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CHANGES IN SALT INTAKE AND BLOOD-PRESSURE
632 that because of the small differences found, the shortness of the follow-up, and the shortfalls in experimental design "this treatment should not be generally advocated, despite its possible benefits, until these results have been confirmed by further work". We are committed to further longitudinal study of the group reported, and have set up a new study which will overcome most of the patient selection criteria problems encountered in the preliminary trial. Notwithstanding this, we would welcome an independent trial. R. B. ELLIOTT R. CROSSLEY J. Department of Paediatrics, C. C. BERRYMAN of Auckland School of Medicine, University A. G. JAMES Auckland, New Zealand
SALT AND HYPERTENSION
SIR,-There is still great reluctance to accept that hypertension is by excessive salt intake in genetically susceptible individuals, and our short report’ of a link between blood pressure
caused
(BP) and table added salt has, predictably, attracted criticism. Further details will be published elsewhere, but perhaps a few points could be made. Table added salt contributes only about 30% of the total salt intake ; nevertheless our data did show a statistical correlation with BP, as Dahl3 had shown, using a similar technique. Statistical analysis showed two independent effects-one between table added salt and BP, and an independent age effect which is probably due to salt already present in the diet. Our study was done on hospital inpatients and outpatients, but all severely ill patients were excluded and the pre-illness salt score was determined. The fact that the population was not entirely random does not invalidate the study. Thus Tibetan Lamas who take large quantities of highly salted butter tea as part of their ritual have a high incidence of hypertension; in the Nepalese, who take little salt, hypertension is very rare. Studies on selected populations, on their own, do not prove a link between salt and hypertension, but, when taken with other epidemiological evidence, they are useful links. Our study was limited to subjects over 39 years because hypertension does not usually manifest itself before this age. In the oft cited Miall study about half the participants were under 40, thus making it more difficult to demonstrate a relation between salt and BP. The information was collected by four doctors independently: three recorded the salt intake score and then looked up the BP in the case notes, while the fourth recorded the salt score and then took the BP. Statistical analysis showed no difference between the observers. Our study was not wholly blind, and this is a justifiable criticism; however, most important 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 1904and subse3 quent milestones include the Kempner rice diet and Dahl’s studies3 in the salt leading to concepts that only produces hypertension genetically susceptible individuals, and that salt acts as an initiator of the hypertensive process. Established hypertension does not therefore respond to salt restriction, and the main role of salt restriction is in prevention. Epidemiological studies have established that hypertension is rare in societies with a low salt intake. The latest major advance has been the work of Garay and colleagues5 who have shown that the cellular cation pump is under genetic control in man, thus explaining the unique susceptibility of some individuals to the ingestion of salt. Certain academics in the U.K. point out that the evidence is not watertight and that a link between salt and hypertension is not proven. I cannot deny the logic of this view, but what are the conse-
quences ? If we withhold advice on salt moderation and continue to investigate such matters as sodium metabolism and renin we will learn more basic physiology and keep several academic units at work, but I suspect that from a practical point of view it will get us nowhere. A vast amount of research has already been done in hypertension without any practical spin-off. A clinical trial of salt restriction would take many years to produce an answer. Surely the American view, as expressed by bodies such as the National Research Council,6 is more reasonable. By all means let research continue but let us now advise a reduction in salt intake. Drastic changes in diet are not necessary: simply avoiding table added salt and reducing the intake of highly salted foods would reduce the risk of 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 Science and Technology of the U.S. House of Representatives that 60 million Americans have high blood pressure and that hypertension is the primary cause of the 500 000 cases of stroke and 175 000 stroke deaths which take place in the United States every year and a major contributor to the 1 250 000 heart attacks and 650 000 heart attack deaths. Such a major health problem, which is not restricted to the United States, needs a multifactorial approach. Established hypertension needs hypotensive drugs, but a general reduction in sodium 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 Japan consumed 20-30 g of salt per day.’ In 1960 Dahl2 reviewed evidence that salt ingestion may be related to hypertension and reported epidemiological findings in human hypertension.From observations in north-eastern Japan, Sasaki3 suggested that interaction between genetic and environmental factors is important in the causation of human hypertension.33 We have tried to assess the in salt intake and bloodpressure in individual subjects over 20 years. The volunteers were chosen from farming people in Oinomori and Kanaya villages, in the north-east.3Their average age, both male and female, was 46. Three consecutive 24 h urine samples were collected from the same person in 1961 and 1981. Blood-pressure was measured once or twice a year by mass surveys from 1954 in Oinomori and from 1958 in Kanaya, respectively, up to 1975, and the changes in bloodpressure for each person were calculated from the records obtained during the entire period (see table). The salt intake of these farming people decreased from 17 - 0 g per day in 1961 to 11’ 9 g in 1981 and the blood-pressure did not rise with advancing age. NAOSUKE SASAKI Department of Hygiene, MASAO TAKAHASHI Hirosaki University, SHO FUKUSHI School of Medicine, KPOCJO TAKEMORI Hirosaki 036, Japan
changes
6. Towards healthful diets. 1.
Washington, DC: Food and Nutrition Board, National Academy of Sciences, 1980. Sasaki N. High blood pressure and the salt intake of the Japanese. Jap HeartJ 1962, 3:
313-24. 2. Dahl LK. Possible role of salt intake
in the development of essential hypertension In Bock KD, Cottier PT, eds. Essential hypertension. Berlin: Springer, 1960: 53-65. 3. Saski N. Epidemiological studies on hypertension in Northeast Japan. In- Kesteloot II, Joossens JV, eds. Epidemiology of arterial blood pressure. Hague: Martinus Nijhoff, 1980: 367-77.
CHANGES IN SALT INTAKE AND BLOOD-PRESSURE
R, McConnochie K, Box DEO, Fennerty AG, Green JR. Blood pressure and salt intake: an intrapopulation study. Lancet 1981; i: 1097. Finn R, McConnochie K, Green JR. Salt and hypertension. In: Rees AR, Purcell H, eds. Disease and the environment. Chichester: John Wiley (in press). Dahl LK. Salt and hypertension. Am J Hum Nutr 1972; 25: 231-44. Ambard L, Beaujard E. Causes de hypertension arterielle. Arch Gen Med 1904; 1: 520-30. 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.
1. Finn
2. 3. 4 5.
*p
fp
Students’ paired comparing urine data for 1961 and 1981.
SALT AND HYPERTENSION
SIR,-There is still great reluctance to accept that hypertension is by excessive salt intake in genetically susceptible individuals, and our short report’ of a link between blood pressure
caused
(BP) and table added salt has, predictably, attracted criticism. Further details will be published elsewhere, but perhaps a few points could be made. Table added salt contributes only about 30% of the total salt intake ; nevertheless our data did show a statistical correlation with BP, as Dahl3 had shown, using a similar technique. Statistical analysis showed two independent effects-one between table added salt and BP, and an independent age effect which is probably due to salt already present in the diet. Our study was done on hospital inpatients and outpatients, but all severely ill patients were excluded and the pre-illness salt score was determined. The fact that the population was not entirely random does not invalidate the study. Thus Tibetan Lamas who take large quantities of highly salted butter tea as part of their ritual have a high incidence of hypertension; in the Nepalese, who take little salt, hypertension is very rare. Studies on selected populations, on their own, do not prove a link between salt and hypertension, but, when taken with other epidemiological evidence, they are useful links. Our study was limited to subjects over 39 years because hypertension does not usually manifest itself before this age. In the oft cited Miall study about half the participants were under 40, thus making it more difficult to demonstrate a relation between salt and BP. The information was collected by four doctors independently: three recorded the salt intake score and then looked up the BP in the case notes, while the fourth recorded the salt score and then took the BP. Statistical analysis showed no difference between the observers. Our study was not wholly blind, and this is a justifiable criticism; however, most important 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 1904and subse3 quent milestones include the Kempner rice diet and Dahl’s studies3 in the salt leading to concepts that only produces hypertension genetically susceptible individuals, and that salt acts as an initiator of the hypertensive process. Established hypertension does not therefore respond to salt restriction, and the main role of salt restriction is in prevention. Epidemiological studies have established that hypertension is rare in societies with a low salt intake. The latest major advance has been the work of Garay and colleagues5 who have shown that the cellular cation pump is under genetic control in man, thus explaining the unique susceptibility of some individuals to the ingestion of salt. Certain academics in the U.K. point out that the evidence is not watertight and that a link between salt and hypertension is not proven. I cannot deny the logic of this view, but what are the conse-
quences ? If we withhold advice on salt moderation and continue to investigate such matters as sodium metabolism and renin we will learn more basic physiology and keep several academic units at work, but I suspect that from a practical point of view it will get us nowhere. A vast amount of research has already been done in hypertension without any practical spin-off. A clinical trial of salt restriction would take many years to produce an answer. Surely the American view, as expressed by bodies such as the National Research Council,6 is more reasonable. By all means let research continue but let us now advise a reduction in salt intake. Drastic changes in diet are not necessary: simply avoiding table added salt and reducing the intake of highly salted foods would reduce the risk of 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 Science and Technology of the U.S. House of Representatives that 60 million Americans have high blood pressure and that hypertension is the primary cause of the 500 000 cases of stroke and 175 000 stroke deaths which take place in the United States every year and a major contributor to the 1 250 000 heart attacks and 650 000 heart attack deaths. Such a major health problem, which is not restricted to the United States, needs a multifactorial approach. Established hypertension needs hypotensive drugs, but a general reduction in sodium 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 Japan consumed 20-30 g of salt per day.’ In 1960 Dahl2 reviewed evidence that salt ingestion may be related to hypertension and reported epidemiological findings in human hypertension.From observations in north-eastern Japan, Sasaki3 suggested that interaction between genetic and environmental factors is important in the causation of human hypertension.33 We have tried to assess the in salt intake and bloodpressure in individual subjects over 20 years. The volunteers were chosen from farming people in Oinomori and Kanaya villages, in the north-east.3Their average age, both male and female, was 46. Three consecutive 24 h urine samples were collected from the same person in 1961 and 1981. Blood-pressure was measured once or twice a year by mass surveys from 1954 in Oinomori and from 1958 in Kanaya, respectively, up to 1975, and the changes in bloodpressure for each person were calculated from the records obtained during the entire period (see table). The salt intake of these farming people decreased from 17 - 0 g per day in 1961 to 11’ 9 g in 1981 and the blood-pressure did not rise with advancing age. NAOSUKE SASAKI Department of Hygiene, MASAO TAKAHASHI Hirosaki University, SHO FUKUSHI School of Medicine, KPOCJO TAKEMORI Hirosaki 036, Japan
changes
6. Towards healthful diets. 1.
Washington, DC: Food and Nutrition Board, National Academy of Sciences, 1980. Sasaki N. High blood pressure and the salt intake of the Japanese. Jap HeartJ 1962, 3:
313-24. 2. Dahl LK. Possible role of salt intake
in the development of essential hypertension In Bock KD, Cottier PT, eds. Essential hypertension. Berlin: Springer, 1960: 53-65. 3. Saski N. Epidemiological studies on hypertension in Northeast Japan. In- Kesteloot II, Joossens JV, eds. Epidemiology of arterial blood pressure. Hague: Martinus Nijhoff, 1980: 367-77.
CHANGES IN SALT INTAKE AND BLOOD-PRESSURE
R, McConnochie K, Box DEO, Fennerty AG, Green JR. Blood pressure and salt intake: an intrapopulation study. Lancet 1981; i: 1097. Finn R, McConnochie K, Green JR. Salt and hypertension. In: Rees AR, Purcell H, eds. Disease and the environment. Chichester: John Wiley (in press). Dahl LK. Salt and hypertension. Am J Hum Nutr 1972; 25: 231-44. Ambard L, Beaujard E. Causes de hypertension arterielle. Arch Gen Med 1904; 1: 520-30. 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.
1. Finn
2. 3. 4 5.
*p
fp
Students’ paired comparing urine data for 1961 and 1981.