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Salt and Blood Pressure:the Next Chapter

ADVICE on dietary salt intake has been

controversial ever since Dahl originally proposed thathypertension in westernised cultures was a disease ofexcessive salt intake.1 Controversy has arisen as theresult of two factors: advice about the management ofindividual patients has been confused with populationadvice about the optimum level of salt intake,2 and theplethora of writings on healthy intake of salt has notbeen matched by an abundance of convincing data.Funding for projects that will reduce the consumptionof antihypertensive drugs or force a major change infood processing in the interests of health is unlikely tobe provided by industry, and studies involving largepopulations are expensive exercises even for

government. Consequently, advice about dietarycontrol of blood pressure has been based on estimatesof risks and benefits that would fail to obtain a licencefor an antihypertensive drug.Despite this unsatisfactory state of affairs, evidence

from various sources is now beginning to converge,although the hard light of science is still blended withthe light in the eyes of enthusiasts on both sides of thedebate. Several studies on the effects of moderate saltrestriction in patients with essential hypertension havenow been reported. The qualification "moderate" iscritical. Diets with an extremely low salt content (eg,the Kempner rice-fruit diet) undoubtedly lower bloodpressure3 but are unacceptable to the healthypopulation. Less stringent salt restriction was believedto be ineffective.4 Thus, when antihypertensive drugscame on to the market, there was little interest inreducing salt intake, either in the management ofhypertension or as a population measure. This viewchanged when recommendations to treat milder

1 Dahl LK. Salt and hypertension Am J Clin Nutr 1972; 25: 231-44.2. Brown JJ, Lever AF, Robertson JIS, et al. Salt and hypertension. Lancet 1984, ii: 456.3 Kemprier W Treatment of hypertensive vascular disease with rice diets. Am J Med

1948, 4: 545-77.4. Medical Research Council. The rice diet in the treatment of hypertension. Lancet

1950; ii: 509-13.

aegrees or nyperiension- vasny mcreasea me

population potentially exposed to lifelong therapy.Simultaneously, epidemiologists made a powerfulcase for the public health benefits of small reductionsin the population blood pressure.6 The outcome hasbeen a growing interest over the past decade innon-pharmacological means of reducing blood

pressure.7 The effect of reductions in salt intake byhalf to two-thirds in hypertensive patients and healthysubjects came into sharp focus.

Conflicting data from clinical trials were partlyattributable to poor design, inadequate controls, andinsufficient numbers. However, both positive andnegative results were reported from essentially similarcarefully designed studies.8-lO The probableexplanation has important implications forrecommendations on salt intake. The fall in bloodpressure (as might be predicted on statistical grounds)was related to the initial blood pressure of the patientsrecruited. However, the crucial fact is that the

regression line relating change in blood pressure toinitial pressure appears to cross the zero change linewhen initial pressures are in the borderline range. 11,12Moderate salt restriction therefore has not loweredblood pressure in normotensive subjects and patientswith borderline blood pressures, and the effect hasbeen small in mild hypertension. 11,12 Australianresearchers have now reported results that accordclosely with the regression line constructed from

previous studies.13 This trial, unlike most of its

predecessors, has the strength of numbers since 103patients completed the protocol, of whom 50 (initialblood pressure 155/95) were maintained on a low-saltdiet that reduced urinary sodium from 142 to 90 mmolper day. Blood pressures in this group fell by 5-5/2-8mm Hg compared with controls, who received thesame diet but with added sodium supplements.

Small falls in blood pressure in large groups couldconceal much greater falls in certain individuals,whose identification would help managementconsiderably. The substantial differences in

responsiveness to salt restriction have generated theconcept of salt-sensitive hypertension;14 it has been

5. Swales JD, Ramsay LE. Coope JR, et al. Treating mild hypertension: agreement fromlarge trials. Report from the British Hypertension Society working party. Br Med J1989; 298: 694-98.

6. Rose G. Strategy of prevention: lessons from cardiovascular disease. Br Med J 1981;282: 1847-51.

7. Joint National Committee on Detection, Evaluation and Treatment of High BloodPressure. Non-pharmacological approaches to the control of high blood pressure.Hypertension 1986; 8: 444-67.

8. MacGregor GA, Markandu ND, Best FE, et al Double-blind randomised crossovertrial of moderate sodium restriction in essential hypertension. Lancet 1982; i.

351-55.

9. Watt GCM, Edwards C, Hart JT, et al. Dietary sodium restriction for mild

hypetension in general practice. Br Med J 1983; 286: 432-3610. Grobbee D, Hofman A, Roelandt JT, et al Sodium restriction and potassium

supplementation in young people with mildly elevated blood pressure. J Hypertens1987; 5: 115-19.

11. Grobbee DE, Hofman A. Does sodium restriction lower blood pressure? Br Med J1986; 293: 27-29.

12. Swales JD. Salt intake and blood pressure In Sheppard MC, ed. Advanced medicine.London: Ballière Tindall, 1988, 336-43.

13 Australian National Health and Medical Research Council Dietary Salt StudyManagement Committee Fall in blood pressure with modest reduction in dietarysalt intake in mild hypertension. Lancet 1989; i. 399-402.

14. Weinberger MH, Miller JZ, Luft FC, et al Definitions and characteristics of sodiumsensitivity and blood pressure resistance. Hypertension 1986; 8 (suppl II). 127-34.

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suggested that this condition is geneticallydetermined15 and a genetic marker has beendescribed.16 However, the evidence for a discretesubgroup of hypertensive individuals with

reproducible salt-sensitivity is not strong; it is morelikely that the mechanisms protecting blood pressureagainst volume depletion are weaker in some peoplethan in others. The prime candidate in this context isthe renin-angiotensin system; the blood pressureresponse to salt depletion is enhanced when this systenis blocked and there is a close relation between theblood pressure response to salt restriction and initialrenin levelsY Whilst there may be a geneticcomponent in renin responsiveness,18 salt sensitivitymay be attributable to factors influencing renin

responsiveness secondarily, such as ageing.19 Theunderlying concept of salt-sensitivity is undeniablyattractive, but before use of the term becomesestablished the disorder requires much bettercharacterisation.There is an immense difference between clinical

management of selected hypertensive patients andadvice given to the population at large. The suggestionthat a moderate reduction in salt intake would lowerthe whole population blood pressure - distributioncurve is based not on intervention trials in healthysubjects, which have proved negative, 12 but onassociations in intercultural studies between sodiumintake and blood pressure. 1,20 The assumptionsimplicit in such advice are seldom made clear in publichealth campaigns. These assumptions are that therelation between salt intake and blood pressurereported in some studies is causal, that it is reversible,that the risk-benefit analysis is favourable, and that theappropriate degree of reduction in intake isachievable.Two major studies have now superseded previous

investigations into the relation between salt intake andblood pressure. The Intersalt study21 recruited 200subjects from each of 52 centres in thirty-twocountries. After adjustment for age and sex, sodiumexcretion and systolic blood pressure were

significantly positively correlated in 15 centres andnegatively in 2. The numbers for diastolic blood

pressure were 4 and 1, respectively. However, sincesome of this relation could be due to other dietaryfactors, multiple regression analysis was carried outafter adjustment for body mass index, alcohol

15. Skrabal F, Aubock J, Hortnagl H Low sodium/high potassium diet for prevention ofhypertension: probable mechanisms of action. Lancet 1981; ii 895-900.

16. Weinberger MH, Miller JZ, Fineberg NS, et al Association of haptoglobin withsodium sensitivity and resistance of blood pressure Hypertension 1987; 10: 443-46.

17. Cappucio FP, Markandu ND, Sagnella GA, et al. Sodium restriction lowers highblood pressure through a decreased response of the renin system. Direct evidenceusing saralasin. J Hypertens 1985; 3: 243-47.

18. Luft FC, Weinberger MH, Grim CE Sodium sensitivity and resistance in

normotensive humans Am J Med 1982, 72: 726-36.19. Weidmann P, Myttenaere-Bursztein S de, Maxwell MH, et al. Effect of ageing on

plasma renin and aldosterone in normal man Kidney Int 1975, 8: 325-33.20. Glieberman L. Blood pressure and dietary salt in human populations. Ecol Food Nutr

1973; 2: 143-56.21. Intersalt Cooperative Research Group Intersalt: an international study of electrolyte

excretion and blood pressure Results for 24 hour urinary sodium and potassiumexcretion. Br Med J 1988; 297: 319-28.

consumption, and urinary potassium. The resultsindicated that confounding factors accounted for someof the observed associations, since the number ofpositive associations fell to 8 for systolic blood

pressure and to 3 for diastolic blood pressure (equalledby 3 significantly negative associations). Whenregression coefficients were pooled, a very weakrelation between sodium excretion and systolic (butnot diastolic) blood pressure remained, so that achange of 100 mmol in daily sodium intake would beassociated with a change in systolic pressure of 2-2 mmHg and of 0- 1 mm Hg in diastolic pressure afteradjustment for such factors as body mass index andalcohol intake. The weak residual association couldhave two explanations. Either the imprecision ofmeasures of blood pressure and salt intake could havediluted a stronger association, or assessment of

confounding factors was insufficient to eliminate aspurious relation. These results are consistent with asecond large-scale study in a single culture.22 Bloodpressure and urinary sodium excretion were measuredin a random sample of 7354 Scottish subjects. A veryweakly positive correlation between blood pressureand sodium excretion disappeared when adjustmentswere made for body mass index, alcohol consumption,and urinary potassium.

Reporting of these extremely important results willbe greeted with a sense of relief in many quarters.Surely the debate about optimum sodium intakeshould now move from an anthropological setting tothat of properly conducted intervention trials. Suchstudies are essential if the other assumptions behindpublic health advice are to be examined. Two reportspublished lately with slightly discordant results pointthe way in this direction. A large public healthprogramme, conducted over a 5-year period in twoBelgian towns, produced a reduction in sodium intakeof 25 mmol per day in women; there was no significantinfluence in men. 23 Whilst more intensive individualadvice and follow-up would probably have been moresuccessful, this study throws doubt upon the efficacyof the public health campaigns hitherto employed.The major finding was quite unexpected, however: asubstantial fall in blood pressure had occurred duringthe course of the investigation unrelated to sodiumexcretion. If this finding is representative, it suggeststhat an unwitting success has been achieved and theunderlying reasons would repay inquiry.A second intervention trial was conducted more

intensively but in a smaller, captive group of

subjects.24 Ellison et al reduced sodium intake in apopulation of 309 children at boarding school through

22. Smith WCS, Crombie IK, Tavendale RT, et al. Urinary electrolyte excretion, alcoholconsumption, and blood pressure in the Scottish heart health study. Br Med J 1988;297: 329-30.

23 Staessen J, Bulpitt CJ, Fagard R, et al Salt intake and blood pressure in the generalpopulation a controlled intervention trial in two towns. J Hypertens 1988; 6:965-73.

24 Ellison RC, Capper AL, Stephenson WP, et al. Effects on blood pressure of a decreasein sodium use in institutional food preparation: the Exeter-Andover project J ClinEpidemiology 1989; 42: 201-08.

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modification of the food purchasing policy. A 23%reduction in estimated sodium intake was associatedwith a fall of 1 -7 mm Hg in systolic blood pressure andof 1.5 mm Hg in diastolic blood pressure.

Unfortunately, the changes in diet were monitoredonly by diary, which makes assessment of the extentand nature of the change imprecise. Nevertheless, thisstudy points the way to further and more definitiveinvestigations.The appearance of studies of adequate size and

design is the most encouraging feature of thiscontentious area. The possibility that, while furtherstudies are being undertaken, other and potentiallymuch more potent influences on blood pressure thandietary electrolytes are at work may be frustrating forthe investigators but encouraging for the population atlarge.

UK Obstetrics and the New HealthService

OBSTETRICIANS in the UK are looking a littlebattle weary; they, more than most in acute medicine,have been buffeted in the past few years by changes insociety’s expectations, the spread of litigation, andgovernmental manoeuvres in manpower andeconomics. How are they coping with these hazardsand where will the discipline be in the 1990s?Medical students commonly report that obstetrics

is one of the most enjoyable subjects in their clinicalcurriculum. Does this enthusiasm persist sufficientlyto carry them into the discipline after qualifying? Asurvey of final year students by the Royal College ofObstetricians and Gynaecologists in 1984 showed that7% wanted to pursue a career.1 Is that proportionmaintained five years later? Already students say thatthey are apprehensive about the hassles surroundingthe specialty. First were the noisy and demandingconsumer groups who attacked obstetricians and

midwives, seeking more patient power; they nowmake less strident demands and seem a little moresatisfied with the work that doctors and midwives are

doing. Later came the frustrated reactions of parentswho, having expected a perfect child, were

disappointed in their hopes and so, aided by lawyers,caused the numbers of medicolegal cases and theclaims for damages to rocket. The isolated peak onwhich obstetrics had been hoist by one of the medicaldefence societies has now been much reduced after the

suggestions about Crown Indemnity for doctors

practising in the National Health Service. Moreover,the courts are beginning to understand that neonatalhypoxia and its complications are often related toproblems in pregnancy and are not attributable toevents at the time of delivery.2 These moves mayencourage students to believe that they can follow

1. Royal College of Obstetricians and Gynaecologists The role of women doctors inobstetrics and gynaecology. London: RCOG, 1987: 4.

2 Illingworth RS Why blame the obstetrician? Br Med J 1979, i: 979-81.

their first inclinations to become obstetricians inreasonable peace.Among those who have already chosen to train in

obstetrics, there are other dissatisfactions. Hours ofduty are long and the middle years are demanding, notallowing an easy family life for doctors of either sex. Acensus conducted by the RCOG in 1988 showed thatapproximately a quarter of those passing theMRCOG examination between 1978 and 1982 hadleft the specialty, the commonest reason given beingdomestic difficulties. Only a fifth of the leaversbelieved there were poor job opportunities. A 1987RCOG report! showed that only 40% of men andwomen who remained in the specialty were happywith their lot. The workload of consultants is often far

greater than that recommended two years ago by theRCOG-a quarter of those staying in obstetricswould have preferred to work six sessions a weekrather than full-time in such an intensive specialty. 3

In the next five year there are bound to be changesdictated by the apparently conflicting aims of

Achieving a Balance4 and the need to shorten the hoursworked by doctors-in-training. It will be hard toreconcile the implications of each of these

philosophies, and after the next round of tacticalbattles middle-grade trainees might be worse off. A2-3% increase in numbers of consultant obstetriciansis urgently needed and may be possible if the Secretaryof State secures another two billion pounds for thehealth service. Wider use of six-session consultant andsenior registrar posts may renew the interest of bothmale and female obstetricians in the 1990s. The

Department of Health should take note of thesereasonable requests if it wants any consultantobstetricians still to be in post to provide care for thenext generation of women.The RCOG controls strictly the conditions of

postgraduate training at all levels. Registrar posts areregulated through inspection and recognition; theentry to higher training is by the MRCOG part IIexamination; while the exit from training isdetermined by the RCOG at accreditation. The

College should play this powerful hand of three aces ifthe Department of Health tries to reduce trainingstandards under the cloak of manpower needs.Another threat to those who want to deliver a good

obstetric service comes from the white-paper Workingfor Patients and its spindly infrastructure of subsidiarypapers.6’ The puny offspring are all so vague that localhealth service managers with pecuniary ideas mighttry to use this opportunity to make money8 and soupset many of the better run obstetric endeavours-

3. Royal College of Obstetricians and Gynaecologists. Workload for consultantobstetricians and gynaecologists. London RCOG, 1987. 4-6.

4. Hospital Medical Staffing: achieving a balance Consultative document issued onbehalf of the UK Health Departments, the Joint Consultants Committee, andChairmen of Regional Health Authorities, July 1986.

5. Brahams D. Junior doctors and hours of work Lancet 1989, i. 795-966. Working for Patients (CM 555). London: HM Stationery Office, 1989.7. Black D. A Black look at a white paper. J R Coll Physicians Lond 1989; 23: 66-678 Bevan G, Holland W, Mays N. Working for which patients and at what cost? Lancet

1989; i: 947-49