Systematic review of long term effects of advice to reduce dietary salt in adults
BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7365.628 (Published 21 September 2002) Cite this as: BMJ 2002;325:628All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Sir,
Hooper and her colleagues in their meta-analysis of randomised trials
of individual dietary advice to reduce salt intake conclude that such
intervention will have little effect on health.1 They do not
satisfactorily distinguish whether salt reduction per se only confers a
small benefit or whether it could confer a large one but people in
practice fail to reduce their salt intake to any material extent. As a
result the reader may conclude from the paper that reducing salt intake is
unimportant.
This is not the case. Reducing the present average salt consumption
in Britain by 3g per day (about one third) would reduce average blood
pressure by about 5mmHg systolic in people over 50 and thereby reduce the
incidence of heart attack and strokes by about 15% and 22% respectively.2
A reduction of 6g would reduce blood pressure by about twice as much with
a corresponding additional reduction in the risk of heart attacks and
stroke. Reducing salt intake throughout the community would thus have a
major impact in the prevention of cardiovascular disease.
The obstacle to prevention is that nearly all the salt we eat is
hidden, added to a wide range of foods in manufacturing and processing.
Only about 15% is discretionary in the sense that an individual can alter
his or her intake through their own cooking and by adding salt at the
table. It is therefore not surprising that trials of advising people to
alter their salt intake will demonstrate little effect.
There is no doubt that when salt intake is reduced blood pressure
falls. The trials that show this best were not included in the meta-
analysis of Hooper and her colleagues. They were ones in which dietary
advice was reinforced by the provision of low salt staple foods such as
bread, which is a major contributor to hidden salt in the national diet.3-
5
While the effect of avoiding discretionary salt is modest it is none
the less real, achievable and worthwhile. Unfortunately it will have been
underestimated in the analysis of Hooper and her colleagues because the
participants in the trials they analysed will have included people who
would have already stopped taking steps to avoid using discretionary salt
thus diluting the effect.
For these reasons we believe the analysis of these trials and the
conclusions drawn are uninformative other than confirming the observation
that little is to be gained by one to one dietary advice. The public
health challenge is to gradually alter the amount of salt used in the
manufacturing and processing of food. Over a ten or 15 year period salt
intake could be reduced by two thirds. This would cause no untoward
effects and confer substantial health benefits.
MR Law
NJ Wald
Department of Environmental &Preventive Medicine,
Wolfson Institute of Preventive Medicine,
Barts & The London,
Queen Mary School of Medicine & Dentistry,
Charterhouse Square,
London EC1M 6BQ
References
1. 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: 628-32.
2. Law MR, Frost CD, Wald NJ. By how much does dietary salt
reduction lower blood pressure? BMJ 1991; 302: 811-824.
3. Sacks FM, Svetkey LP, Vollmer WM et al. Effects on blood pressure
of reduced sodium and the dietary approaches to stop hypertension (DASH)
diet. N Eng J Med 2001; 344: 3-10.
4. Cappuccio FP, Markandu ND, Carney C, Sagnella GA, MacGregor GA.
Double-blind randomised trial of modest salt restriction in older people.
Lancet 1997; 350: 850-54.
5. Korhonen MH, Litmanen H, Rauramaa R, Vaisanen, Niskanen L,
Uusitupa MIJ. Adherence to the salt restriction diet among people with
mildly elevated blood pressure. European Journal of Clinical Nutrition
1999; 53: 880-88
Competing interests: No competing interests
I am puzzled at the BMJ's decision to publish the paper from Hooper
and colleagues on long-term effects of advice to reduce salt intake in
adults (21 September, p 628). The paper adds nothing new to the literature. We already have
substantial evidence accumulated over several decades that reducing salt
intake lowers blood pressure1-3. It has also been clear for many years
that advice targeted at individuals will not produce substantial and
sustained reductions in salt intake as most salt in our diet is added by
the food industry to processed food such as bread, cooked meat and
breakfast cereals4. It is true that we have limited data on mortality and
on cardiovascular events from sodium restriction trials. This is clearly
an important issue but again it is one that has been repeatedly
highlighted in the literature in recent years1-3.
The discussion section of this paper has elements of spin worthy of
tabloid journalism with selective and uncritical citation of relevant
papers and a lack of context. The arguments seem largely based on a
simplistic, individually based model of health promotion. There is only
cursory reference to the fact that dietary salt restriction is a
population health issue that needs to be tackled at the population level,
both by regulation and collaborative work with the food industry. The
authors raise the spectre of possible harm from sodium restriction,
raising the possibility of adverse effects on cardiovascular disease and
all cause mortality. This speculation, which clearly goes well beyond the
clinical trial data, is largely based on two papers from Alderman5-6 that
have been extensively criticised in correspondence and reviews1-4. They
fail to cite the paper by Tuomilehto and colleagues linking higher dietary
salt intake with increased risk of cardiovascular events and increased
mortality7. Given that the current high levels of dietary salt intake
amongst children and adults can be largely attributed to salt added to
processed food at concentrations well in excess of physiological
requirements, the notion that efforts to achieve modest reductions in salt
intake will have adverse effects on health is implausible to say the
least. Meta-analysis is a powerful tool but it does not absolve its
practitioners from the need to exercise their critical faculties.
The caption on the front cover of the BMJ edition in which this paper
was published falls short of the standard expected from a peer-reviewed
international medical scientific journal. I assume it is a source of
embarrassment to the authors of this paper.
1. He J, Whelton PK. Salt intake, hypertension and risk of
cardiovascular disease: an important public health challenge. Int J
Epidemiol 2002;31:327-31.
2. Elliott P, Stamler J. Evidence on salt and blood pressure is
consistent and persuasive. Int J Epidemiol 2002;31:316-19.
3. MacGregor G, de Wardener HE. Salt, blood pressure and health. Int
J Epidemiol 2002; 31:320-7.
4. Perry IJ. Dietary salt intake and cerebrovascular damage. Nutr Metab
Cardiovasc Dis. 2000;10:229-35.
5. Alderman MH, Cohen H, Madhavan S. Dietary sodium intake and
mortality: the National Health and Nutrition Examination Survey (NHANES I)
[see comments]. Lancet 1998;351(9105):781-5.
6. Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH. Low urinary
sodium is associated with greater risk of myocardial infarction among
treated hypertensive men [see comments]. Hypertension 1995;25(6):1144-52.
7. Tuomilehto J, Jousilahti P, Rastenyte D, et al. Urinary sodium
excretion and cardiovascular mortality in Finland: a prospective study.
Lancet 2001;357(9259):848-51.
Competing interests: No competing interests
Neither the safety nor benefit of long term reduced sodium intake has been established in hypertensi
To The Editor:
Drs. Hooper et al1 have added another fine Cochrane Review - this
time of low salt diets. In an arena where authoritative advise had
generally held sway, this rigorous review establishes what is known and
identifies the questions that need answering before sound public policy
can be articulated.
However, the comment “A low salt diet may help people taking
antihypertensive drugs to stop their medication without loss of blood
pressure control” is a disappointingly obscure conclusion. It is based upon
little data and begs the important question of whether patients are better
off by substituting a low sodium diet for, say, a low dose diuretic. Sodium
restriction is both less effective in lowering BP,2 and substantially more
expensive3 than conventional therapy. More importantly, no clinical trial
data support the notion that low sodium provides cardioprotection
equivalent (or superior) to antihypertensive drugs. Different approaches
to BP control, with equal efficacy in terms of the surrogate endpoint,
differ significantly in terms of stroke and heart attack.4 A randomized
clinical trial could determine the health effect of a low sodium diet, but
there is precious little at this point to justify such an undertaking.
Surprisingly, after so many years of recommending a low sodium diet for
hypertensive patients, only one prospective observational study linking
baseline sodium intake to health outcomes has been published. That study
revealed a significant independent inverse relationship of sodium intake
and CVD morbidity.5
I believe that the Cochrane recommendations could be supplemented by
a clear statement indicating that neither the safety nor benefit of long
term reduced sodium intake in hypertensive patients has been established.
Yours truly,
Michael H. Alderman
References:
1. Hooper L, Bartlett C, Smith GD, Ebrahim S. Systematic review of long
term effects of advice to reduce dietary salt in adults. BMJ 2002;325;628-
636.
2. Cheung MMY, Law, CY, Ho GYY, Ng PPY, Kumana CR, Lau CP. Efficacy of non
-pharmacological treatment of hypertension. AJH 2001;14(4), Part 2:141A.
3. Elliott, WJ. Cost-minimization analysis of discontinuing
antihypertensive medication: The Tone Study. AJH 2001;14(4), Part 2:141A-
141A.
4. Lindholm LH, Ibsen H, Dahlof B, et al: Cardiovascular morbidity and
mortality in patients with diabetes in the losartan intervention for
endpoint reduction in hypertension study (LIFE): A randomised trial
against atenolol. Lancet 2002;359:1004-1010.
5. Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH. Low urinary
sodium associated with greater risk of myocardial infarction among treated
hypertensive men. Hypertension 1995;25(6):1144-1152.
Competing interests: No competing interests
Dear Sir
We read the article and editors comment with great interest
and were very surprised at the conclusions drawn in the editorial on
reviewing the article 1.
From the data presented it would seem clear that a modest salt
reduction leads to a significant fall in blood pressure. Indeed on a
global basis a reduction of salt intake would have a huge impact on blood
pressure (a 1-2 mmHg fall which could save “millions” of lives). On can
only assume that the article has been misinterpreted in the comments or at
least the findings undervalued. As clinicians one strives to alter life
style patterns to improve well being. Sodium restriction results in
altered intake of other nutrients and therefore would tend to exert a
positive beneficial effect, which should not be overlooked in a broader
picture. This present article in no way aids this or helps to put further
pressure on industry to reduce the salt content in food.
From a physiological point of view it needs to be remembered that the
kidney functions to avidly retain salt not as in many Westernised and
other cultures where it tries desperately to remove sufficient salt to
maintain salt homeostasis.
It was clearly noted in chimpanzee experiments, that salt loading led
to the development of which resolved on discontinuing salt 2. Similar
observations have been noted in humans 3 and population based studies 4.
Historically the average consumption of sodium was in the order of at most
1-2 g a day, while at present the average person consumes between 7-10 g
per day of sodium 4. Do we really need compelling data to convince us to
return to the biological norm. Finally the huge benefit to the efficacy of
many anti-hypertensive drugs favours the continued philosophy to reduce
salt intake.
We therefore should at all times be stressing to people to reduce
salt intake to as low a value as possible. Certainly we should be striving
to reach a level of less than 6 g /day of salt (equivalent of
approximately 2.4g of sodium) 5.
1. Systematic review of long term effects of advice to reduce dietary
salt in adults. Lee Hooper, Christopher Bartlett, George Davey Smith, and
Shah Ebrahim. BMJ 2002; 325: 628
2. Denton D, Weisinger R, Mundy NI et al. The effects of increased
salt intake on blood pressure of chimpanzees. Nat Med 1995; 1: 1009.
3. Hofman A, Hazebroek A, Valkenburg HA, A randomised trial of sodium
intake and blood pressure in newborn infants. JAMA 1983; 250: 370.
4. Gleibermann L. Blood pressure and dietary salt in human
populations. Ecol Food Nutr 1973; 2: 143-156.
5. Joint National Committee on Prevention, detection, Evaluation and
treatment of high Blood pressure. The sixth report. Arch Intern Med 1997;
157; 2413-2446.
Dr Sunil Bhandari
Honorary Senior Lecturer
Consultant Nephrologist/Physician
Hull Royal Infirmary,
Hull and East Yorkshire NHS trust,
Kingston upon Hull
HU3 2JZ
Competing interests: No competing interests
I fully understand the requirement for research but in all honesty,
on when working on the ground, the main problem with controlling
hypertension is due to patient non compliance with diet etc. Patient
education because of the limited time doctors are given is also poor. It
is vital to provide individuals with the necessary education about CHD and
other conditions related to hypertension. Only then will motivation and
compliance improve.
I often find that patients react well to providing them with leaflets
to educate them. In the age of the internet, there are various communities
to assist them.
Dietary education is very poor indeed. There is a national shortage
of dieticians and the importance of weight reduction, low salt intake and
the necessary food changes are not provided to patients. Without education
the doctor will be banging his head against the brick wall.
Medication compliance is good once the mechanism is explained to each
patient. Personally, I find providing them with details of associations
gives them a plan so to speak to improve their lifestyle.
This is the website of the Blood Pressure Association for any GPs out
there who wish to provide their patients with a print out. I find them
helpful and informative reducing the time needed to educate your patients.
Blood Pressure Association
http://www.bpassoc.org.uk/home.htm
By post
Blood Pressure Association
60 Cranmer Terrace
London
SW17 0QS
By telephone or fax:
Telephone: 020 8772 4994
Membership Line: 020 8774 4983
International: +44 208 772 4994
Fax : 020 8772 4999
Kind Regards
Dr Rita Pal
Competing interests: No competing interests
The systematic review of advice to reduce dietary salt in adults by
Hooper et al[1] highlights a common misconception through the
inconsistent and interchangeable use of ‘sodium’ and ‘salt’. It is
accepted that salt has an adverse effect on blood pressure. Studies have
demonstrated that restriction of dietary ‘sodium’ improves blood pressure,
although to varying degrees. However, these studies have considered sodium
in the form of sodium chloride i.e. table salt. Approximately 95% of
dietary sodium is in the form of sodium chloride. As such, in referring to
dietary sodium, we are making reference to table salt. I would advocate
scientific accuracy in referring to ‘salt’ as either ‘salt’, ‘table salt’
or ‘sodium chloride’, but certainly not sodium (Na+)!
Why this need you might ask? It would seem that all sodium in its
associations are not created equal, particularly when referring to
influences on blood pressure.
American Heart Association Dietary Guidelines[2] qualify salt as
sodium chloride. In a statement by the AHA Nutrition Committee[3],
referenced in the Dietary Guidelines, the following appears:
“full expression of NaCl-sensitive hypertension depends on the
concomitant intake of both sodium and chloride. In both experimental
models and humans, blood pressure is not increased by a high dietary
sodium intake provided as non-chloride salts of sodium.”
A number of small studies[4,5], have been undertaken to determine the
impact of sodium with chloride and other anions such as bicarbonate on
blood pressure. Essentially, the findings support the adverse influence of
chloride ions when associated with sodium on blood pressure, and do not
implicate other associated anions such as bicarbonate. The weight of
evidence is very much against the use of sodium chloride (salt) and not
sodium in other forms.
Such scientific accuracy becomes essential in health awareness
campaigns, such as advising patients to reduce their ‘sodium’ intake. If
we are concerned about their blood pressure, we should make it clear we
refer to salt (sodium chloride), as many foods and medicines may contain
sodium in other forms e.g. bicarbonate. Would we be keen to deprive
ourselves of a favourite food or an effective medicine through a failure
to correctly define what constitutes a good or bad sodium ion?
In conclusion, evidence-based medicine should encourage us to qualify
our use of the words salt or sodium in the context of hypertension as
‘salt’, ‘table salt’ or ‘sodium chloride’, but not just any sodium!
[1] Hooper L, Bartlett C, Smith GD, Ebrahim S. Systematic review of
long term effects of advice to reduce dietary salt in adults. BMJ
2002;325: 628-636.
[2] Nutrition Committee of the American Heart Association. AHA
Dietary Guidelines Revision 2000: A Statement for Healthcare
Professionals. Circulation 2000; 102: 2284 –2299.
[3] Theodore A. Kotchen and David A. McCarron for the Nutrition
Committee
Dietary Electrolytes and Blood Pressure. A Statement for Healthcare
Professionals From the American Heart Association Nutrition Committee.
Circulation 1998; 98: 613-617.
[4] Luft FC, Zemel MB, Sowers JA, Fineberg NS, Weinberger MH. Sodium
bicarbonate and sodium chloride: effects on blood pressure and electrolyte
homeostasis in normal and hypertensive man. J Hypertens 1990 Jul;8(7):663-
70.
[5] Kurtz TW, Morris RC Jr. Dietary chloride as a determinant of
"sodium-dependent" hypertension. Science 1983 Dec 9; 222(4628): 1139-41.
Competing interests: No competing interests
EDITOR - The finding that small reductions in salt intake (2
grams/day) have a less but significant effect on blood pressure[1] than
larger reductions (5 grams/day) is hardly surprising; but nevertheless on
a population basis this would have a large effect on reducing strokes,
heart failure and coronary heart disease.
However, Hooper et al do not ask the obvious question - "Why is it so
difficult for people to restrict salt intake long term?". The authors
claim that the interventions used were highly intensive, but the majority
of the studies give no details as to how and what advice was offered, so
how do they know this? Furthermore, 75% of the western population's salt
intake now comes from processed food[2], for example one quarter of the
present UK salt consumption comes from bread. It is therefore vital to
either avoid processed foods or to provide processed foods with less salt
in these studies. Unfortunately, none of the studies provided reduced salt
foods. The interpretation of their study is not helped by the front cover
writer of the BMJ who appears to have read a different paper and
completely misinterpreted the important positive findings in their paper.
The confusion is increased by the authors' own press release[3] which
rightly puts the blame for the difficulty in reducing salt intake squarely
on the food industry and states that it is important to reduce salt intake
and that this would have a major effect on blood pressure and would be
easy to do if the salt content of processed food was reduced.
This confusion is compounded by errors in the meta-analysis. For
instance, the 18 month TOPH trial (phase I) was included as a long term
intervention trial over "60 months", but salt intake was reduced for only
18 months in this study with all participants returning to their normal
diet after 18 months, and yet the authors included this as a study of salt
restriction over 5 years. There are also misquoted references, and in
particular the authors have not read the correspondence following these
papers. The authors fail to put into perspective the comparison of
reducing salt intake to other lifestyle or dietary interventions in
preventing cardiovascular disease. The totality of evidence for reducing
salt, including epidemiological, intervention, migration, treatment,
animal and molecular biology studies is stronger than for any of the other
non-pharmacological treatment. Ninety-five percent of the population are
at risk from developing cardiovascular disease[4], and 40% die from it.
There are no studies showing a reduction in mortality in controlled trials
of the effects of stopping smoking, reducing fat intake alone (without
fish oil supplements), reducing salt intake or losing weight, or for that
matter increasing fruit and vegetable consumption or increasing exercise.
Indeed, for most of these factors there has been no attempt to do long
term studies, even on intermediate variables. This is due to the innate
difficulty of conducting and funding long term dietary and lifestyle
changes and now the ethics of randomly putting a group of people, for
instance on a high salt intake for the rest of their lives. The question
that Hooper et al need to consider is what strength of evidence is needed
to give dietary and lifestyle advice to try and prevent cardiovascular
disease as there will not be mortality data.
Their study clearly indicates the importance of reducing salt intake
in the population, even by small amounts, and in particular, as they
agree, in the treatment of high blood pressure whether on its own or in
conjunction with medical therapy where there is clear evidence of major
additive effects[5].
The editor of the BMJ needs to publish a retraction of his very
misleading front cover and read the authors' own press release.
Graham A. MacGregor, Professor of Cardiovascular Medicine,
Blood Pressure Unit, St. George's Hospital Medical School, Cranmer
Terrace, London SW17 0RE.
g.macgregor@sghms.ac.uk
Feng J. He, Cardiovascular Research Fellow,
Blood Pressure Unit, St. George's Hospital Medical School, Cranmer
Terrace, London SW17 0RE.
References
[1] 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;325:628-32.
[2] Nestle M. Food politics - How the food industry influences
nutrition and health. University of California Press, London, England
2002.
[3] New ways of reducing salt intake needed to make a long-term
impact on blood pressure. University of Bristol, Media release.
http://bris.ac.uk/Depts/Info-Office/news/archive/salt.htm
[4] Beaglehole R. Global cardiovascular disease prevention: time to
get serious. Lancet 2001;358:661-3.
[5] MacGregor GA, Markandu ND, Singer DRJ, Cappuccio FP, Shore AC,
Sagnella GA. Moderate sodium restriction with angiotensin converting
enzyme inhibitor in essential hypertension: a double blind study. BMJ
1987;294:531-4.
Competing interests: No competing interests
Sir
I would go further and ask what problems are to be encountered with
insufficient salt intake; in Traditional Chinese Medicine we expect
insufficiency of salt (by this I mean natural salt not refined) to
seriously affect the 'kidney system' (hypothalamic-pituitary-adrenal
axis); 'hypo-kidney' amongst other complaints are treatable with increased
salt intake.
Regards
John H.
Competing interests: No competing interests
Sir,
More and more, words like "is unclear", "is not sure" and so on are
published in serious medical journals like yours. More and more trust is
disappearing when one reads that every thing you knew "could be" false.
It is really very disappointing reading yesterday that your
knowledge about preparatory exercices before sport "could not" be helping
(against previous knowledge...or beliefs?), reading today vague meta-
analytical comments on salt reduction and its impact on health (which
"could not be" sure...).
The list is longer every month. It is of course necessary to revise
our positions as well as to "analyse analysis". I would like, however, clear statements about these different matters. It is very
negative to throw a suspicion on a specific belief without giving in
return a clear demonstration of the contrary.
If salt reduction is reducing blood pressure, could it not be helping
health, perhaps in an indirect way? How helpful for us, simple
medical doctors are these destructive articles?
If you have THE demonstration that something is actually false or not
working, please demonstrate. If you cannot present a STRONG demonstration,
please do not continue to undermine our faith, our trust.
Competing interests: No competing interests
Salt consumption and commercial interests
On the front cover of your 21 September 2002 issue there is a banner
heading that "SALT REDUCTION IN INDIVIDUALS is hard to achieve, harder to
sustain, and maybe not worth the effort". This admonition is based on
Hooper et al's accompanying paper1, but this states that "cutting salt
concentrations in processed foods .....can achieve small reduction in
blood pressure across the whole population for sustained periods of time"
and that ..."across the whole population the effect may be substantial".
Furthermore as the main source of dietary salt is in processed food and
the food industry appears to be willing to co-operate, a reduction in the
salt content of food is not hard to achieve, or to sustain.
There is a suggestion that the front cover's comments were engendered
by Hooper et al's reference to two papers by Alderman and his
colleagues2,3 which claimed that a reduction in habitual salt intake
increases the risk of myocardial infarction. In the first paper 24hr
urinary salt excretion was estimated after a 5 day period of salt
restriction and parallelism between 24hr urinary salt excretion,
creatinine clearance and creatinine excretion demonstrated that there were
serious problems with urine collection4. Therefore the estimations of 24hr
urinary sodium excretion (on which was based the dietary intake of sodium)
were irrelevant and insecure. In the second paper salt consumption was
based on 24hr dietary recall of "nutrient intake" in 11,348 subjects
between 1971-1975, who were examined 20 years later. The data revealed
that many of the subjects held grossly incorrect ideas of what they were
consuming. For instance, 25% had a salt intake below 4.5g/day for men and
3g/day for women (i.e. well below the 6g/day now recommended) with a
calorie intake about 50% lower than the national recommended daily
allowance4.
Furthermore it was remarkable that 20 years later the women on
such a near starvation diet were on average 4kg heavier than the 25% on
the high salt intake who were eating twice as many calories. Calculations
based on such data are invalid.
These papers were widely publicised by The
Salt Institute, a public relations body in the USA supported by commercial
interests. It conducts a campaign to oppose
Government action to lower salt intake. The Institute offered to
distribute reprints of the second paper as a "professional courtesy". Dr.
Alderman was a consultant to the Salt Institute.
1 Hooper L, Bartlett C, Smith GD, Ebrahim S. Systemic review of long
term effects of advice to reduce dietary salt in adults. BMJ 2002;325:628-
32.
2 Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH. Low sodium is
associated with greater risk of myocardial infarction among treated
hypertensive men. Hypertension 1995;25:1144-52.
3 Alderman MH, Cohen H, Madhavan S. Dietary sodium intake and mortality:
the national health and nutrition examination survey (NHANES.1). Lancet
1998;351:781-785.
4 de Wardener HE. Salt reduction and cardiovascular risk: the anatomy of a
myth. J Human Hypertens 1999;13:1-4.
Competing interests:
None declared
Competing interests: No competing interests