Download - Salt, blood pressure and health

© 2001 British Nutrition Foundation Nutrition Bulletin, 26, 133–139

*Editor’s note. John Swales (MA MD FRCP FmedSci), Professor of

Clinical Medicine, was President of the British Hypertension Society

from 1982–4 and the author of five books and over 200 papers. He

was seconded to the Department of Health as Director of R & D

for the NHS between 1996 and 1998. This article was originally

submitted as a review paper. Sadly, Professor Swales passed away

(aged 64 years) on 17 October 2000, after a short illness. The peer-

refereeing process for this paper could not therefore be completed.

Correspondence about this article is welcomed and should be

addressed to the Editor.

NEWS AND VIEWS: RESEARCH

Salt, blood pressure and health

John Swales*

Clinical Sciences Building, Royal Infirmary, University of Leicester, UK

Introduction

The healthy individual has a right to feel confused by

the contradictory advice being given about dietary salt.

Some experts advocate a reduction in salt intake for

everyone, while others say this advice is unjustified in

those who do not suffer from high blood pressure. It is

not surprising that this has been described as one of the

most polarised fields in medical science. In spite of the

divergent views, evidence accruing over the last few

years has been remarkably consistent. We should there-

fore beware of older work claiming an enormous saving

of life if we all reduced our salt intake. In 1998, experts

for the leading American scientific journal, Science, eval-

uated the most widely quoted study that made this

claim. They concluded that the study was ‘so flawed as

to be effectively meaningless’.

People with high blood pressure in our society eat no

more salt than anyone else. In clinical trials, even major

reductions in salt intake, larger than could be achieved

normally, produce little or no reduction in blood pres-

sure. Blood pressure rises with age in developed soci-

eties, and this has been linked to salt intake in the

‘Intersalt Study’, but differences in blood pressure

between the developed and the developing world could

equally well be due to the other multiple differences in

stress and life. Nuns living in closed orders, for instance,

seem equally protected from this increase in blood pres-

sure, although their diet contains as much salt as others.

It is not of course possible for most of us to avoid

stress in such a radical way as this. Is there anything a

healthy individual can do to avoid the dangers of high

blood pressure? Here, there is scientific agreement.

Reducing weight, taking a diet high in fruit and vegeta-

bles, indulging in regular physical exercise and avoiding

excessive alcohol intake are all sensible, health-

promoting measures that help to lower blood pressure

and also carry other health benefits. The tragedy of the

salt controversy is that it has tended to distract atten-

tion from these sensible measures by unjustified and

controversial claims.

The significance of blood pressure

The modern debate about salt and blood pressure is

now reaching the end of its fifth decade, although hints

of it can be traced back to ancient Chinese literature.

The last few years must seem particularly bewildering

for those without any special knowledge. Claims that

there is a consensus amongst experts are countered by

a distinguished scientific journalist writing ‘if ever there

were a controversy over the interpretation of scientific

data, this is it’ (Taubes 1998).

I believe that the salt controversy is important to

everyone for two reasons. Firstly, reducing the burden

of high blood pressure would undoubtedly produce

major public health benefits. Secondly, it demonstrates

the pitfalls in trying to combine scientific accuracy and

caution with persuasive, credible public health advice.

High blood pressure is a major cause of ill-health and

death in developing countries. Because it injures blood

vessels, it is the most important risk factor in strokes,

an important contributor to heart attacks and kidney

disease and probably to deteriorating mental function

in the elderly. There is some exciting recent work sug-

gesting that high blood pressure even plays a role in

patients with Alzheimer’s disease. Over the last 30 years,

it has become clear that lowering blood pressure helps

to prevent strokes, heart attacks and kidney disease. No-

133

one now denies the importance of blood pressure

control in maintaining health, and we now have excel-

lent drugs that can achieve this in most patients.

This is the nub of the problem that confronts those

who provide health care. The risks associated with

blood pressure apply to everyone. Risk of suffering a

stroke, for instance, can be reduced by a modest lower-

ing of blood pressure even in those people who have

what used to be called ‘normal’ blood pressure. This

represents a very small benefit to the individual whose

blood pressure is not particularly high, but added up

across the whole population would have a major impact

upon the total number of strokes. Of course, mass

medication is not a realistic prospect, and so, medical

research has had to find other, hopefully harmless, ways

of reducing blood pressure through diet and lifestyle.

We have to be sure of our ground before advocating

such changes. Advising us to alter the way we organise

our lives may be attractive to those who run the UK

National Health Service (NHS), as it costs the NHS little

or nothing and may save it some of the costs of treat-

ing illness. However, there are personal and social costs

for even the simplest modification of diet. Those who

advocate change have to behave with the same degree

of responsibility they would be expected to employ in

prescribing a drug for a patient. Unfortunately, this has

not always been the case amongst enthusiasts for the

various ‘healthy’ diets and writers of ‘healthy’ recipe

books.

Scientific ‘evidence’

The UK NHS and other healthcare systems across the

world are undergoing a quiet revolution in the way in

which scientific evidence is used in decision-making.

This is the result of some tragic shortcomings in the tra-

ditional approach, which became clear about 10 years

ago. It became quite evident that so-called ‘expert’

advice was likely to be deeply flawed on occasions,

reflecting as it did conventional wisdom and prejudice.

This was demonstrated in a seminal study from Harvard

by Antman and his coworkers (Antman et al. 1992).

Treatment of heart attacks has improved vastly in recent

years with the development of thrombolytic ‘clot-

busting’ drugs, which are now used routinely. In the

early days, there were fears about drugs that inhibited

one of the body’s normal mechanisms for preventing

bleeding. Theoretically, these drugs could make matters

worse for victims of a heart attack, indeed, they are

harmful in a small minority of patients. By the mid-

1970s however, clinical trials had been performed that

showed net benefit for patients and subsequent trials

134 John Swales


simply reinforced that conclusion. Antman et al.however, went on to look at the expert advice being

given to doctors through textbook chapters and reviews

in specialist journals. Thrombolysis was rarely men-

tioned until the late 1980s and where it was referred to

at all, it was as an ‘experimental treatment’. Other

advice consistently recommended treatment that could

not be supported at all from clinical trial evidence and

that may actually have been harmful. When the only evi-

dence cited in favour of a treatment is that an ‘expert

group’ has recommended it, one should recall that

such expert groups tend to consist of selected individ-

uals of rather similar outlook with their own view of

accepted wisdom. The track record has not been good,

but what can be put in their place? The ‘experts’ tended

to select trials that supported their view and ignored or

denigrated those that did not, giving a misleading

impression of the overall conclusions of research.

Modern databases now allow immediate access to all

the relevant information on methods of preventing and

treating disease. This provides the basis for the ‘sys-

tematic review’, which figures increasingly in decision-

making in the NHS. Of course, a broad range of

expertise is still required in screening this evidence and

interpreting its relevance, but the day of the old-

fashioned expert setting out with their own firmly held

views and finding evidence to support them is now

passing. The NHS now funds two groups, the Cochrane

Centre and the Centre for Reviews and Dissemination,

which carry out systematic reviews to very high, care-

fully defined standards.

The second seminal episode in medical history under-

lined the caution required in interpreting ‘epidemiologi-

cal associations’. Because two things tend to happen

together, we cannot assume that they are cause and

effect. I think the best illustration of this fallacy was

provided by George Bernard Shaw in the Doctor’sDilemma, when he wrote:

‘Thus it is easy to prove that the wearing of tall hats

and the carrying of umbrellas prolongs life and confers

immunity from disease, for the statistics show that the

classes which use these articles are bigger, healthier and

live longer than the class which never dreams of pos-

sessing such things’ (Shaw 1911).

This may seem obvious. Nevertheless, a similar

assumption proved fatal for many people in the 1980s.

Many patients, after a heart attack, develop extra heart-

beats (sometimes felt as palpitations, although often

only picked up by carrying out an electrocardiogram).

When a particular form of these palpitations (ventricu-

lar extrasystoles) is present, patients are much more

likely to have a second, fatal heart attack, probably as

Salt, blood pressure and health 135


a result of a more serious disturbance of heart rhythm.

There is, in other words, an association between ven-

tricular extrasystoles and death from heart disease. For

many years, doctors assumed, quite reasonably, that this

was a causal relationship and gave patients drugs to

suppress the extra beats. It was only at the end of the

1980s that a trial was set up to assess the benefits of

this treatment (CAST Investigators 1989). The CAST

(Cardiac Arrhythmia Suppression Trial) has strongly

influenced the evidence used as a basis for providing

doctors with guidance. The trial was never completed.

In April 1989, it was discontinued. Deaths in the treated

group were over twice as great as in the control group

and it was no longer ethically acceptable to proceed

with it.

It has been calculated that more Americans died from

this treatment than died in the Vietnam War. The lesson

for doctors was in some ways a hard one. Not only was

an epidemiological association a flawed basis for treat-

ment, but clinical experience in quite carefully moni-

tored groups of patients had failed to detect evidence of

harm. This is not surprising. The overall annual mor-

tality rate is quite low even in these patients and an indi-

vidual doctor’s experience of patients dying will be quite

limited. An increase of one or two patients in a year is

likely to be attributed to chance. The message was quite

simple, and again points to the danger of unsupported

‘expert’ views. Where it is feasible to carry out clinical

trials, these should be done before recommendations are

made and, where several such trials have been carried

out, a proper systematic review from relevant databases

of evidence is needed. No regulatory agency would

accept unsupported clinical experience or carefully

selected clinical trials as sufficient evidence that a drug

did no harm.

Salt and blood pressure: the associations

Preventive medicine and public health have been much

slower to take on board these messages. It is to be hoped

that a much more scientific Food Standards Agency,

funded to carry out its own research and reviews, will

change this. It will not be easy. It is much more difficult

to carry out a randomised controlled trial in a healthy

population than in a group of patients. Nevertheless, in

the case of blood pressure, we have something that is

eminently measurable and can be studied easily in clini-

cal trials. If claims are made that a particular dietary

change will influence blood pressure, these can be exam-

ined with just as much rigour as is used for evaluating

a drug.

It is also true, however, that clinical trials are not so

good at picking up the net, very small, beneficial and

harmful effects of an intervention when these occur over

a long period of time. On other occasions, a trial may

be impossible. The role of smoking in lung cancer and

heart disease is a good example of an important risk,

the evidence for which is entirely based upon epidemi-

ological associations. Why should we accept this and

not all associations? Austin Bradford Hill, who, with

Richard Doll, discovered the tobacco lung cancer rela-

tionship, as well as designing the first randomised

clinical trial, laid down some important principles (Hill

1965). Besides being biologically plausible, associations

needed to be strong and consistent. They needed to

show a gradient, so that weaker influences were associ-

ated with less effect, and they needed to be specific. This

was true both of the smoking/cancer association and the

cholesterol/heart disease association. The association of

tobacco with lung cancer, for instance, was required to

be unique to tobacco and not due to other factors that

are associated with tobacco, such as social class and

diet. The existence of such ‘confounders’ is one of the

major pitfalls in ascribing causality to an association.

How far does the salt/blood pressure association meet

these criteria? The short answer is that it cannot,

because there is no such simple association. Individuals

with high blood pressure take no more dietary salt than

anyone else. It has been impossible to show any associa-

tion between blood pressure and measured salt intake

when this has been rigorously sought in quite large

studies of populations such as the study carried out

in Scotland some years ago (Smith et al. 1988). This is

in striking contrast to, for example, the relationship

between cholesterol and heart disease where the evi-

dence for causality is now strong.

It is surprising, under such circumstances, that so

much emphasis in the public debate has been placed on

a different type of association study, ‘Intersalt’ (Intersalt

Cooperative Group 1988). This looked at salt intake

across a wide range of cultures extending from the

United States to the Yanamamo Indians of South

America. The latter, like some of the other populations

examined, take extremely small quantities of salt, well

below the level that could ever be achieved in developed

societies. Even so, when other factors that can influence

blood pressure were taken into account, it proved

impossible to show any relationship between salt intake

(measured by the sodium content of urine) and diastolic

blood pressure. In addition, only a minuscule change in

systolic blood pressure was shown over extremely large

differences in salt intake. In the reports of Intersalt, this

finding took second place to a different sort of analysis,

which proved more positive, although it had not fea-

tured at all in the original objectives of the study. Blood

pressure rises with age in developed societies, but

remains at low levels throughout life in nonurban unde-

veloped societies such as the Yanamamo. Intersalt noted

a strong relationship between the rise in blood pressure

with age and measured salt intake. The advocates of

salt reduction have attached great importance to this

finding. As an isolated finding, however, its significance

is doubtful. For one thing, the phrase ‘rise in blood pres-

sure with age’ is not, of course, based upon following

the same individuals through their natural lifespan. It is

based upon a single snapshot. The lifetime experience

of an older subject in Europe will include a childhood

perhaps spent in the war years, while a 30-year-old will

have quite a different background, both in respect to

diet and to working environment.

In fact, there are even stronger grounds to doubt the

assumption of causality in Intersalt. Although the rela-

tionship of blood pressure with salt intake is so con-

tentious, the relationship with other dietary and

environmental factors is much more clear-cut. Societies

such as the Yanamamo differ in many respects from

those who live in developed societies. Some of these dif-

ferences are dietetic, others reflect quite different

lifestyles, the effects of which are much more difficult

to measure and incorporate in statistical analyses. Diet

may be important. Increasing the amount of fruits and

vegetables, for instance, lowered blood pressure sub-

stantially without any reduction in salt intake in one

important recent study (Appel et al. 1997). Clearly, diet

was radically different in the examined populations in,

for instance, the components derived from vegetable

and animal sources.

More important however, we have more direct evi-

dence that the rise in blood pressure with age in the

developed world is not related to salt, or perhaps any

other dietary component. This comes not from another

cross-sectional study such as Intersalt, but a genuine

longitudinal study in which the same individuals were

carefully followed. In a classic piece of work, Timio fol-

lowed nuns who had entered a closed order for 20 years

(Timio et al. 1988). Unlike a control population of

women from the same background, these nuns showed

no rise in blood pressure with age. By the end of the

study, the differerence in systolic blood pressure

between the two groups was 30 mm Hg; a difference

about three times as great as could be produced by

giving the control women a blood-pressure-lowering

drug. This difference could not be accounted for by salt

or any other dietary component looked at, by body

weight or by childbearing.

It is difficult to treat the salt/blood pressure associa-

136 John Swales


tion evidence as though it were comparable to the evi-

dence that links tobacco and lung cancer or cholesterol

and heart disease. There are closer parallels in the field

of blood-pressure research, however. There has been

no difficulty in demonstrating an association between

bodyweight and blood pressure, or between heavy

alcohol intake and blood pressure. This counters some

of the arguments used to explain the weakness of the

salt/blood pressure association evidence: that measure-

ments are too imprecise; that a lifetime’s exposure is

required; or that only predisposed individuals will

respond with high blood pressure. All such arguments

suggest a degree of special pleading for fundamentally

negative findings. This is fairly unusual in the applica-

tion of epidemiology to medicine. In most cases, posi-

tive associations are critically examined for possible

confounding factors creating spurious relationships. In

this case, negative findings are scrutinised for reasons

why they have failed to detect effects that really are

present.

The physiological evidence

Some physiologists are prominent in the campaign to

reduce salt intake. Indeed at one stage, a physiological

theory claimed that hypertension in humans was wholly

due to excessive intake of salt causing secretion of a cir-

culating inhibitor that raised blood pressure. Claims

were made to have isolated this inhibitor repeatedly for

many years but work could not be reproduced. The

theory has never been withdrawn, but very little is heard

of it now at blood-pressure conferences. Having com-

mitted themselves in this way, some of the original pro-

ponents of the theory figure amongst the most vocal

advocates of salt-restricted diets.

There is, on the other hand, no doubt that changing

salt balance can influence blood pressure, as it does, for

instance, in some patients with renal disease. If salt

depletion is allowed to develop in some animal models,

high blood pressure does not occur. Mild salt depletion

on the other hand is not effective, and in some situa-

tions actually raises blood pressure. All this is, of course,

a very long way from the effects of a modest reduction

in dietary salt in humans. Some physiological statements

in this context are quite misleading. We often hear, for

instance, that humans take 20 times as much salt as they

require. The unspoken implication of this statement,

which is based on the fact that most of the sodium

ingested is excreted in the urine, is that we could reduce

salt intake by 95% and nothing would change. This is

not the case. When salt intake is changed, the fluid com-

ponents of the body are slightly altered and a variety of



physiological systems are activated in order to preserve

the circulation. One of these is the renin–angiotensin

system. Blood concentrations of the hormone renin and

its active component angiotensin II rise. These perform

an important role in maintaining blood pressure, but

they have come under a shadow recently as cell physi-

ologists have implicated them in the changes giving rise

to atheromatous plaques, which cause heart attacks,

and the structural alterations in heart muscle that are

seen in cardiac failure. All this is a long way from

disease in humans, but there is now some indirect, but

disturbing, clinical evidence that the renin system is

not always benign. The ACE (angiotensin-converting

enzyme) inhibitor class of drug, which blocks the renin

system, has been used to treat hypertension for the last

20 years. Recently, an ACE inhibitor has been used

to treat patients at high risk of heart attacks. There

was a dramatic reduction in the incidence of heart

attacks that was not explicable by effects on blood

pressure. This type of trial requires confirmation, but

there is clearly a danger that we will be advocating a

dietary change that activates the renin–angiotensin

system and then prescribing drugs to block it, in both

cases with the intention of decreasing the incidence of

vascular disease.

Detecting harm

Physiological reasoning can, therefore, point in both

directions. The answer you get on the possible benefits

or harmful effects of salt restriction depends on whether

you ask an organ physiologist or a cell physiologist.

Other potentially harmful effects have been demon-

strated in experimental studies, such as increased activ-

ity of the sympathetic nervous system and increases in

blood cholesterol. These require quite severe salt restric-

tion, approaching that of the Yanamamo Indians,

however, and their application to milder degrees of salt

restriction is debatable.

Surely, there must be more direct evidence to demon-

strate that salt restriction is safe? Studies have reported

a higher incidence of myocardial infarction in those who

eat less salt, but these are subject to exactly the same

problems with unrecognised confounding as other

observational work (Alderman et al. 1995). One trial

that examined subjective changes in patients found

increased fatigability (Wassertheil-Smoller et al. 1991),

but no trials of salt restriction have been large enough

or continued long enough to give any information on

possibly more serious adverse events. We are therefore

left with the simple reassurance that either there is no

evidence of harm or alternatively, that clinical experi-

ence indicates that salt restriction is not harmful. As far

as the former is concerned, the absence of evidence of

harm in the absence of relevant trials does not reassure

regulatory authorities when they evaluate drugs, and

dietary advice requires us to be just as circumspect. As

far as the second statement is concerned, those making

it should reflect on the experience with CAST, in a

situation where adverse effects were much more likely

to be recognised, but were not. The unfortunate truth

is that, if the population intake of salt were reduced to

the levels being recommended, and there was an

unfavourable impact, say upon the incidence of heart

attacks, it would be impossible to detect it against the

background changes in incidence that are already occur-

ring. A deterioration in the statistics would generate an

endless debate about what exactly was responsible, but

no means of resolving the uncertainty. This is what

happens when public health measures are taken in the

absence of good scientific evidence.

The evidence from trials

If a drug were being introduced into the new NHS, the

first question that the recently inaugurated National

Institute for Clinical Excellence (NICE) would ask is

‘what have clinical trials shown?’ It would then require

a systematic review of these, for the reasons given

above. If the same question were asked about salt

restriction, fairly clear answers emerge. Two systematic

reviews have been published in the Journal of the American Medical Association in the last 4 years

(Midgley et al. 1996; Graudal et al. 1998). One identi-

fied 28 randomised trials of acceptable quality, the other

56. The conclusions were almost identical. Despite a

major reduction in salt intake, much greater than

that currently under consideration, there was no signifi-

cant impact at all on diastolic blood pressure, and a

minuscule reduction of systolic blood pressure (1.0–

1.2 mm Hg). Even these findings may have been affected

by a tendency of researchers to publish only positive

studies, and by the other changes in diet that occur when

subjects change to salt restriction. Thus, one of these

reviews showed that, overall, small effects upon systolic

blood pressure were seen even when no change in

sodium intake occurred. Both reviews concluded that

their results provided no support for a population

reduction in salt intake.

These discouraging results have dampened the enthu-

siasm for population salt restriction in Canada (Taubes

1998; Fodor et al. 1999), but in the UK, such work

has been discounted on the grounds of irrelevance. How

can short-term trials reflect lifetime experience? The

longest study included in these meta-analyses was

3 years, and most were only of 1–2 weeks’ duration.

However, there was no evidence of a progressive fall in

blood pressure and a British meta-analysis, which only

looked at trials of 6 months duration or over, found no

significant impact on blood pressure, while weight

reduction and alcohol restriction continued to have an

effect (Ebrahim & Smith 1998). Indeed, the remarkable

feature about trials of diet in blood pressure has been

the consistency with which weight reduction and

alcohol restriction in heavy drinkers has been demon-

strated to lower blood pressure. This parallels the

consistency with which these factors have been

demonstrated to be associated with blood pressure in

epidemiological studies.

One systematic review is informative, not because of

its content, but because of the way it has been used. In

1991, the British Medical Journal published a paper

that claimed that a reduction in salt intake would have

a major impact upon blood pressure and prevent 40 000

deaths a year in the UK (Law et al. 1991). This was an

analysis of 78 trials in people with high as well as

normal blood pressure. The size of the fall in blood pres-

sure was a remarkable 8–50-fold greater than that

reported in the more recent papers. Some of the older

trials showed really massive falls. The reason the

authors obtained such a discrepant result is not difficult

to find. Most of the trials they included are nonran-

domised, dating in one case back to 1947, before the

first randomised trial was reported. Nonrandomised

studies are anathema to the experts in the field such as

the Cochrane Collaboration, because of their strong ten-

dency to produce misleading results. Why is this? When

blood pressure is measured repeatedly in the same indi-

vidual, over the course of time, it falls as he or she

becomes used to the procedure. If, therefore, we cross

them over from a normal- to a low-salt diet after a week,

we will observe a fall in blood pressure even if the diet

has no effect. Randomisation avoids this by randomly

allocating subjects to different diets. When Taubes

wrote his Political Science of Salt, he sought expert

opinions on the 1991 analysis (Taubes 1998). The

overall conclusion was that it was ‘so flawed as to beeffectively meaningless’. Why mention it therefore, par-

ticularly as it is now fairly out of date? Last year, I

carried out a citation analysis, using an American sci-

entific literature database (Swales 1999). This shows

how many times a paper has been quoted in the medical

and scientific literature. I was extremely surprised by the

result. With one exception (one citation difference in

1997), this ‘flawed’ analysis was cited more frequently

than any other, up to and including 1998.

138 John Swales


Consensus and nonconsensus

This should not have surprised anyone who has read

Taubes’ paper (Taubes 1998). Despite its manifest short-

coming, the conclusions of the older analysis are more

congenial than those reached by the more recent and

rigorous analyses. A public campaign is unlikely to be

successful in the face of unsupportive high-quality work.

Selective quotation of favourable evidence, whatever the

reservations about it, is one approach to creating an

impression of scientific agreement. The other is to claim

that a scientific consensus has been reached. In view of

the predominantly negative nature of both association

and intervention studies, this would seem a difficult

task. Even if ad hoc explanations based upon unproven

assumptions are persuasive to some, it is unlikely that

there will be widespread acceptance of such a case.

Recently Members of Parliament received a letter on

behalf of CASH (Consensus Action on Salt and Hyper-

tension), stating that a reduction in salt intake would

save ‘approximately 34 000 lives a year’. An ‘Early Day

Motion’ resulted from this. The figure is presumably

derived from the 1991 analysis, although this is not

stated. None of the more recent analyses of clinical trials

support this in the slightest. The Canadians are well

ahead of us in their approach to these issues. The Cana-

dian Hypertension Society, The Canadian Coalition for

High Blood Pressure Prevention and Control, The

Laboratory Centre for Disease Control, and the Heart

and Stroke Foundation jointly commissioned a report

based upon a systematic review of all the published evi-

dence. The consensus conclusion was that: ‘Restriction

of salt intake for the normotensive population is not rec-

ommended at present, because of insufficient evidence

that this would lead to a reduced incidence of hyper-

tension’ (Fodor et al. 1999).

Conclusions

The significance of the salt-restriction controversy

extends well beyond the immediate issue. It provides a

litmus test of how far social policy on lifestyle and

health is to be influenced by objective and independent

scientific advice and how far it is to be influenced by

campaigns and pressure groups. In this instance, the

path trodden by the NHS in recent years provides a

good model. There may come a point at which decisions

have to be made in spite of quite significant reservations.

Indeed, in the real world, this will often be the case.

What is quite unacceptable is an attempt to pervert the

course of democratic discussion by the selective use of

demonstrably flawed evidence and the pretence that



there is a scientific consensus when there manifestly is

not.

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