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Double Standards Revisited
- Ron Law (24 January 2003)
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Dietary Sodium Poorly Calculated
- Bill D. Misner (24 January 2003)
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Salt - Misleading Front Cover and Letter
- Graham A. MacGregor, Feng J. He (31 January 2003)
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Ron Law, Risk Analyst Beyond Alternative Solutions
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MacGregor & He do well to point out that there are no controlled trials showing a reduction in mortality on stopping smoking, reducing fat intake alone (without fish oil supplements), reducing salt intake, losing weight, increasing fruit and vegetable consumption, or increasing exercise. Add to that cholesterol reduction, and you have a series of multi-billion dollar medical industries not evidence based. Isn't it a double standard that whenever a vitamin or mineral is touted as a likely candidate for risk reduction that the medical hounds bay for randomised, double-blind, placebo-controlled clinical studies? Who's going to fund such studies over a 20 year period to "prove" that folic acid reduces the incidence of cancer of the colon by 50-75%? The innate difficulty of conducting and funding such trials, not to mention the medical politics, does indeed mean that such studies will never be undertaken. MacGregor & He ask a very pertinent question, "what strength of evidence is needed to give dietary and lifestyle advice to try to prevent cardiovascular disease?" A cynic might wonder what the recommendations regarding the plethora of risk reduction possibilities associated with longterm folic acid would be if folic acid was patentable and 'owned' by one of the large pharmaceutical companies? Competing interests: None declared |
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Bill D. Misner, Director R & D E-CAPS Inc. E-CAPS Inc. Spokane, Wa. USA 99205
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I conducted 70 computerized dietary analysis on elite endurance athletes over a 6 year period. Most of the subjects stated they consumed low sodium in a healthy balanced diet. Sodium intake was therfore expected to be less than the 2400 mg upper recommended amount. Only 2 subjects of the 70 recorded less than 2400 mg; both subjects were vegetarians. The 68 remaining subjects consumed dietary sodium from food alone ranged from 5500 to 8000 mg sodium per day. If additional salt were added to their foods, it was not recorded. The total sodium came from the food alone, especially from packaged or processed store shelf items. Most people assume that their sodium intake is low when in fact it is likely not low unless their diet consists of unprocessed grains, nuts, seeds, fruits, and vegetables. Bill D. Misner Ph.D. C.S.M.T. Competing interests: The author designed a low sodium electrolyte capsule for endurance athletes. |
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Graham A. MacGregor, Professor of Cardiovascular Medicine Blood Pressure Unit, St. George’s Hospital Medical School, Cranmer Terrace, London SW17 0RE., Feng J. He
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In Hooper et al's reply to the correspondence published about their meta-analysis on salt, they make no attempt to answer any of the very relevant questions put to them[1]. Indeed, they remind us of many current politicians who when asked relevant questions about their policies do not answer them, but attack the questioner! Furthermore, they lack critical insight into the literature or have failed to read or acknowledge it. The follow-up study of TOPH-I trial quite clearly states that this was an 18- month intervention study where salt intake was reduced with the objective of examining whether an 18-month period of salt restriction would have a longer-term effect on blood pressure, in spite of the fact participants went back to their usual salt intake[2]. This is clearly stated in the paper[2] and is not, as Hooper et al state, a 60-month trial of salt restriction. Hooper et al claim that an increase in cholesterol occurs with salt restriction. Again, they have not adequately reviewed the literature. Graudal et al's meta-analysis was severely contaminated by trials of very short-term (many for only five days) and huge changes in salt intake (e.g. 20 grams/day). With these acute large changes in salt intake there are large changes in blood volume and it is not surprising that in the short term there is an increase in cholesterol. However, longer-term trials of more modest reduction in salt intake have shown no increase in cholesterol[3]. Furthermore, Hooper et al again quote Alderman's so called "mortality" studies uncritically and have clearly not read, or have chosen to ignore, the detailed correspondence and papers that followed. Indeed, one of these papers criticising Alderman's study was commissioned by one of the authors of Lee Hooper's meta-analysis for the International Journal of Epidemiology[4]. In the first paper Alderman claimed that reducing salt intake in treated hypertensives caused myocardial infarction. The group with the low salt intake were in fact there because most of them were unable to collect a complete 24-hour urine and therefore had less salt in the urine and were wrongly placed in the low salt group. There was no evidence from the paper to show they were on a low salt intake at the time of entry to the study, and furthermore no measurements were made during the study. In the second study, taken from the NHANES-1 dietary survey, no assessment of discretionary salt was made (The study was conducted in the 1980s when approximately half of the salt intake would be in the form of discretionary salt, ie salt added to cooking or at the table). Furthermore it was clear even to superficial reading of the results that the paper was nonsense. Those on a supposedly lower salt intake were on a calorie intake that was equivalent to a starvation diet, and yet were heavier than those who were said to be on a high salt intake, in spite of the fact that these people had a much higher calorie intake. These two studies cannot be quoted as serious evidence in any discussion about the long term effects of salt restriction. Hooper et al also criticise the very well controlled double blind trials of salt restriction we have conducted. They have not read, or have ignored, the correspondence following our paper in the Lancet where we clearly pointed out that the falls in blood pressure in our trials of salt restriction alone are within two standard deviations of the other trials[5]. Our studies were conducted double blind with slow sodium and placebo and did achieve the expected changes in salt intake, unlike the very small changes that occurred in Hooper et al's meta-analysis. It is not surprising that if people change their salt intake by larger amounts, there are much larger changes in blood pressure, as evidenced in the DASH Sodium Study. Furthermore, they also ignore the fact that some of our studies they criticise were conducted with patients already on an ACE inhibitor. Even a simple understanding of the physiology of the renin- angiotensin system and sodium balance should indicate to Lee Hooper et al that once the renin system is blocked, salt restriction becomes more effective. Indeed, this is exactly what we found – the average fall in blood pressure in untreated patients with essential hypertension with a reduction in salt intake of approximately 5 grams/day for one month was 7.9/4.0 mmHg[6-8], whereas in patients already taking Captopril the same reduction in salt intake caused a fall in blood pressure of 13/9 mmHg[9]. Furthermore, if Hooper et al looked at our paper in the Lancet of a double blind study of three salt intakes[7], they will see that the falls in blood pressure with the three salt intakes are identical to those found with the same changes in the salt intake in the DASH Sodium Study. Their lack of rigour in analysing their own meta-analysis is further revealed by the comment at the end of their letter stating that in one of the studies entered into the meta-analysis anti-hypertensive drugs were involved and were altered during the study. How this study can be included in their meta-analysis of salt restriction alone is not clear. We have recently published a meta-analysis of salt restriction studies with duration of one month or more[3]. This meta-analysis demonstrates that with an average reduction of 4.5 grams/day in salt intake the blood pressure falls by 5/3 mmHg in hypertensive and by 2/1 mmHg in normotensive individuals. Furthermore, there was a clear dose response to salt restriction. We now need to address the important question of how to make it easier for people to reduce their salt intake by amounts that do cause worthwhile falls in blood pressure, ie from the current salt intake of 10 to 12 grams per day to the recommended intake of 5 to 6 grams per day. This is going to be difficult for the majority of the population, where 75% of salt intake now comes courtesy of the food industry hidden in processed food. Nevertheless, just because something is difficult to do and is opposed by a large and financially powerful industry, it does not, in our view, mean we should give in, although it would appear that Hooper et al and presumably the editor of the BMJ are happy to do this. In relation to the grossly misleading front cover of the BMJ, we note that the editor agrees with us by the title of our letter (which he decided). However, he has not apologised or offered any explanation. We feel that in the circumstances the editor of the BMJ should explain himself. Graham A. MacGregor Feng J. He References [1] MacGregor GA, He FJ, Perry IJ, Law MR, Wald NJ, Hooper L, Bartlett C, Davey Smith G, and Ebrahim S. Long term effects of advice to reduce dietary salt. BMJ 2003;326:222-4. [2] He J, Whelton PK, Appel LJ, Charleston J, Klag MJ. Long-term effects of weight loss and dietary sodium reduction on incidence of hypertension. Hypertension 2000; 35: 544-550. [3] He FJ, MacGregor GA. Effect of modest salt reduction on blood pressure. A meta-analysis of randomised trials. Implications for public health. J Hum Hypertens 2002;16:761-770. [4] MacGregor GA, de Wardener HE. Salt, blood pressure and health. Int J Epidemiol 2002;31:320-7. [5] Cappuccio FP, Markandu ND, Carney C, Sagnella GA, MacGregor GA. Modest salt restriction in older people. Lancet 1997;350:1703. [6] MacGregor GA, Markandu ND, Best FE, Elder DM, Cam JM, Sagnella GA, Squires M. Double-blind randomised crossover trial of moderate sodium restriction in essential hypertension. Lancet 1982;1:351-5. [7] MacGregor GA, Markandu ND, Sagnella GA, Singer D, Cappuccio FP. Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension. Lancet 1989;2:1244-7. [8] Cappuccio FP, Markandu ND, Carney C, Sagnella GA, MacGregor GA. Double-blind randomised trial of modest salt restriction in older people. Lancet 1997;350:850-4. [9] MacGregor GA, Markandu ND, Singer DRJ, Cappuccio FP, Shore AC, Sagnella GA. Moderate sodium restriction with angiotensin converting enzyme inhibitor in essential hypertension: a double blind study. BMJ 1987;294:531-4. Competing interests: None declared |
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