632

that because of the small differences found, the shortness of thefollow-up, and the shortfalls in experimental design "thistreatment should not be generally advocated, despite its possiblebenefits, until these results have been confirmed by further work".We are committed to further longitudinal study of the groupreported, and have set up a new study which will overcome most ofthe patient selection criteria problems encountered in the

preliminary trial. Notwithstanding this, we would welcome anindependent trial.

Department of Paediatrics,University of Auckland School of Medicine,Auckland, New Zealand

R. B. ELLIOTT

J. R. CROSSLEYC. C. BERRYMANA. G. JAMES

SALT AND HYPERTENSION

SIR,-There is still great reluctance to accept that hypertension iscaused by excessive salt intake in genetically susceptible in-

dividuals, and our short report’ of a link between blood pressure(BP) and table added salt has, predictably, attracted criticism. Fur-ther details will be published elsewhere, but perhaps a few pointscould be made.Table added salt contributes only about 30% of the total salt in-

take ; nevertheless our data did show a statistical correlation withBP, as Dahl3 had shown, using a similar technique. Statistical

analysis showed two independent effects-one between table addedsalt and BP, and an independent age effect which is probably due tosalt already present in the diet. Our study was done on hospital inpa-tients and outpatients, but all severely ill patients were excluded andthe pre-illness salt score was determined. The fact that the popula-tion was not entirely random does not invalidate the study. ThusTibetan Lamas who take large quantities of highly salted butter teaas part of their ritual have a high incidence of hypertension; in theNepalese, who take little salt, hypertension is very rare. Studies onselected populations, on their own, do not prove a link between saltand hypertension, but, when taken with other epidemiologicalevidence, they are useful links. Our study was limited to subjectsover 39 years because hypertension does not usually manifest itselfbefore this age. In the oft cited Miall study about half the par-ticipants were under 40, thus making it more difficult to

demonstrate a relation between salt and BP. The information wascollected by four doctors independently: three recorded the salt in-take score and then looked up the BP in the case notes, while thefourth recorded the salt score and then took the BP. Statistical

analysis showed no difference between the observers. Our study wasnot wholly blind, and this is a justifiable criticism; however, mostimportant scientific observations have been open.There is a mass of other evidence pointing to a causal link between

salt and BP. The relation was first suggested in 1904 and subse-quent milestones include the Kempner rice diet and Dahl’s studies3

3

leading to the concepts that salt only produces hypertension ingenetically susceptible individuals, and that salt acts as an initiatorof the hypertensive process. Established hypertension does nottherefore respond to salt restriction, and the main role of salt restric-tion is in prevention. Epidemiological studies have established thathypertension is rare in societies with a low salt intake. The latest ma-jor advance has been the work of Garay and colleagues5 who haveshown that the cellular cation pump is under genetic control in man,thus explaining the unique susceptibility of some individuals to theingestion of salt.

Certain academics in the U.K. point out that the evidence is notwatertight and that a link between salt and hypertension is not pro-ven. I cannot deny the logic of this view, but what are the conse-

1. Finn R, McConnochie K, Box DEO, Fennerty AG, Green JR. Blood pressure and saltintake: an intrapopulation study. Lancet 1981; i: 1097.

2. Finn R, McConnochie K, Green JR. Salt and hypertension. In: Rees AR, Purcell H,eds. Disease and the environment. Chichester: John Wiley (in press).

3. Dahl LK. Salt and hypertension. Am J Hum Nutr 1972; 25: 231-44.4 Ambard L, Beaujard E. Causes de hypertension arterielle. Arch Gen Med 1904; 1:

520-30.5. Garay RP, Degher G, Pernollet KG, Devynck MA, Heyer P. Inherited defect in a

Na-K co-transport system in erythrocytes from essential hypertensive patients.Nature 1980; 284: 281-83.

quences ? If we withhold advice on salt moderation and continue toinvestigate such matters as sodium metabolism and renin we willlearn more basic physiology and keep several academic units atwork, but I suspect that from a practical point of view it will get usnowhere. A vast amount of research has already been done inhypertension without any practical spin-off. A clinical trial of saltrestriction would take many years to produce an answer. Surely theAmerican view, as expressed by bodies such as the NationalResearch Council,6 is more reasonable. By all means let researchcontinue but let us now advise a reduction in salt intake. Drastic

changes in diet are not necessary: simply avoiding table added saltand reducing the intake of highly salted foods would reduce the riskof hypertension in genetically susceptible individuals.In April, 1981, Dr Robert I. Levy, director of the National Heart,

Lung and Blood Institute, stated before the Committee of Scienceand Technology of the U.S. House of Representatives that 60million Americans have high blood pressure and that hypertensionis the primary cause of the 500 000 cases of stroke and 175 000stroke deaths which take place in the United States every year and amajor contributor to the 1 250 000 heart attacks and 650 000 heartattack deaths. Such a major health problem, which is not restrictedto the United States, needs a multifactorial approach. Establishedhypertension needs hypotensive drugs, but a general reduction insodium intake could have a major preventive effect.

Department of Medicine,Royal Liverpool Hospital,Liverpool L7 8XP RONALD FINN

CHANGES IN SALT INTAKE AND BLOOD-PRESSURE

SiR,—Traditionally the inhabitants of north-eastern Japanconsumed 20-30 g of salt per day.’ In 1960 Dahl2 reviewedevidence that salt ingestion may be related to hypertension andreported epidemiological findings in human hypertension. Fromobservations in north-eastern Japan, Sasaki3 suggested thatinteraction between genetic and environmental factors is importantin the causation of human hypertension.3 3We have tried to assess the changes in salt intake and blood-

pressure in individual subjects over 20 years. The volunteers werechosen from farming people in Oinomori and Kanaya villages, inthe north-east.3 Their average age, both male and female, was 46.Three consecutive 24 h urine samples were collected from the sameperson in 1961 and 1981. Blood-pressure was measured once ortwice a year by mass surveys from 1954 in Oinomori and from 1958in Kanaya, respectively, up to 1975, and the changes in blood-pressure for each person were calculated from the records obtainedduring the entire period (see table). The salt intake of these farmingpeople decreased from 17 - 0 g per day in 1961 to 11’ 9 g in 1981 andthe blood-pressure did not rise with advancing age.

Department of Hygiene,Hirosaki University,School of Medicine,Hirosaki 036, Japan

NAOSUKE SASAKIMASAO TAKAHASHISHO FUKUSHIKPOCJO TAKEMORI

6. Towards healthful diets. Washington, DC: Food and Nutrition Board, NationalAcademy of Sciences, 1980.

1. Sasaki N. High blood pressure and the salt intake of the Japanese. Jap Heart J 1962, 3:313-24.

2. Dahl LK. Possible role of salt intake in the development of essential hypertension InBock KD, Cottier PT, eds. Essential hypertension. Berlin: Springer, 1960: 53-65.

3. Saski N. Epidemiological studies on hypertension in Northeast Japan. In- KestelootII, Joossens JV, eds. Epidemiology of arterial blood pressure. Hague: MartinusNijhoff, 1980: 367-77.

CHANGES IN SALT INTAKE AND BLOOD-PRESSURE

*p<O - 05; fp<p-01, 4:p<0.Students’ paired comparing urine data for 1961 and 1981.