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For Debate
The salt dilemma: some answers, many questions
M Gary Nicholls and A Mark Richards
MJA 1999; 170: 178-180
| Introduction |
The many studies linking dietary sodium intake with blood pressure
present conflicting views on the benefits and risks of salt
restriction. Reviews, and more recently meta-analyses (which, as
discussed by Swales,46 must be viewed with
caution), have become commonplace in the struggle to reach firm
conclusions about the importance of dietary sodium in contributing
to raised blood pressure levels and the cardiovascular
complications of hypertension. The continuing debate reflects
inadequacies in the information.
We present a personal view of, firstly, whether moderate dietary
sodium restriction in Western society reduces arterial pressure;
secondly, whether such dietary sodium restriction reduces the
complications of hypertension; thirdly, whether sodium
restriction has adverse effects; and finally, whether a population
approach to reducing dietary sodium is practical.
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Does moderate restriction of dietary sodium reduce arterial
pressure? | |
Most studies of dietary sodium restriction have been short term.
Furthermore, vital methodological features (eg, using objective
techniques for measuring blood pressure, and randomisation of
dietary regimens) have often been ignored. Many of these trials would
be considered unacceptable were antihypertensive drugs rather than
dietary sodium being scrutinised.
From our overview of studies in Western countries, we conclude that
restricting a population's dietary sodium intake to about 80-100
mmol/day has a minor and variable effect on arterial pressure. A
majority of people show a small fall in arterial pressure, but a
sizeable minority exhibit no change or even a slight rise. An
antihypertensive effect is most readily seen in the elderly, in
African Americans and in people with moderate to severe
hypertension.37,47-49 Younger subjects
and those who are normotensive or have mild hypertension generally
exhibit little or no fall in arterial pressures.49,50
Individual blood pressure responses relate in part to activation of
the renin-angiotensin and sympathetic systems as dietary sodium
intake is reduced.41,51-53
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Effects of dietary sodium restriction on complications of
hypertension | |
We are not aware of interventional data demonstrating that moderate
dietary sodium restriction either reduces or increases the
complications of hypertension, namely stroke, myocardial
infarction, cardiac failure or renal failure.
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Does dietary sodium restriction have adverse effects? | |
Dietary sodium restriction stimulates the renin-angiotensin
system, plasma aldosterone and circulating
catecholamines,12 most obviously in young
subjects. Whether long term activation of these neurohormonal
systems is hazardous is a vexed question. Some researchers (with
Laragh and colleagues usually leading) consider that heightened
activity of the renin-angiotensin system constitutes a risk factor
for coronary heart disease, stroke, retinopathy and left
ventricular hypertrophy, especially in hypertensive
patients.14,21,44,54-57 Others have
found no evidence to support the view that the renin-angiotensin
system constitutes a cardiovascular risk factor in hypertensive or
normotensive subjects.58-60 Recently, the report
from the first National Health and Nutrition Examination Survey
(NHANES I) added fuel to the controversy by documenting an inverse
association between all-cause mortality and sodium intake in a
representative sample of 11 346 adults in the United
States.6 Vigorous debate followed in
the letters columns of journals, much of it focused on the adequacy (or
otherwise) of using a single assessment of sodium intake based on diet
recall.
There is no lack of animal and experimental information
demonstrating the vascular and cardiac toxicity of angiotensin
II,61 which, when added to the
accumulated data from New York in particular,14,21,44 raises questions
about the advisability of restricting dietary sodium intake over
years and decades. These data, however, are difficult to reconcile
with evidence that a high dietary sodium intake (which should
suppress renin secretion) is claimed to have adverse effects on blood
vessels and the heart beyond, and perhaps independent of, any action
via an increase in arterial pressure.62-64 Information from a
small number of laboratories suggests that raised levels of
aldosterone, like angiotensin II, may have adverse effects,
particularly on the heart.65,66 Whether a chronic
threefold elevation in aldosterone levels with restriction of
dietary sodium12 could offset to a greater
or lesser extent any benefits from a concomitant fall in arterial
pressure is unknown.
It can be argued that diuretic-based antihypertensive treatment,
the effects of which are in many ways similar to those of dietary sodium
restriction, has been shown to reduce the cardiovascular
complications of hypertension notwithstanding stimulation of
angiotensin II, aldosterone and catecholamine levels.67-69 However,
these were intervention trials of about three to five years' duration
and often in elderly people with hypertension. Extrapolation from
short term, diuretic-based trials in elderly patients to longer term
dietary sodium restriction in young and middle-aged subjects could
be hazardous.
Dietary sodium restriction has been claimed to increase plasma
levels of total and low density lipoprotein cholesterol, to reduce
insulin sensitivity, to impair sleep and worsen fatigue, and to be
undesirable in pregnancy.12,70-73 Whether such
changes are significant or important in the long term is unknown. Some
bravely dismiss such possibilities outright.74
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The practicality of reducing dietary sodium in whole populations | |
Although there are exceptions,75 most researchers have
found it difficult to achieve a substantial reduction in dietary
sodium consumption in a majority of subjects in Western
populations.76,77
Many foods, particularly processed foods, have a high sodium
content, and presumably this is preferred by many. If food companies
reduced the sodium content of foods considerably, a daily intake in
the range of 80-100 mmol/day would be more readily attained. But
should industry be encouraged, even forced, to reduce the sodium
content of foods when evidence of benefit over risk remains so
tenuous?
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Conclusions |
- Dietary sodium restriction is advisable in all patients with
hypertension who are receiving antihypertensive drugs, with the
possible exception of monotherapy with a calcium channel
antagonist, as the antihypertensive action of this drug is arguably
little altered by the level of dietary sodium intake.
- Dietary sodium restriction is advisable as a trial over a period of
months in all patients with mild to moderate hypertension,
especially the elderly,49,78 as part of a "hygienic"
approach to reduce blood pressure, which should include weight loss
in the obese, restriction of alcohol intake in heavy drinkers, and
regular exercise in the sedentary.
- The realities of life dictate that few patients can alter more than
one or two lifestyle habits in the long term, and, given a choice of
which to pursue based on evidence of benefit versus risk, we recommend
weight loss, restriction of alcohol and regular moderate exercise
ahead of dietary sodium restriction. Other lifestyle changes might
repay further investigation.79
As noted already, the medical literature relating to dietary sodium,
blood pressure and its complications is vast and conflicting. The
controversy is well reflected in a recent overview in
Science, in which the real difficulties attending
interpretation of the Intersalt study,80 and especially
reanalysis of the original data,81 are
discussed.3 More information of an
objective nature is required before we admonish whole populations to
restrict dietary sodium intake, as, in our view (which has not changed
in 14 years82), the balance between
benefit and risk is unknown. Regarding lifestyle matters and general
health (not just in relation to hypertension), energy is better
directed to areas where the evidence is more secure, such as smoking
cessation, prevention of obesity and regular moderate exercise.
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Conflict of interest | |
None. We do not have any connection with or receive funds from the food
and salt industries or any related commercial interests.
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| | Authors' details | |
Department of Medicine, Christchurch Hospital, Christchurch, New
Zealand.
M Gary Nicholls, FRACP, Professor of Medicine.
A Mark Richards, FRACP, Professor of Medicine.
Reprints will not be available from the authors. Correspondence:
Professor M G Nicholls, Department of Medicine, Christchurch
Hospital, PO Box 4345, Christchurch, New Zealand.
Email: bgriffinATchmeds.ac.nz
©MJA 1998
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