hypertensive Individuals
The characteristics of individual trials included in the metaanalysis
were reported in detail elsewhere19 and are summarized
here. Seven hundred thirty-four hypertensive individuals
were studied in 17 trials.17,18,21–35 Median age was 50
years (ranging from 24 to 73 years). The study duration
varied from 4 weeks to 1 year (median, 6 weeks). The median
24-hour urinary sodium on the usual salt intake was
161 mmol (9.5 g of salt per day), ranging from 125 to
191 mmol (7.4 to 11.2 g of salt per day), and on the reduced
salt intake it was 87 mmol (5.1 g of salt per day), ranging
from 57 to 117 mmol (3.4 to 6.9 g of salt per day). The
median net change in 24-hour urinary sodium was 78 mmol
(4.6 g of salt per day), ranging from 53 to 117 mmol (3.1
to 6.9 g of salt per day).
The pooled estimates of changes in blood pressure were
5.0 0.4 mm Hg (mean SEM, P 0.001; 95% confidence
interval [CI], 5.8 to 4.2 mm Hg) for systolic and
2.7 0.2 mm Hg (P 0.001; 95% CI, 3.2 to
2.3 mm Hg) for diastolic pressure.
To examine whether there was a dose-response relation
between the changes in 24-hour urinary sodium and the
changes in blood pressure, we performed weighted linear
regression and assumed a zero intercept. The assumption for
using this model was that the absence of a change in urinary
sodium would be associated with no change in blood pressure,
ie, all other factors being equal between 2 randomized
treatments. The results showed a significant dose response to
salt reduction (P 0.001 for both systolic and diastolic
pressures; Figure 1). A reduction of 50 mmol/d (3 g/d) in salt
intake predicts a fall in blood pressure of 3.6/1.9 mm Hg. A
reduction of 100 mmol/d (6 g/d) predicts a fall in blood
pressure of 7.1/3.9 mm Hg. A reduction of 150 mmol/d (9
g/d) in salt intake would cause a fall in blood pressure of
10.7/5.8 mm Hg.
Trials in Normotensive Individuals
Two thousand two hundred twenty normotensive individuals
were studied in 11 trials.18,35–43 Median age was 47 years
(ranging from 22 to 67 years). The study duration varied from
4 weeks to 3 years (median, 4 weeks). The median 24-hour
urinary sodium on the usual salt intake was 154 mmol (9.1 g
of salt per day), ranging from 128 to 200 mmol (7.5 to 11.8 g
of salt per day), and on the reduced salt intake it was 82 mmol
(4.8 g of salt per day), ranging from 56 to 135 mmol (3.3 to
7.9 g of salt per day). The median net change in 24-hour
urinary sodium was 74 mmol (4.4 g of salt per day), ranging
from 40 to 118 mmol (2.4 to 6.9 g of salt per day).
The pooled estimates of changes in blood pressure were
2.0 0.3 mm Hg (P 0.001; 95% CI, 2.6 to
1.5 mm Hg) for systolic and 1.0 0.2 mm Hg (P 0.001;
95% CI, 1.4 to 0.6 mm Hg) for diastolic pressure. The
dose-response analysis with fixing the intercept showed a
Figure 1. Relation between the net change in 24-hour urinary
sodium excretion and blood pressure in the meta-analysis.
Open circles represent normotensives and solid circles represent
hypertensives. The slope is weighted by the inverse of the
variance of the net change in blood pressure. The size of the
circle is proportional to the weight of the trial.
1094 Hypertension December 2003
significant dose response to salt reduction (P 0.001 for
systolic and P 0.05 for diastolic pressures; Figure 1). A
reduction of 3, 6, and 9 g/d in salt intake predicts a fall in
blood pressure of 1.8/0.8, 3.6/1.7, and 5.4/2.5 mm Hg,
respectively.
Trials in All Individuals
When all individuals were grouped together, there were 2954
subjects (25% were hypertensives). Median age was 49 years
(ranging from 22 to 73 years). The study duration varied from
4 weeks to 3 years (median, 5 weeks). The pooled estimates
of changes in blood pressure were 2.9 0.2 mm Hg
(P 0.001; 95% CI, 3.4 to 2.5 mm Hg) for systolic and
1.7 0.2 mm Hg (P 0.001; 95% CI, 2.0 to
1.4 mm Hg) for diastolic pressure. The dose-response
analysis with fixing the intercept showed a significant dose
response to salt reduction (P 0.001 for systolic and P 0.001
for diastolic pressures). A reduction of 3, 6, and 9 g/d in salt
intake predicts a fall in blood pressure of 2.5/1.4, 5.0/2.8, and
7.5/4.2 mm Hg, respectively.
Dose Response Between Salt Intake and Blood
Pressure in Our Previous Double-Blind Study and
the DASH-Sodium Study
The best way to study the dose-response relation between salt
intake and blood pressure is to look at the blood pressure
responses to several levels of salt intake for a long term. So
far, there are only 2 well-controlled trials that studied 3 salt
intakes, each for 4 weeks. One is our double-blind study in 19
patients with untreated essential hypertension,17 and the other
is the Dietary Approaches to Stop Hypertension (DASH)-
Sodium study,18 in which 79 untreated hypertensives and 116
normotensives were studied on the normal American diet, and
81 untreated hypertensives and 121 normotensives were
studied on the DASH diet.
In our double-blind study with 3 salt intakes, the blood
pressure decreased by 8/5 mm Hg when salt intake, as judged by
24-hour urinary sodium, changed from 190 to 108 mmol/24 h
(11.2 to 6.4 g/d), and the blood pressure decreased by
8/4 mm Hg when salt intake changed from 108 to 49 mmol/24
h (6.4 to 2.9 g/d).17 The DASH-Sodium study showed that in all
individuals (ie, both hypertensives and normotensives) who
were studied on the normal American diet, the blood pressure
decreased by 2.1/1.1 mm Hg when salt intake changed from 141
to 106 mmol/24 h (8.3 to 6.2 g/d) and by 4.6/2.4 mm Hg when
salt intake changed from 106 to 64 mmol/24 h (6.2 to 3.8 g/d).18
In those who were studied on the DASH diet, the blood pressure
decreased by 1.3/0.6 mm Hg when salt intake changed from 144
to 107 mmol/24 h (8.5 to 6.3 g/d) and by 1.7/1.0 mm Hg when
salt intake changed from 107 to 67 mmol/24 h (6.3 to 3.9 g/d).18
To study the dose-response relation between salt intake and
blood pressure, we performed linear regression analysis on
these 2 studies by using the mean 24-hour urinary sodium and
mean blood pressure at 3 salt intakes. For the purpose of
comparison, we included only a subgroup of hypertensive and
normotensive individuals who were studied on the normal
American diet in the DASH-Sodium study. As shown in
Figure 2, the 2 studies showed a very similar dose-response
relation between salt intake and blood pressure. Within the
range of 11.2 to 2.9 g of salt per day, the lower the salt intake,
the lower the blood pressure. In patients with essential
hypertension, a reduction of 3, 6, and 9 g/d in salt intake
predicts a fall in blood pressure of 5.6/3.2, 11.2/6.4, and
16.8/9.6 mm Hg, respectively, in the double-blind, salt reduction
study. In the DASH-Sodium study, the same reductions
in salt intake predict a fall in blood pressure of 5.3/2.9,
10.5/5.7, and 15.8/8.6 mm Hg, correspondingly. The DASHSodium
study also showed that in normotensive individuals,
there was a dose response to salt reduction (Figure 2). A
reduction of 3, 6, and 9 g/d in salt intake predicts a fall in
blood pressure of 3.5/1.8, 7.0/3.5, and 10.5/5.3 mm Hg,
respectively, in normotensives.
Comparison of the Dose-Response Relation Among
3 Studies
To compare the dose-response relation among 3 studies, we
superimposed the regression lines found in the 2 studies with
Figure 2. Dose-response relation
between 24-hour urinary sodium and
blood pressure in the double-blind salt
reduction study and the DASH-Sodium
study.
He and MacGregor Salt, Blood Pressure, and Dose Response 1095
3 salt intakes on our meta-analysis (Figure 3). There was a
similar dose response in all 3 studies. However, the regression
line from our meta-analysis was flatter. This is not
surprising, because some less well-controlled studies were
included in the meta-analysis, and the diversity of patients
recruited to different trials (eg, age, ethnic group, baseline
blood pressure and potassium intake) might also have affected
the blood pressure responses. Table 1 shows the
predicted falls in blood pressure with reductions of 3, 6, and
9 g/d of salt intake in 3 studies. A reduction of 3 g/d in salt
intake would have an effect on blood pressure, but the effect
would be doubled with a 6 g/d reduction and tripled with a 9
g/d reduction in salt intake.
Discussion
Our meta-analysis of randomized, longer-term, salt reduction
trials demonstrates a dose response to salt reduction. More
importantly, the dose response found in our meta-analysis is
consistent with the dose response found in the 2 wellcontrolled
trials with 3 salt intakes. Within the range of 12 to
3 g of salt per day, the lower the salt intake, the lower the
blood pressure. The current public health recommendations to
reduce salt intake from 9 to 12 g/d to 5 to 6 g/d will have a
major effect on blood pressure but are no means ideal. A
further reduction to 3 g of salt per day will have a much
greater effect on blood pressure.
One important point is that it is not clear from the 3 studies
whether the dose response to salt reduction is linear or
nonlinear. In hypertensives, both the DASH-Sodium study
and our double-blind study of 3 salt intakes showed a
nonlinear dose response for systolic pressure, ie, a steeper
dose response at a lower level of salt intake. In other words,
for a given reduction in salt intake, the fall in systolic blood
pressure is larger when salt intake is at a lower level.
Figure 3. Comparison of the
dose-response relation among 3
studies.
TABLE 1. Predicted Falls in Blood Pressure With Salt Reduction in 3 Studies
Study and Measure
Reduction in Salt Intake
3 g/d (50 mmol/d) 6 g/d (100 mmol/d) 9 g/d (150 mmol/d)
Hypertensive Normotensive Hypertensive Normotensive Hypertensive Normotensive
Meta-analysis of modest salt reduction19
Fall in systolic blood pressure, mm Hg 3.6 1.8 7.1 3.6 10.7 5.4
Fall in diastolic blood pressure, mm Hg 1.9 0.8 3.9 1.7 5.8 2.5
Double-blind salt reduction study17
Fall in systolic blood pressure, mm Hg 5.6 11.2 16.8
Fall in diastolic blood pressure, mm Hg 3.2 6.4 9.6
DASH-Sodium study18
Fall in systolic blood pressure, mm Hg 5.3 3.5 10.5 7 15.8 10.5
Fall in diastolic blood pressure, mm Hg 2.9 1.8 5.7 3.5 8.6 5.3
DASH indicates Dietary Approaches to Stop Hypertension.
1096 Hypertension December 2003
However, for diastolic blood pressure in both the DASHSodium
study and our double-blind study, the dose-response
relation appears to be linear, and in the DASH-Sodium study
in normotensives, there appears to be a linear dose response
for both systolic and diastolic blood pressure.
For the purpose of comparison, only subgroup data of the
DASH-Sodium study were included in our analyses. It is of
note that the overall results of the DASH-Sodium study
showed a nonlinear dose response to salt reduction both on
the normal American diet and on the DASH diet, indicating
that salt reductions have greater effects on blood pressure
with salt intake at lower levels. In our meta-analysis, we
assumed a linear relation between the change in 24-hour
urinary sodium and the change in blood pressure. This, if
anything, would underestimate the effect of salt reduction on
blood pressure at lower levels of salt intake if the doseresponse
relation were nonlinear.
The recent UK National Diet and Nutrition Survey, which
was carried out between 2000 and 2001 in a nationally
representative sample of 1495 adults aged 19 to 64 years,
showed that 24-hour urinary sodium was 187 mmol (11.0 g/d
of salt) for men and 139 mmol (8.1 g/d of salt) for women.44
However, 24-hour urinary sodium is an underestimate of
dietary salt intake. A study by Pietinen45 showed that the
24-hour urinary sodium was, on average, 93% of dietary salt
intake. Therefore, the average salt intake in the United
Kingdom is actually between 8.7 and 11.8 g/d. A conservative
estimate of the impact on cardiovascular disease (ie, from
the falls in blood pressure in all individuals in the meta-analysis)
indicates that a reduction of 3 g/d in salt intake would
result in a fall in blood pressure of 2.5/1.4 mm Hg, and this
would reduce strokes by 12% (estimated from systolic) to
14% (from diastolic) and ischemic heart disease (IHD) by 9%
to 10%.3 In the United Kingdom, the total number of stroke
deaths is 60 666 per year, and the total number of IHD deaths
is 124 037 per year.46 Therefore, a reduction of 3 g/d in salt
intake would prevent 7300 to 8300 stroke deaths and
10 600 to 12 400 IHD deaths per year. As shown in Table 2,
the effects on strokes and IHD would be almost doubled if
salt intake were reduced by 6 g/d and tripled with a 9 g/d
reduction. A reduction of 9 g/d in salt intake (eg, from 12 to
3 g/d) would result in a fall in blood pressure of 7.5/
4.2 mm Hg, and this would reduce strokes by approximately
one third and IHD by one quarter. In the United Kingdom,
this would prevent 20 500 stroke deaths and 31 400 IHD
deaths per year. These numbers of stroke and IHD deaths
prevented are likely to be an underestimate, because the falls
in blood pressure in the much better controlled DASHSodium
study18 and our double-blind study17 are larger and
would have an even greater impact.
It is important to note that even in normotensives alone,
salt reductions would have large effects on stroke and IHD. A
reduction of 3 g/d in salt intake would lower blood pressure
by 1.8/0.8 mm Hg, and this would reduce strokes by 9% and
IHD by 6% in normotensives alone. A reduction of 6 g/d
would reduce strokes by 17% and IHD by 12%, and a
reduction of 9 g/d would reduce strokes and IHD by 24% and
18%, respectively, in normotensives.
In our article, we reported the reductions in blood pressure,
stroke, and IHD death with reductions of 3, 6, and 9 g/d in salt
intake. The long-term target should be to reduce salt intake to
3 g/d. Therefore, if individuals have a salt intake of 12 g/d,
then they need to reduce salt intake by 9 g/d, and if
individuals have a salt intake of 9 g/d, then they need to
reduce salt intake by 6 g/d. The effects of these reductions in
salt intake on blood pressure, stroke, and IHD deaths are
shown in Table 1 and Table 2.
The levels of salt intake in many countries are similar to
those in the United Kingdom. The percentage reduction in
stroke and IHD applies to many countries. Therefore, the
reductions in stroke and IHD worldwide, if salt intake were
reduced from the current intake of 9 to 12 g/d to the
now-recommended levels of 5 to 6 g/d, would be immense.
The effects on stroke and IHD would be much greater if salt
intake were reduced further, ie, to 3 g/d.
Although we calculated only the numbers of stroke and
IHD deaths that could be prevented with reductions in salt
intake, the percentage reductions in stroke and IHD apply to
the incidence as well. Approximately 50% of patients who
suffer stroke or heart attack survive; therefore, there would be
a proportionate reduction in the numbers of these people. This
would result in a reduction in disability and major cost
savings both to individuals, their families, and the Health
Service. Furthermore, high blood pressure is an important
risk factor for heart failure. A reduction in salt intake would
therefore have a major effect on heart failure.
From our studies, it is not clear whether reducing salt
intake to 3 g/d has a greater effect on blood pressure,
TABLE 2. Predicted Reductions in Stroke and IHD Deaths With Reductions in Salt Intake
Measure
Reduction in Salt Intake
3 g/d (50 mmol/d) 6 g/d (100 mmol/d) 9 g/d (150 mmol/d)
SBP DBP SBP DBP SBP DBP
Fall in BP in all participants, mm Hg
(from the meta-analysis)
2.5 1.4 5 2.8 7.5 4.2
Reduction in stroke death, % 12 14 23 25 32 36
Stroke deaths prevented in UK, n/y 7300 8300 13,700 15,500 19,300 21,600
Reduction in IHD death, % 9 10 16 19 23 27
IHD deaths prevented in UK, n/y 10,600 12,400 20,300 23,600 29,100 33,700
Blood pressure fall taken from the meta-analysis. IHD indicates ischemic heart disease; SBP, systolic blood
pressure; DBP, diastolic blood pressure; and BP, blood pressure.
He and MacGregor Salt, Blood Pressure, and Dose Response 1097
because no randomized trials with a duration of 4 or more
weeks have reduced salt intake to 3 g/d. However, the
observational epidemiologic studies suggest that within the
range of 14 to 0.01 g of salt per day, there is a dose response
between salt intake and blood pressure, ie, the lower the salt
intake, the lower the blood pressure.4,47 Despite the potential
greater benefits of reducing salt intake to 3 g/d, it is
currently impractical to achieve a reduction to 3 g/d, given
the current amount of salt in processed foods that accounts for
75% to 80% of our salt intake.48
In conclusion, our meta-analysis of longer-term salt reduction
trials and the 2 well-controlled studies with 3 salt intakes
demonstrate a consistent dose-response relation between salt
intake and blood pressure within the range of 12 to 3 g of salt
per day. Importantly, the dose-response relation exists in both
hypertensive and normotensive subjects. The current public
health recommendations to reduce salt intake from 9 to 12 g/d
to 5 to 6 g/d will have a major effect on blood pressure and
cardiovascular disease but are not ideal. A reduction to 3 g of
salt per day will have a much greater effect and should now
become the long-term target for population salt intake
worldwide.
Perspectives
The totality of evidence that links salt intake to blood
pressure is now overwhelming. Current recommendations are
to reduce salt intake from 9 to 12 g/d to 5 to 6 g/d. Our article
demonstrates that although these reductions will have a major
effect on blood pressure and cardiovascular disease, reducing
salt intake further to 3 g/d will have additional large effects.
Therefore, the target of 5 to 6 g/d should be seen as an interim
target, and the long-term target for population salt intake
worldwide should now be 3 g/d. This will be difficult,
particularly because in most developed countries, 75% to
80% of salt intake now comes from salt added to processed
foods. In our view, the strategy should be that the food
industry should gradually reduce the salt concentration of all
processed foods, starting with a 10% to 25% reduction, which
is not detectable by consumers, and continuing a sustained
reduction over the course of the next decade. This strategy
has now been adopted in the United Kingdom by both the
Department of Health and Food Standards Agency, and
several leading supermarkets and food manufacturers have
already started to implement such changes. Of all the dietary
changes to try and prevent cardiovascular disease, a reduction
in salt intake is the easiest change to make, because it can be
done without the consumers’ knowledge but will require the
cooperation of the food industry. Clearly, it would be helpful
if individuals also reduced the amount of salt that they add to
their own cooking or to their food. If this strategy were
implemented and achieved and the 3 g/d target were reached
throughout the world, there would be immense reductions in
strokes, heart attacks, and heart failure.
Acknowledgments
We are very grateful to the DASH-Sodium Steering Committee for
providing us with data necessary for calculating the dose-response
relation.
References
1. Ezzati M, Lopez AD, Rodgers A, Vander Hoorn S, Murray CJL, and the
Comparative Risk Assessment Collaborating Group. Selected major risk
factors and global and regional burden of disease. Lancet. 2002;360:
1347–1360.
2. Murray CJL, Lauer JA, Hutubessy RCW, Niessen L, Tomijima N,
Rodgers A, Lawes CMM, Evans DB. Effectiveness and costs of interventions
to lower systolic blood pressure and cholesterol: a global and
regional analysis on reduction of cardiovascular-disease risk. Lancet.
2003;361:717–725.
3. Prospective studies collaboration. Age-specific relevance of usual blood
pressure to vascular mortality: a meta-analysis of individual data for 1
million adults in 61 prospective studies. Lancet. 2002;360:1903–1913.
4. Intersalt Cooperative Research Group. Intersalt: an international study of
electrolyte excretion and blood pressure: results for 24-hour urinary
sodium and potassium excretion. BMJ. 1988;297:319–328.
5. Poulter N, Khaw KT, Hopwood BEC, Mugambi M, Peart WS, Rose G,
Sever PS. The Kenyan Luo migration study: observations on the initiation
of a rise in blood pressure. BMJ. 1990;300:967–972.
6. Forte JG, Pereira Miguel JM, Pereira Miguel MJ, de Padua F, Rose G.
Salt and blood pressure: a community trial. J Hum Hypertens. 1989;3:
179–184.
7. Lifton RP. Molecular genetics of human blood pressure variations.
Science. 1996;272:676–680.
8. Denton D, Weisinger R, Mundy NI, Wickings EJ, Dixson A, Moisson P,
Pingard AM, Shade R, Carey D, Ardaillou R, Paillard F, Chapman J,
Thillet J, Michel JB. The effect of increased salt intake on blood pressure
of chimpanzees. Nat Med. 1995;1:1009–1016.
9. Midgley JP, Matthew AG, Greenwood CM, Logan AG. Effect of reduced
dietary sodium on blood pressure: a meta-analysis of randomized controlled
trials. JAMA. 1996;275:1590–1597.
10. Cutler JA, Follmann D, Allender PS. Randomized trials of sodium
reduction: an overview. Am J Clin Nutr. 1997;65(suppl):643s–651s.
11. Graudal NA, Gallae AM, Garred P. Effect of sodium restriction on blood
pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride:
a meta-analysis. JAMA. 1998;279:1383–1391.
12. Hooper L, Bartlett C, Davey Smith G, Ebrahim S. Systematic review of
long term effects of advice to reduce dietary salt in adults. BMJ. 2002;
325:628–634.
13. Joint WHO/FAO expert consultation on diet, nutrition and the prevention
of chronic diseases. 2003, Geneva. Available at http://www.who.int/hpr/
NPH/docs/who_fao_experts_report.pdf. Accessed October 21, 2003.
14. Scientific Advisory Committee on Nutrition, Salt and Health. 2003. The
Stationery Office. Available at http://www.sacn.gov.uk/pdf/saltfinal/pdf.
Accessed October 21, 2003.
15. Whelton PK, He J, Appel LJ, Cutler JA, Havas S, Kotchen TA, Roccella
EJ, Stout R, Vallbona C, Winston MC, Karimbakas J. National High
Blood Pressure Education Program Coordinating Committee. Primary
prevention of hypertension: clinical and public health advisory from The
National High Blood Pressure Education Program. JAMA. 2002;288:
1882–1888.
16. Dahl KL, Knudsen KD, Heine MA, Leitl GJ. Effects of chronic excess
salt ingestion: modification of experimental hypertension in the rat by
variations in the diet. Circ Res. 1968;22:11–18.
17. MacGregor GA, Markandu ND, Sagnella GA, Singer D, Cappuccio FP.
Double-blind study of three sodium intakes and long-term effects of
sodium restriction in essential hypertension. Lancet. 1989;2:1244–1247.
18. Sacks FM, Svetkey LR, Vollmer WM, Appel LJ, Bray GA, Harsha D,
Obarzanek E, Conlin PR, Miller ER, Simons-Morton DG, Karanja N, Lin
PH. Effects on blood pressure of reduced dietary sodium and the dietary
approaches to stop hypertension (DASH) diet. N Engl J Med. 2001;
344:3–10.
19. He FJ, MacGregor GA. Effect of modest salt reduction on blood pressure:
a meta-analysis of randomised trials: implications for public health. J
Hum Hypertens. 2002;16:761–770.
20. Snedecor GW, Cochran WG. Statistical Methods. 8th ed. Ames, Iowa:
Iowa State University Press; 1989:149–176.
21. Parijs J, Joossens JV, der Linden LV, Verstreken G, Amery AKPC.
Moderate sodium restriction and diuretics in the treatment of hypertension.
Am Heart J. 1973;85:22–34.
22. Morgan TO, Myer JB. Hypertension treated by sodium restriction. Med J
Aust. 1981;2:396–397.
23. MacGregor GA, Markandu ND, Best FE, Elder DM, Cam JM, Sagnella
GA, Squires M. Double-blind randomised crossover trial of moderate
sodium restriction in essential hypertension. Lancet. 1982;1:351–355.
1098 Hypertension December 2003
24. Watt GCM, Edward C, Hart JT, Heart M, Walton P, Foy CJW. Dietary
sodium restriction for mild hypertension in general practice. BMJ. 1983;
286:432–436.
25. Silman AJ, Locke C, Mitchell P, Humpherson P. Evaluation of the
effectiveness of a low sodium diet in the treatment of mild to moderate
hypertension. Lancet. 1983;1:1179–1182.
26. Puska P, Iacono JM, Nissinen A, Korhonen HJ, Vartiainen E, Pietinen P,
Dougherty R, Leino U, Mutanen M, Moisio S, Huttunen J. Controlled,
randomised trial of the effect of dietary fat on blood pressure. Lancet.
1983;1:1–5.
27. Richards AM, Nicholls MG, Espiner EA, Ikram H, Maslowski AH,
Hamilton EJ, Wells JE. Blood-pressure response to moderate sodium
restriction and to potassium supplementation in mild essential hypertension.
Lancet. 1984;1:757–761.
28. Erwteman TM, Nagelkerke N, Lubsen J, Koster M, Dunning AJ.
-Blockade, diuretics, and salt restriction for the management of mild
hypertension: a randomised double blind trial. BMJ. 1984;289:406–409.
29. Chalmers J, Morgan T, Doyle A, Dickson B, Hopper J, Mathews J,
Matthews G, Moulds R, Myers J, Nowson C, Scoggins B, Stebbing M.
Australian National Health and Medical Research Council dietary salt
study in mild hypertension. J Hypertens. 1986;4(suppl 6):S629–S637.
30. Grobbee DE, Hofman A, Roelandt JT, Boomsma F, Schalekamp MA,
Valkenburg HA. Sodium restriction and potassium supplementation in
young people with mildly elevated blood pressure. J Hypertens. 1987;5:
115–119.
31. Australian National Health and Medical Research Council Dietary Salt
Study Management Committee. Effects of replacing sodium intake in
subjects on a low sodium diet: a crossover study. Clin Exp Hypertens.
1989;A11:1011–1024.
32. Australian National Health and Medical Research Council Dietary Salt
Study Management Committee. Fall in blood pressure with modest
reduction in dietary salt intake in mild hypertension. Lancet. 1989;1:
399–402.
33. Benetos A, Yang Yan X, Cuche JL, Hannaert P, Safar M. Arterial effects
of salt restriction in hypertensive patients: a 9-week, randomized, doubleblind,
crossover study. J Hypertens. 1992;10:355–360.
34. Fotherby MD, Potter JF. Effects of moderate sodium restriction on clinic
and twenty-four-hour ambulatory blood pressure in elderly hypertensive
subjects. J Hypertens. 1993;11:657–663.
35. Cappuccio FP, Markandu ND, Carney C, Sagnella GA, MacGregor GA.
Double-blind randomised trial of modest salt restriction in older people.
Lancet. 1997;350:850–854.
36. Watt GC, Foy CJ, Hart JT, Bingham G, Edwards C, Hart M, Thomas E,
Walton P. Dietary sodium and arterial blood pressure: evidence against
genetic susceptibility. BMJ. 1985;291:1525–1528.
37. Mascioli S, Grimm RH, Launer C, Svendsen K, Flack J, Gonzalez N,
Elmer P, Neaton J. Sodium chloride raises blood pressure in normotensive
subjects: the study of sodium and blood pressure. Hypertension.
1991;17(suppl I):I-21–I-26.
38. Cobiac L, Nestel PJ, Wing LMH, Howe PRC. A low-sodium diet supplemented
with fish oil lowers blood pressure in the elderly. J Hypertens.
1992;10:87–92.
39. The Trials of Hypertension Prevention Collaborative Research Group.
The effects of nonpharmacologic interventions on blood pressure of
persons with high normal levels: results of the Trials of Hypertension
Prevention, phase I. JAMA. 1992;267:1213–1220.
40. Ruppert M, Overlack A, Kolloch R, Kraft K, Gobel B, Stumpe KO.
Neurohormonal and metabolic effects of severe and moderate salt
restriction in non-obese normotensive adults. J Hypertens. 1993;117:
743–749.
41. Nestel PJ, Clifton PM, Noakes M, McArthur R, Howe PR. Enhanced
blood pressure response to dietary salt in elderly women, especially those
with small waist:hip ratio. J Hypertens. 1993;11:1387–1394.
42. Schorr U, Distler A, Sharma AM. Effect of sodium chloride- and sodium
bicarbonate-rich mineral water on blood pressure and metabolic parameters
in elderly normotensive individuals: a randomized double-blind
crossover trial. J Hypertens. 1996;14:131–135.
43. The Trials of Hypertension Prevention Collaborative Research Group.
Effect of weight loss and sodium reduction intervention on blood pressure
and hypertension incidence in overweight people with high-normal blood
pressure: The Trials of Hypertension Prevention, Phase II. Arch Intern
Med. 1997;157:657–667.
44. Henderson L, Irving K, Gregory J, Bates CJ, Prentice A, Perks J, Swan G,
Farron M. National Diet and Nutrition Survey: Adults Aged 19 to 64.
2003:3:127–136.
45. Pietinen P. Estimating sodium intake from food consumption data. Ann
Nutr Metab. 1982;26:90–99.
46. Coronary heart disease statistics. British Heart Foundation Statistics
Database 2002. http://www.dphpc.ox.ac.uk/bhfhprg/stats/2000/index.
html. Accessed December 17, 2002.
47. Law MR, Frost CD, Wald NJ. By how much does dietary salt reduction
lower blood pressure? I-Analysis of observational data among populations.
BMJ. 1991;302:811–815.
48. Nestle M. Food Politics: How the Food Industry Influences Nutrition and
Health. London, England: University of California Press; 2002.
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