Salt, blood pressure and health

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  • 2001 British Nutrition Foundation Nutrition Bulletin, 26, 133139

    *Editors note. John Swales (MA MD FRCP FmedSci), Professor ofClinical Medicine, was President of the British Hypertension Societyfrom 19824 and the author of five books and over 200 papers. Hewas seconded to the Department of Health as Director of R & Dfor the NHS between 1996 and 1998. This article was originallysubmitted 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 beaddressed to the Editor.


    Salt, blood pressure and health

    John Swales*Clinical Sciences Building, Royal Infirmary, University of Leicester, UK


    The healthy individual has a right to feel confused bythe contradictory advice being given about dietary salt.Some experts advocate a reduction in salt intake foreveryone, while others say this advice is unjustified inthose who do not suffer from high blood pressure. It isnot surprising that this has been described as one of themost polarised fields in medical science. In spite of thedivergent views, evidence accruing over the last fewyears has been remarkably consistent. We should there-fore beware of older work claiming an enormous savingof life if we all reduced our salt intake. In 1998, expertsfor the leading American scientific journal, Science, eval-uated the most widely quoted study that made thisclaim. They concluded that the study was so flawed asto be effectively meaningless.

    People with high blood pressure in our society eat nomore salt than anyone else. In clinical trials, even majorreductions in salt intake, larger than could be achievednormally, 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 theIntersalt Study, but differences in blood pressurebetween the developed and the developing world couldequally well be due to the other multiple differences instress 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 avoidstress in such a radical way as this. Is there anything ahealthy individual can do to avoid the dangers of highblood pressure? Here, there is scientific agreement.Reducing weight, taking a diet high in fruit and vegeta-bles, indulging in regular physical exercise and avoidingexcessive alcohol intake are all sensible, health-promoting measures that help to lower blood pressureand also carry other health benefits. The tragedy of thesalt controversy is that it has tended to distract atten-tion from these sensible measures by unjustified andcontroversial claims.

    The significance of blood pressure

    The modern debate about salt and blood pressure isnow reaching the end of its fifth decade, although hintsof it can be traced back to ancient Chinese literature.The last few years must seem particularly bewilderingfor those without any special knowledge. Claims thatthere is a consensus amongst experts are countered bya distinguished scientific journalist writing if ever therewere a controversy over the interpretation of scientificdata, this is it (Taubes 1998).

    I believe that the salt controversy is important toeveryone for two reasons. Firstly, reducing the burdenof high blood pressure would undoubtedly producemajor public health benefits. Secondly, it demonstratesthe pitfalls in trying to combine scientific accuracy andcaution with persuasive, credible public health advice.

    High blood pressure is a major cause of ill-health anddeath in developing countries. Because it injures bloodvessels, it is the most important risk factor in strokes,an important contributor to heart attacks and kidneydisease and probably to deteriorating mental functionin the elderly. There is some exciting recent work sug-gesting that high blood pressure even plays a role inpatients with Alzheimers disease. Over the last 30 years,it has become clear that lowering blood pressure helpsto prevent strokes, heart attacks and kidney disease. No-


  • one now denies the importance of blood pressurecontrol 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 thosewho provide health care. The risks associated withblood pressure apply to everyone. Risk of suffering astroke, for instance, can be reduced by a modest lower-ing of blood pressure even in those people who havewhat used to be called normal blood pressure. Thisrepresents a very small benefit to the individual whoseblood pressure is not particularly high, but added upacross the whole population would have a major impactupon the total number of strokes. Of course, mass medication is not a realistic prospect, and so, medicalresearch has had to find other, hopefully harmless, waysof reducing blood pressure through diet and lifestyle.We have to be sure of our ground before advocatingsuch changes. Advising us to alter the way we organiseour lives may be attractive to those who run the UKNational Health Service (NHS), as it costs the NHS littleor nothing and may save it some of the costs of treat-ing illness. However, there are personal and social costsfor even the simplest modification of diet. Those whoadvocate change have to behave with the same degreeof responsibility they would be expected to employ inprescribing a drug for a patient. Unfortunately, this hasnot always been the case amongst enthusiasts for thevarious healthy diets and writers of healthy recipebooks.

    Scientific evidence

    The UK NHS and other healthcare systems across theworld are undergoing a quiet revolution in the way inwhich 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 yearsago. It became quite evident that so-called expertadvice was likely to be deeply flawed on occasions,reflecting as it did conventional wisdom and prejudice.This was demonstrated in a seminal study from Harvardby Antman and his coworkers (Antman et al. 1992).Treatment of heart attacks has improved vastly in recentyears with the development of thrombolytic clot-busting drugs, which are now used routinely. In theearly days, there were fears about drugs that inhibitedone of the bodys normal mechanisms for preventingbleeding. Theoretically, these drugs could make mattersworse for victims of a heart attack, indeed, they areharmful in a small minority of patients. By the mid-1970s however, clinical trials had been performed thatshowed net benefit for patients and subsequent trials

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    simply reinforced that conclusion. Antman et al.however, went on to look at the expert advice beinggiven to doctors through textbook chapters and reviewsin specialist journals. Thrombolysis was rarely men-tioned until the late 1980s and where it was referred toat all, it was as an experimental treatment. Otheradvice consistently recommended treatment that couldnot be supported at all from clinical trial evidence andthat may actually have been harmful. When the only evi-dence cited in favour of a treatment is that an expertgroup 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 ofaccepted wisdom. The track record has not been good,but what can be put in their place? The experts tendedto select trials that supported their view and ignored ordenigrated those that did not, giving a misleadingimpression of the overall conclusions of research.Modern databases now allow immediate access to allthe relevant information on methods of preventing andtreating disease. This provides the basis for the sys-tematic review, which figures increasingly in decision-making in the NHS. Of course, a broad range ofexpertise is still required in screening this evidence andinterpreting its relevance, but the day of the old-fashioned expert setting out with their own firmly heldviews and finding evidence to support them is nowpassing. The NHS now funds two groups, the CochraneCentre 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 happentogether, we cannot assume that they are cause andeffect. I think the best illustration of this fallacy was provided by George Bernard Shaw in the DoctorsDilemma, when he wrote:

    Thus it is easy to prove that the wearing of tall hatsand the carrying of umbrellas prolongs life and confersimmunity from disease, for the statistics show that theclasses which use these articles are bigger, healthier andlive longer than the class which never dreams of pos-sessing such things (Shaw 1911).

    This may seem obvious. Nevertheless, a similarassumption proved fatal for many people in the 1980s.Many patients, after a heart attack, develop extra heart-beats (sometimes felt as palpitations, although oftenonly picked up by carrying out an electrocardiogram).When a particular form of these palpitations (ventricu-lar extrasystoles) is present, patients are much morelikely to have a second, fatal heart attack, probably as

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    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. Formany years, doctors assumed, quite reasonably, that thiswas a causal relationship and gave patients drugs tosuppress the extra beats. It was only at the end of the1980s that a trial was set up to assess the benefits ofthis treatment (CAST Investigators 1989). The CAST(Cardiac Arrhythmia Suppression Trial) has stronglyinfluenced the evidence used as a basis for providingdoctors with guidance. The trial was never completed.In April 1989, it was discontinued. Deaths in the treatedgroup were over twice as great as in the control groupand it was no longer ethically acceptable to proceedwith it.

    It has been calculated that more Americans died fromthis treatment than died in the Vietnam War. The lessonfor doctors was in some ways a hard one. Not only wasan epidemiological association a flawed basis for treat-ment, but clinical experience in quite carefully moni-tored groups of patients had failed to detect evidence ofharm. This is not surprising. The overall annual mor-tality rate is quite low even in these patients and an indi-vidual doctors experience of patients dying will be quitelimited. An increase of one or two patients in a year islikely to be attributed to chance. The message was quitesimple, and again points to the danger of unsupportedexpert views. Where it is feasible to carry out clinicaltrials, these should be done before recommendations aremade and, where several such trials have been carriedout, a proper systematic review from relevant databasesof evidence is needed. No regulatory agency wouldaccept unsupported clinical experience or carefullyselected clinical trials as sufficient evidence that a drugdid no harm.

    Salt and blood pressure: the associations

    Preventive medicine and public health have been muchslower to take on board these messages. It is to be hopedthat a much more scientific Food Standards Agency,funded to carry out its own research and reviews, willchange this. It will not be easy. It is much more difficultto carry out a randomised controlled trial in a healthypopulation than in a group of patients. Nevertheless, inthe case of blood pressure, we have something that iseminently measurable and can be studied easily in clini-cal trials. If claims are made that a particular dietarychange will influence blood pressure, these can be exam-ined with just as much rigour as is used for evaluatinga drug.

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

    good at picking up the net, very small, beneficial andharmful effects of an intervention when these occur overa long period of time. On other occasions, a trial maybe impossible. The role of smoking in lung cancer andheart 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 andnot all associations? Austin Bradford Hill, who, withRichard Doll, discovered the tobacco lung cancer rela-tionship, as well as designing the first randomised clinical trial, laid down some important principles (Hill1965). Besides being biologically plausible, associationsneeded to be strong and consistent. They needed toshow a gradient, so that weaker influences were associ-ated with less effect, and they needed to be specific. Thiswas true both of the smoking/cancer association and thecholesterol/heart disease association. The association oftobacco with lung cancer, for instance, was required tobe unique to tobacco and not due to other factors thatare associated with tobacco, such as social class anddiet. The existence of such confounders is one of themajor pitfalls in ascribing causality to an association.

    How far does the salt/blood pressure association meetthese criteria? The short answer is that it cannot,because there is no such simple association. Individualswith high blood pressure take no more dietary salt thananyone else. It has been impossible to show any associa-tion between blood pressure and measured salt intakewhen this has been rigorously sought in quite largestudies of populations such as the study carried out in Scotland some years ago (Smith et al. 1988). This isin striking contrast to, for example, the relationshipbetween cholesterol and heart disease where the evi-dence for causality is now strong.

    It is surprising, under such circumstances, that somuch emphasis in the public debate has been placed ona different type of association study, Intersalt (IntersaltCooperative Group 1988). This looked at salt intakeacross a wide range of cultures extending from theUnited States to the Yanamamo Indians of SouthAmerica. The latter, like some of the other populationsexamined, take extremely small quantities of salt, wellbelow the level that could ever be achieved in developedsocieties. Even so, when other factors that can influenceblood pressure were taken into account, it provedimpossible to show any relationship between salt intake(measured by the sodium content of urine) and diastolicblood pressure. In addition, only a minuscule change insystolic blood pressure was shown over extremely largedifferences in salt intake. In the reports of Intersalt, thisfinding 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. Bloodpressure rises with age in developed societies, butremains at low levels throughout life in nonurban unde-veloped societies such as the Yanamamo. Intersalt noteda strong relationship between the rise in blood pressurewith age and measured salt intake. The advocates of salt reduction have attached great importance to thisfinding. As an isolated finding, however, its significanceis doubtful. For one thing, the phrase rise in blood pres-sure with age is not, of course, based upon followingthe same individuals through their natural lifespan. It isbased upon a single snapshot. The lifetime experienceof an older subject in Europe will include a childhoodperhaps spent in the war years, while a 30-year-old willhave quite a different background, both in respect todiet and to working environment.

    In fact, there are even stronger grounds to doubt theassumption of causality in Intersalt. Although the rela-tionship of blood pressure with salt intake is so con-tentious, the relationship with other dietary andenvironmental factors is much more clear-cut. Societiessuch as the Yanamamo differ in many respects fromthose who live in developed societies. Some of these dif-ferences are dietetic, others reflect quite differentlifestyles, the effects of which are much more difficultto measure and incorporate in statistical analyses. Dietmay be important. Increasing the amount of fruits andvegetables, for instance, lowered blood pressure sub-stantially without any reduction in salt intake in oneimportant recent study (Appel et al. 1997). Clearly, dietwas radically different in the examined populations in,for instance, the components derived from vegetableand animal sources.

    More important however, we have more direct evi-dence that the rise in blood pressure with age in thedeveloped world is not related to salt, or perhaps anyother dietary component. This comes not from anothercross-sectional study such as Intersalt, but a genuinelongitudinal study in which the same individuals werecarefully 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 ofwomen from the same background, these nuns showedno rise in blood pressure with age. By the end of thestudy, the differerence in systolic blood pressurebetween the two groups was 30 mm Hg; a differenceabout three times as great as could be produced bygiving the control women a blood-pressure-loweringdrug. This difference could not be accounted for by saltor any other dietary component looked at, by bodyweight or by childbearing.

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

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    tion evidence as though it were comparable to the evi-dence that links tobacco and lung cancer or cholesteroland heart disease. There are closer parallels in the fieldof blood-pressure research, however. There has been no difficulty in demonstrating an association betweenbodyweight and blood pressure, or between heavyalcohol intake and blood pressure. This counters someof the arguments used to explain the weakness of thesalt/blood pressure association evidence: that measure-ments are too imprecise; that a lifetimes exposure isrequired; or that only predisposed individuals willrespond with high blood pressure. All such argumentssuggest a degree of special pleading for fundamentallynegative findings. This is fairly unusual in the applica-tion of epidemiology to medicine. In most cases, posi-tive associations are critically examined for possibleconfounding factors creating spurious relationships. Inthis case, negative findings are scrutinised for reasonswhy they have failed to detect effects that really arepresent.

    The physiological evidence

    Some physiologists are prominent in the campaign toreduce salt intake. Indeed at one stage, a physiologicaltheory claimed that hypertension in humans was whollydue to excessive intake of salt causing secretion of a cir-culating inhibitor that raised blood pressure. Claimswere made to have isolated this inhibitor repeatedly formany years but work could not be reproduced. Thetheory has never been withdrawn, but very little is heardof 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 vocaladvocates of salt-restricted diets.

    There is, on the other hand, no doubt that changingsalt balance can influence blood pressure, as it does, forinstance, in some patients with renal disease. If saltdepletion is allowed to develop in some animal models,high blood pressure does not occur. Mild salt depletionon 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 reductionin dietary salt in humans. Some physiological statementsin this context are quite misleading. We often hear, forinstance, that humans take 20 times as much salt as theyrequire. The unspoken implication of this statement,which is based on the fact that most of the sodiumingested is excreted in the urine, is that we could reducesalt intake by 95% and nothing would change. This isnot the case. When salt intake is changed, the fluid com-ponents of the body are slightly altered and a variety of

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    physiological systems are activated in order to preservethe circulation. One of these is the reninangiotensinsystem. Blood concentrations of the hormone renin andits active component angiotensin II rise. These performan important role in maintaining blood pressure, butthey have come under a shadow recently as cell physi-ologists have implicated them in the changes giving riseto atheromatous plaques, which cause heart attacks,and the structural alterations in heart muscle that areseen in cardiac failure. All this is a long way fromdisease in humans, but there is now some indirect, butdisturbing, clinical evidence that the renin system is not always benign. The ACE (angiotensin-convertingenzyme) inhibitor class of drug, which blocks the reninsystem, has been used to treat hypertension for the last20 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 heartattacks that was not explicable by effects on blood pressure. This type of trial requires confirmation, butthere is clearly a danger that we will be advocating adietary change that activates the reninangiotensinsystem and then prescribing drugs to block it, in bothcases with the intention of decreasing the incidence ofvascular disease.

    Detecting harm

    Physiological reasoning can, therefore, point in bothdirections. The answer you get on the possible benefitsor harmful effects of salt restriction depends on whetheryou 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 inblood cholesterol. These require quite severe salt restric-tion, approaching that of the Yanamamo Indians,however, and their application to milder degrees of saltrestriction is debatable.

    Surely, there must be more direct evidence to demon-strate that salt restriction is safe? Studies have reporteda higher incidence of myocardial infarction in those whoeat less salt, but these are subject to exactly the sameproblems with unrecognised confounding as otherobservational work (Alderman et al. 1995). One trialthat examined subjective changes in patients foundincreased fatigability (Wassertheil-Smoller et al. 1991),but no trials of salt restriction have been large enoughor continued long enough to give any information onpossibly more serious adverse events. We are thereforeleft with the simple reassurance that either there is noevidence of harm or alternatively, that clinical experi-

    ence indicates that salt restriction is not harmful. As faras the former is concerned, the absence of evidence ofharm in the absence of relevant trials does not reassureregulatory authorities when they evaluate drugs, anddietary advice requires us to be just as circumspect. Asfar as the second statement is concerned, those makingit should reflect on the experience with CAST, in a situation where adverse effects were much more likelyto be recognised, but were not. The unfortunate truthis that, if the population intake of salt were reduced tothe levels being recommended, and there was anunfavourable impact, say upon the incidence of heartattacks, it would be impossible to detect it against thebackground changes in incidence that are already occur-ring. A deterioration in the statistics would generate anendless debate about what exactly was responsible, butno means of resolving the uncertainty. This is whathappens when public health measures are taken in theabsence of good scientific evidence.

    The evidence from trials

    If a drug were being introduced into the new NHS, thefirst question that the recently inaugurated NationalInstitute for Clinical Excellence (NICE) would ask iswhat have clinical trials shown? It would then requirea systematic review of these, for the reasons givenabove. If the same question were asked about saltrestriction, fairly clear answers emerge. Two systematicreviews 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 amajor reduction in salt intake, much greater than that currently under consideration, there was no signifi-cant impact at all on diastolic blood pressure, and aminuscule reduction of systolic blood pressure (1.01.2 mm Hg). Even these findings may have been affectedby a tendency of researchers to publish only positivestudies, and by the other changes in diet that occur whensubjects change to salt restriction. Thus, one of thesereviews showed that, overall, small effects upon systolicblood pressure were seen even when no change insodium intake occurred. Both reviews concluded thattheir results provided no support for a populationreduction in salt intake.

    These discouraging results have dampened the enthu-siasm for population salt restriction in Canada (Taubes1998; Fodor et al. 1999), but in the UK, such work has been discounted on the grounds of irrelevance. Howcan short-term trials reflect lifetime experience? The

  • longest study included in these meta-analyses was3 years, and most were only of 12 weeks duration.However, there was no evidence of a progressive fall inblood pressure and a British meta-analysis, which onlylooked at trials of 6 months duration or over, found nosignificant impact on blood pressure, while weightreduction and alcohol restriction continued to have aneffect (Ebrahim & Smith 1998). Indeed, the remarkablefeature about trials of diet in blood pressure has beenthe consistency with which weight reduction andalcohol 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 inepidemiological studies.

    One systematic review is informative, not because ofits content, but because of the way it has been used. In1991, the British Medical Journal published a paperthat claimed that a reduction in salt intake would havea major impact upon blood pressure and prevent 40 000deaths a year in the UK (Law et al. 1991). This was ananalysis of 78 trials in people with high as well asnormal blood pressure. The size of the fall in blood pres-sure was a remarkable 850-fold greater than thatreported in the more recent papers. Some of the oldertrials showed really massive falls. The reason theauthors obtained such a discrepant result is not difficultto find. Most of the trials they included are nonran-domised, dating in one case back to 1947, before thefirst randomised trial was reported. Nonrandomisedstudies are anathema to the experts in the field such asthe Cochrane Collaboration, because of their strong ten-dency to produce misleading results. Why is this? Whenblood pressure is measured repeatedly in the same indi-vidual, over the course of time, it falls as he or shebecomes used to the procedure. If, therefore, we crossthem over from a normal- to a low-salt diet after a week,we will observe a fall in blood pressure even if the diethas no effect. Randomisation avoids this by randomlyallocating subjects to different diets. When Taubeswrote his Political Science of Salt, he sought expertopinions on the 1991 analysis (Taubes 1998). Theoverall 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, Icarried out a citation analysis, using an American sci-entific literature database (Swales 1999). This showshow many times a paper has been quoted in the medicaland scientific literature. I was extremely surprised by theresult. With one exception (one citation difference in1997), this flawed analysis was cited more frequentlythan any other, up to and including 1998.

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    Consensus and nonconsensus

    This should not have surprised anyone who has readTaubes paper (Taubes 1998). Despite its manifest short-coming, the conclusions of the older analysis are morecongenial than those reached by the more recent andrigorous analyses. A public campaign is unlikely to besuccessful in the face of unsupportive high-quality work.Selective quotation of favourable evidence, whatever thereservations about it, is one approach to creating animpression of scientific agreement. The other is to claimthat a scientific consensus has been reached. In view ofthe predominantly negative nature of both associationand intervention studies, this would seem a difficulttask. Even if ad hoc explanations based upon unprovenassumptions are persuasive to some, it is unlikely thatthere will be widespread acceptance of such a case.Recently Members of Parliament received a letter onbehalf of CASH (Consensus Action on Salt and Hyper-tension), stating that a reduction in salt intake wouldsave approximately 34 000 lives a year. An Early DayMotion resulted from this. The figure is presumablyderived from the 1991 analysis, although this is notstated. None of the more recent analyses of clinical trialssupport this in the slightest. The Canadians are wellahead of us in their approach to these issues. The Cana-dian Hypertension Society, The Canadian Coalition forHigh Blood Pressure Prevention and Control, The Laboratory Centre for Disease Control, and the Heartand Stroke Foundation jointly commissioned a reportbased upon a systematic review of all the published evi-dence. The consensus conclusion was that: Restrictionof salt intake for the normotensive population is not rec-ommended at present, because of insufficient evidencethat this would lead to a reduced incidence of hyper-tension (Fodor et al. 1999).


    The significance of the salt-restriction controversyextends well beyond the immediate issue. It provides alitmus test of how far social policy on lifestyle andhealth is to be influenced by objective and independentscientific advice and how far it is to be influenced bycampaigns and pressure groups. In this instance, thepath trodden by the NHS in recent years provides agood model. There may come a point at which decisionshave 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 thecourse of democratic discussion by the selective use ofdemonstrably flawed evidence and the pretence that

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    there is a scientific consensus when there manifestly isnot.


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