HOME
Salt and Blood Pressure
H L MENCKEN
The importance of high blood pressure
If your blood pressure is persistently high, this increases your risk of a heart attack, congestive heart failure, stroke, and damage to your eyes and kidneys. Symptoms of hypertension include cramps, dizziness, nosebleeds, chest pain, nervousness, coronary artery disease, aneurysm, stroke, kidney failure and retinal haemorrhage.
It seems obvious, therefore, that if your blood pressure is too high, you should seek to reduce it to a normal level. But, therein lies the problem, for we have to define firstly what 'high' means in this context, and then determine what is the healthiest way to correct any fault.
Hypertension
The human heart is nothing more than a big pump. When it contracts, it forces blood through the arteries. At this point blood pressure is at a peak, known as systolic, the top number when you have a blood pressure test. Between heartbeats, the heart relaxes and pressure drops. Pressure measured at this time is called diastolic, the bottom number. These numbers are the pressure needed to raise a column of mercury to that height in millimetres (mm Hg). If blood volume increases or the blood vessels' walls don't expand enough, more pressure is needed to push blood around the circulatory system.
Blood pressure is measured with a sphygmomanometer. This consists of a rubber cuff with a tube running to a measuring device. The cuff is usually wrapped around the arm just above the elbow and a stethoscope or electronic sensor is placed over the brachial artery. The cuff is then inflated with air to such a pressure that the brachial artery is closed and no blood flows down the arm. Then the air is allowed to escape slowly from the cuff. When the pressure is just less than the pressure in the artery, a jet of blood will spurt through the artery and be detected by the sensor. This is the systolic measurement. As more air is allowed to escape, the pressure falls until the point at which the blood flow is continuous between heartbeats. This is detected by the sensor and recorded as the diastolic pressure. Blood pressure is expressed as the systolic pressure over the diastolic pressure, e.g. 125 over 70 or 125/70.
Hypertension has been variously defined as a systolic pressure higher than: 100 + your age, then 100 + half your age (systolic), then a fixed figure: 160/100, then 140/90, and currently 120/90, numbers that have been steadily deceasing over the years. This has had the effect of turning more and more healthy people into patients: now, practically everybody is classified as a patient although the vast majority have no obvious medical symptoms to show for it. But it does help to sell drugs! (Sorry if I sound cynical, but a recent paper suggested that people with perfectly normal blood pressure readings were 'pre-hypertensive' thus making them into potential patients as well.)
This measurement, however, can be misleading, particularly among the elderly. As arteries become stiffer, usually with age, a greater pressure in the sphygmomanometer is required to close them, giving the impression of a higher blood pressure than is, in fact, present. Blood pressure is also affected by your physical condition at the time it is measured. If you are working hard, your muscles use up more nutrients and oxygen, and produce more waste products. Blood, which carries all nutrients throughout the body and removes waste from muscles, must be pumped round faster. Under these conditions a raised blood pressure is quite normal. Similarly, when you rest, your blood pressure falls. Even asleep in bed, if you turn over there will be a change in blood pressure. There are also significant variations dependent upon where you are when your blood pressure is measured. When you are at home with your family, it will be at its lowest. With friends it will be higher, and when you are with strangers it will be higher still. Individual blood pressure variations measured in trials ranged from 133/86 to 154/92.[1] So blood pressure varies constantly.
Interarm blood pressure differences are common
If you have had your blood pressure measured in one arm, and your doctor said it was high, did he measure it in your other arm too? Or in your legs? A large difference between blood pressure measurements in different limbs is generally believed to indicate the possibility of disease involving the major arteries and their tributaries in the upper part of the body. For this reason measuring blood pressure at several sites is thought essential as a single measurement tells only part of the story.
In 1997 researchers at the State University of New York reported that large differences in blood pressure between the right and left arms are actually quite common.[2] Their study involved 610 patients who had their blood pressure measured in both arms either simultaneously or sequentially (right arm first followed immediately by the left arm). The researchers discovered that the mean systolic blood pressure difference was about 10 while the mean diastolic pressure difference was 8.5 and 6.7 for sequential and simultaneous measurements respectively. The researchers suggest that initial blood pressure measurements should be made in both arms while follow-up measurements should always be made in the same arm. They also suggest that the arm with the higher measurement should be used when monitoring hypertension. The researchers also found that patients with known coronary heart disease tended to have a greater interarm systolic pressure difference than did people with no heart disease (14.5 mm Hg compared to 10.4 mm Hg). They did, however, conclude that even a difference as large as 20 may not be indicative of a problem.
High blood pressure and heart disease
People with high blood pressure do seem to suffer a greater degree of heart disease, but it is quite obvious from the history of both those conditions that the forces responsible for each are different and independent of each other. The evidence from the United States of the pattern of the rise and fall of coronary heart disease, if plotted against the incidence of hypertension, shows that death rates from the latter decreased in log-linear fashion after 1950 while deaths from the former were still rising.[3]Why blame salt?
As in other 'diseases of civilisation', hypertension is generally blamed on an item of food we eat: in this case, salt. In fact, salt was one of the first dietary items to be indicted by the 'healthy eating' faddists. You will see in The Cholesterol Myth how weak the argument against fat is; in the case against salt it is practically non-existent. Nevertheless, the argument is that salt increases blood pressure and that raised blood pressure causes stroke, brain haemorrhage and heart disease.
For centuries salt, or to give it its scientific name, sodium chloride (NaCl), has been regarded as one of the most important items of diet for health. Salt was so important that people were actually paid in salt (it is the origin of the word 'salary'), and it was used extensively as a valuable commodity for bartering. Then, suddenly, in the 20th Century it became a killer: indicted as a cause of hypertension and, thence, of stroke and of heart disease. The evidence on which this was based arose from poorly controlled cross-cultural studies carried out earlier in the century. At least in the debates on the desirability of fats and fibre, trials were carried out in an attempt to provide evidence to support the hypotheses, but no similar trials have been carried out in the case of salt. The salt hypothesis has no large-scale studies to back it up. The intervention studies that have been carried out are confined to small numbers of people with high blood pressure, and many of these have failed to show that lowering salt intake has any significant effect on blood pressure in those with hypertension. And no tests have been conducted on those whose blood pressure is normal to show that reducing salt intake will reduce the risk of their becoming hypertensive.
Salt is a naturally occurring chemical that is vital to the body. It is an essential constituent of secretions such as perspiration and tears, and it plays a major part in the regulation of fluids within the body. The reason why some people have permanently high blood pressure is not known but the mechanisms which regulate and stabilise blood pressure in the body are many and extremely complex. They are also very efficient: when people eat more salt than is required by the body, it is excreted in the urine and, if they eat less than the body needs, the kidneys conserve it.[4] Those living in the tropics, and particularly in desert conditions, know only too well the value of salt. Too little is a serious threat to health. Deaths from sunstroke and dehydration are not usually caused by the loss of water but by the loss of salt.
Hypertension is rare in primitive cultures out of contact with civilisation, untouched by Western living stresses and eating little salt. When these people move into a Western situation their blood pressure tends to rise. Comparing cultures in an attempt to pin the cause of disease on just one difference are notoriously unreliable. If we look at individuals in any one country or culture, we find that salt plays not the slightest part in hypertension: those with the condition have not been shown to eat more salt than those without it. We also find that if hypertensives do reduce their salt intake, in some their blood pressure goes down but in others it goes up.
Studies on rats show that salt restriction is associated with an increased susceptibility to haemorrhage and kidney problems and the long-term effects of salt restriction on humans are unknown[5] — although it is known that there are problems with erection in men and fatigue with only moderate reductions of sodium.[6]
Clinical, placebo controlled studies using drugs on people with mild to moderate hypertension have shown no benefit in terms of total mortality: there being a similar number of deaths in the drug intervention groups as there was in the group taking the placebo.[7] But those taking the drugs, propranolol, a beta blocker, and bendrofluazide, a diuretic, also had to endure such side-effects as gout, diabetes and impotence.[8]
Diagnosis is harmful
Strangely, the placebo group also suffered similar side-effects, although to a lesser degree, and this points to another side-effect of this and similar interventions. It is recognised by most that diagnosis itself increases stress as it focuses the patient's mind on the possibility of not recovering and of having to be careful what he or she does; it adds uncertainty; and it adds reliance on others. It also sets the patient apart from the normal and healthy: When people who feel fine are told that they have a life-threatening disease, such as hypertension, it alters their whole attitude to life in ways which can have serious consequences affecting their psychological well-being, attitude to their work and marital and social relationships.[9] For example, those treated for hypertension were more likely to complain of more symptoms and were more depressed than untreated hypertensives; they were also more prone to absenteeism and they lost the ability to enjoy social and recreational activities.[10]
So a recent trend is particularly worrying: A friend of mine, an apparently healthy man aged 84, has normal blood pressure. When he tried to arrange insurance, for a holiday abroad in 2004, his insurance company asked for medical details, which were duly supplied by his doctor. They then refused to insure him because he was 'hypertensive'.
But he knew he wasn't. He contacted his doctor to clarify the situation.
It turned out that, although he did not have high blood pressure and unknown to him, his doctor had put him a blood-pressure lowering drug, a beta-blocker 'so that he doesn't become hypertensive'! Frankly, I am appalled. This is indicative of the sort of medical mindset we have today — to give someone drugs that they don't need.
Even today (2005), the long-term safety of low-salt diets has not been tested. Nevertheless, a number of committees recommended in the early 1980s that the general public should reduce its intake of dietary salt. In Britain the two most influential committees were, again, NACNE and COMA.
The bizarre reference
NACNE's report stated that a comparison between Western and primitive societies appeared to show that raised blood pressure was due to an excess consumption of salt. Its reference for this statement, one purporting to demonstrate the benefit of a reduction of salt, was Abstracts of the 18th annual conference of cardiovascular epidemiology 1978, in the Cardiovascular Disease Newsletter No. 28. The choice of such a reference is bizarre to say the least. Many thousands of papers have been published in the medical journals over the years, which failed to show any benefit from reducing salt intake. These are not mentioned. Perhaps the committee had too much difficulty finding one that would support their recommendations. NACNE's choice of so obscure a reference provoked a storm of complaints from leading scientists from Scotland, England, the USA, Sweden and New Zealand who wrote in The Lancet:[11]
'We are concerned with the way in which this important issue is currently being handled. The idea (or likelihood) that salt in the diet has some positive value is totally ignored. The usual scientific standards for weighing evidence and giving advice which are now well established . . . seem to have been forgotten in an evangelical crusade to present a simplistic view of the evidence which will prove attractive to the media.
Professor Swales of Leicester University also pointed out:
'Such a citation would not even get into the bibliography of hypertension. The use of such a publication to support a major recommendation is not acceptable scientific practice. . . it is fairly apparent that an enormous superstructure is being built on extremely weak foundations.'[12]
COMA too, recommend that the dietary intake of salt should not be increased and that a reduction should be considered. They say: 'We believe that the intake of salt in the United Kingdom diet (approximately 7-10 g per day) is needlessly high'. But the reference they use as evidence in support of this recommendation states: 'but a mechanism whereby salt could lead to the development of essential hypertension has not been established.' and 'detailed investigations within a single community frequently fail to demonstrate such a relationship.'
Not that the lack of evidence has stopped the health educators from proclaiming the gospel, or the food industry from realising that here was yet another golden opportunity for them to increase their very profitable range of 'healthy' foodstuffs sold to an unsuspecting public, this time 'with no added salt'.
Reduce hypertension — but increase heart disease?
And with regard to heart disease, there is a confounding factor in that in Japan, where hypertensive diseases are much more common, studies have shown that an increased consumption of saturated fats and cholesterol have led to a reduction in hypertension. So, if the twin hypotheses that both dietary fat and high blood pressure can cause heart disease are correct, how can one be reduced without aggravating the other? There is also no truth that a high-fibre diet will help to combat high blood pressure.[13]
Where risk factors for both heart disease and hypertension do seem to run in parallel is in birth weight. Low weight at birth and high placenta weight, particularly if the two go together, have been shown to be a common factor in fifty-year-old men with high blood pressure.[14] Similarly, the larger the head circumference in relation to body length, the higher was systolic blood pressure.
The relation between diet towards the end of the first trimester of gestation and subsequent birth-weights was measured in 419 singleton pregnancies.[15] The mothers of low birth-weight babies were found to be consuming a diet significantly lower in some essential nutrients than mothers of larger babies. Among others, the associated nutrients were sodium and chloride. The authors of this study recommend that expectant mothers should increase salt intake.
But still the perceived wisdom is trotted out.
The first National Health and Nutrition Examination Survey (NHANES I) established baseline information during 1971-75 in a representative sample of 20,729 American adults aged twenty-five to seventy-five.[16] Of these, 11,348 underwent medical and nutritional examination.
They were rechecked on 30 June 1992. By then there had been 3,923 deaths, of which 1,970 were due to a cardiovascular disease. Comparing salt intakes, this study found that all-cause mortality was inversely related to salt intake. In other words, those who ate the most salt had the fewest deaths — from any cause. And the same was found for cardiovascular deaths. Dr Helen Whalley writing a feature in the Lancet, talks of the continuing debate on the supposed association between salt and hypertension. She points out that an analysis of the NHANES I survey shows that 'the heart attack fatality rate among those on low-sodium diets was 20% higher that those on normal diets.'[17] She goes on to report a study on the Salt Institute's website on the impact of long-term salt reduction. It found 'a four-fold increase in heart attacks among those on low-salt diets'.
The following year a large meta-analysis was published in an attempt to resolve the controversy.[18] Fifty-eight trials published between 1966 and the end of 1997 were reviewed to estimate the effects of reduced sodium intake on systolic and diastolic blood pressure, particularly as in recent years the debate has been extended by studies indicating that reducing sodium intake has adverse effects. They found that reducing salt intake did reduce blood pressure slightly, but that it increased LDL cholesterol, the so-called 'bad' cholesterol. They conclude that 'These results do not support a general recommendation to reduce sodium intake.'
And in May 2005, Dr Hillel W Cohen, assistant professor of epidemiology and population health, Albert Einstein College of Medicine, New York, presented the results of the latest study to an American Heart Association meeting in Washington, DC. In their study, Cohen's team collected data on 7,278 men and women who participated in the Second National Health and Nutrition Examination Survey (NHANES II). During a follow-up of more than 13 years, the researchers looked for the number of deaths from heart disease and the number of deaths from any other cause.
According to Cohen, they found that the intake of less than 2,400 mg of sodium (6 grams of salt) a day was associated with a fifty percent higher risk of heart disease. And they found that as the intake of salt went down, mortality went up: For each 1,000-mg reduction in salt intake, the risk for cardiovascular mortality rose by one percent.
'We found that those who had an intake of salt that was less than the 2,400-mg recommendation had higher mortality,' Cohen said. 'That was true for all-cause mortality and cardiovascular disease mortality.'
This new research adds to others that upend long-standing advice to limit daily salt intake if you want to protect your heart. In fact, the new study suggests, the less salt you eat, the greater your risk of dying from heart disease.
The controversial findings, challenge U.S. Food and Drug Administration and American Heart Association recommendations that people consume no more than 2,400 milligrams of sodium (about 1 teaspoon of table salt) a day.
Dr Cohen told delegates: 'We believe these data do not support' the current guidelines. 'We are urging those who make these guidelines to go back to their data and look at additional data prior to making universal recommendations.'
Cohen believes that the amount of salt that's right for one person may not be right for another. 'It is likely that there are differences between individuals with regard to sodium intake,' he said. 'And it's clear that the data do not support the current recommendations.'
According to Cohen, some people cannot tolerate high levels of salt, while others can. 'From a biological standpoint, if one's kidneys are working reasonably well, sodium within the usual range of intakes shouldn't be a problem,' he said.
Not surprisingly, the findings were challenged by at least one expert, who called them unreliable.
Blood pressure drugs increase risk of heart attack
It is generally accepted practice to treat people with high blood pressure with antihypertensive drugs in order to prevent heart attacks (myocardial infarctions). This despite the fact that clinical trials and recent population studies have both raised serious questions about the effectiveness of antihypertensive drugs in reducing the incidence of heart attacks. Nevertheless, the prescription of antihypertensive drugs for the prevention of heart attacks continues and there is an increasing trend to prescribe them for people whose blood pressure is only just above normal. Now Swedish researchers report that treating elderly men who have a diastolic blood pressure less than 90 mm Hg with antihypertensive drugs increases their risk of having a heart attack by a factor of four.[19]
Conclusion so far
The case of salt and hypertension is a good illustration of the harm that ill-conceived and unsupported hypotheses can do. Yet, despite the vast amount of evidence that screening the population to identify people with high blood pressure, and vilifying salt, does more harm than good, it is being advocated more and more widely.
Is carbohydrate the culprit?
Despite the many studies which show that salt appears not to be the primary culprit, many still insist that it is. In these circumstances, could it be that another dietary item is confusing the issue?
Dr W L Bloom noticed that salt excretion was greater during fasting than when on a low-salt diet. This suggested either that food in general, or some constituent in food, might be involved in the regulation of salt excretion. In 1962 he conducted a study which showed that salt excretion in the urine dropped to low levels immediately after carbohydrate was eaten.[20] Fat and protein, as well as salt, on the other hand, increased the salt excretion of fasting.
What Dr Bloom is suggesting is that salt is important in cases of hypertension, but that eating carbohydrates prevents the body from ridding itself of excess salt.
Obesity and alcohol may cause hypertension
A study of 1,031 subjects in Oakland, California, who developed hypertension over a six-year period was carried out to determine the possible effects of obesity, weight gain, alcohol usage, and salt consumption on the development of hypertension.[21] The results from this group were compared with the results from a matched group of 1031 subjects with normal blood pressure levels. Obesity and weight gain were shown to be clear precursors of hypertension. Excessive alcohol consumption also related to the development of hypertension, most significantly on a short-term basis. Once again the results concerning the effect of salt intake were inconclusive.
Dietary reducers of blood pressure
Fish oils reduce blood pressure. A daily consumption of fish oils (omega-3 polyunsaturated fatty acids) can significantly lower blood pressure in people suffering from hypertension. The benefit of the fish oils is comparable to that obtainable by sodium reduction and weight loss. A group of medical researchers at the Johns Hopkins Medical School evaluated the results of seventeen clinical trials involving supplementation with fish oils for periods of three months or less.[22] They found that the consumption of three grams per day of fish oil (6-10 capsules) or more led to 'impressive reductions' of the order of 5.5 mm Hg systolic in the blood pressure of hypertensive individuals. However, twenty-eight percent of the participants in the trials reported side effects such as a fishy taste or belching.
Fish and fish oils help protect against the development of atherosclerosis and heart disease. It is believed that fish oils exert their protective effect by lowering blood pressure and the levels of triglycerides and very-low-density lipoprotein (VLDL). Fish oils are also believed to reduce platelet aggregation and to suppress the growth of smooth-muscle cells in the arterial walls. Many people with hypertension also suffer from diabetes and there has been concern that fish oil supplementation may aggravate problems with glucose intolerance. Researchers at the University of Tromso now report that fish oil supplementation lowers blood pressure significantly in people with hypertension and has no effect on glucose control even in people with mild diabetes.[23] The study involved seventy-eight obese volunteers with essential hypertension. The participants were randomly assigned to one of two equal-sized groups. The fish oil group received four fish oil capsules a day (containing a total of 3.4 grams of a mixture of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) for a period of sixteen weeks. The control group received four corn oil capsules a day. At the end of the test period the average (mean) systolic blood pressure had dropped by 4.4 mm Hg and the diastolic pressure by 3.2 mm Hg in the fish oil group. The average blood pressure in the control group did not change. The researchers also found that plasma triglyceride and VLDL levels in the fish oil group decreased significantly (by about nine percent) while they increased significantly (by about twelve per cent) in the control group. There were no changes in cholesterol levels in either group. Extensive tests (oral glucose tolerance, hyperglycemic and hyperinsulemic clamps) were done to evaluate the effect of fish oil supplementation on glucose control. No adverse effects were found. An editorial accompanying the research report concludes that fish or fish oil is useful in the prevention of vascular disease in diabetics. Patients with diabetes should eat fish two to three times a week or, as an alternative, supplement with two to three one gram capsules of fish oil per day.
But, again, not all studies agree. Dr D Kenny, writing in 1992 found that fish oil increased arterial pressure and also the incidence of stroke.[24]
Vitamin C lowers blood pressure. Researchers at the Medical College of Georgia have confirmed that people with a high vitamin C concentration in their blood have lower blood pressures than do people with little vitamin C.[25] They tested 168 healthy people, 56 of whom were taking supplements containing ascorbic acid. They found that both diastolic and systolic blood pressure were about 5 mm Hg lower in people having a high plasma level of vitamin C than in people having a low level. Blood levels of selenium, vitamin A and vitamin E were not found to affect blood pressure, but both obesity and smoking had a significant adverse effect.
Magnesium supplement lowers blood pressure. Dutch and Belgian researchers conducted a double-blind, controlled trial in order to determine if oral supplementation with magnesium is an effective way of lowering blood pressure in women suffering from mild to moderate hypertension.[26] Their experiment involved ninety-one women aged between thirty-five and seventy-seven who did not take anti- hypertensive medication. All the women had a systolic blood pressure between 140 and 185 mm Hg and a diastolic pressure between 90 and 105 mm Hg. The intervention group received 485 mg per day of magnesium aspartate-HCl. At the end of the six-month trial period the systolic blood pressure in the magnesium supplementation group had decreased by 2.7 mm Hg and the diastolic pressure by 3.4 mm Hg when compared to the placebo group. The researchers conclude that oral supplementation with magnesium aspartate-HCl may be effective in lowering blood pressure in people suffering from mild to moderate hypertension who are not taking anti-hypertensive drugs.
Strangely, however, one of the early studies on salt on hypertension rated sea salt worse than table salt.[27] Unlike table salt, which is pure sodium chloride, sea salt also contains other chemicals, including magnesium.
Calcium combats high blood pressure. Researchers at the Oregon Health Sciences University published a major overview on the current knowledge concerning the effect of dietary minerals on high blood pressure.[28] They conclude that the effect of sodium intake on blood pressure is still not clear. It may be that only a subset of people with a genetic defect are sensitive to salt intake. The chloride ion in itself does not seem to increase blood pressure, but when combined with sodium it does cause hypertension in salt-sensitive individuals. A four-year study of 60,000 nurses concluded that women who have a calcium intake of 800 mg/day or more have a twenty-three per cent lower risk of developing high blood pressure than women with an intake of 400 mg/day or less. The benefits of calcium are even greater among pregnant women. Controlled trials have found that women who consume between 1500 and 2000 mg/day of calcium reduce their risk of developing pregnancy-induced hypertension by as much as fifty percent. It has also been shown that maternal calcium intake directly affects the infant's blood pressure. Women with a high calcium intake gave birth to babies with higher birth weights and lower blood pressures. This lower pressure persisted throughout at least the first five years of life.
Relaxation therapy controls high blood pressure. Hypertension is widespread in northern Taiwan. A recent survey found that 27.2 per cent of males and 13.6 per cent of females suffer from this condition.[29] A team of researchers from the National Taiwan University and the University of Hawaii now reports that relaxation techniques, frequent blood pressure measurements, and educational techniques are all effective in controlling hypertension. Their experiment involved 590 patients. The patients were randomly assigned to an intervention group to practise relaxation techniques at home, to have frequent, routine blood pressure measurements by health professionals, to read information packages about hypertension control; or to a control group who received no treatment. The relaxation techniques involved one-on-one instruction sessions, taped messages of progressive relaxation procedures, and encouragement to perform Buddhist meditation. At the end of the two-month test period the average drop in systolic pressure in the relaxation group was 11 mm Hg and the drop in diastolic pressure was 4.7 mm Hg greater than in the control group. The patients who participated in the frequent blood pressure measurement program also lowered their pressure significantly, as did the self-learning group. Almost fifty percent of the members of the relaxation and self-learning groups achieved a drop in systolic pressure of 10 mm Hg or more and a drop in diastolic pressure of 5 mm Hg or more as a result of the program.
Dairy products reduce hypertension
The risk of developing hypertension in African Americans is more than twice that of their white counterparts, and thus they are at dramatically increased risk of excessive mortality from cardiovascular disease.[30] This greater risk is evident in all age groups and both sexes. While overweight and sensitivity to dietary salt are often thought to contribute to this excessive risk, neither fully explains this relation:
- In groups with comparable weights and body mass indexes, African Americans have higher mean blood pressure than whites.
- Salt sensitivity is more prevalent in African Americans, but there is no evidence that salt intake is notably greater in this population.
Over a decade in the late 1980s, early 1990s, a credible body of evidence emerged supporting the concept that maintaining an adequate dietary mineral intake, specifically of calcium, magnesium, and potassium, protects against high blood pressure in humans. Observational and interventional studies in humans and extensive use of laboratory models showed that a significant portion of blood pressure variability in response to salt could be linked to the adequacy of the mineral content of the diet. In particular, a report published in 1998 provided valuable evidence that adequate dietary calcium intake was essential to optimal blood pressure regulation in humans. [31] This benefit on blood pressure of calcium and other minerals found in a diet rich in dairy products, was greatest when these foods are added to the diets of individuals whose dietary patterns were deficient.[32]
Analysis of the first National Health and Nutrition Examination Survey [NHANES I] showed in 1994 for the first time that there were important, relevant dietary intake patterns that predicted blood pressure in Americans,[33] and confirmed an earlier observation that hypertension was associated with a diet poor in dairy products and the minerals calcium, potassium, and magnesium.[34] This analysis showed that the cardiovascular benefits of calcium and potassium were continuous across the age range from 18 to 75 years of age and were evident in both men and women as well as across racial groups. The benefits appeared to have a dose-response relation with a threshold at less than 600—700 mg of calcium per day. Below that, blood pressure and the risk of being hypertensive were greater.
These findings have been confirmed many times since. The evidence in clear food sources that contain dietary calcium rather than supplements are more efficacious.
But note that low calcium can be the result of a diet high in 'healthy' cereal fibre and also with lack of vitamin D.
Conclusion
Over the years the level of blood pressure considered 'normal' has been progressively lowered until now practically everyone is a potential patient. At the same time, the general population has been exhorted to undertake dietary changes which are unsupported by any coherent body of evidence. When the hoped for reductions are not achieved by salt restriction, these 'patients' are prescribed drugs which may be harmful. This is despite the undoubted fact that salt restriction has not been shown to be beneficial in terms either of morbidity or mortality: Most people who suffer strokes today have blood pressures that are well within normal.
Let me leave the last word to Michael Alderman, President of the American Society of Hypertension, Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, who wrote in 1997:[35]
'Public health recommendations must be based on proof of safety and benefit. Even if a low sodium diet could lower the blood pressure of most people (probably not true) and both the diet and the change in blood pressure could be sustained (not established), this alone would not justify a recommendation to reduce sodium intake.
'For such advice to be responsibly given there must be evidence that the change will improve and not impair health. While the advantage of a lower blood pressure, at any level, is well established, it is not true that every method to lower blood pressure would necessarily improve health. Some techniques to lower blood pressure, like giving short acting calcium antagonists, may not be safe.
'All interventions aimed at enhancing or extending life by manipulating a single mechanism inevitably produce a variety of effects, some of which may not be advantageous. Extrapolation from mechanistic thinking demands evidence that the sum total of all the effects of the intervention — and not just one, such as lowering blood pressure — will help and not harm; and particularly here since the target is the whole population.
'A low sodium intake produces many effects, not all of which are salutary. The integrated impact of these effects remains to be established. The scanty evidence directly linking sodium intake to morbidity and mortality is not encouraging.
'Unfortunately, we simply do not know whether a universal change in sodium consumption will cause benefit or harm. Insufficient evidence — for good or ill — is not a sturdy basis for making health policy. Gratuitous exhortation, reflecting the hopes of even the most well meaning authorities, is no substitute for data. Toward this end, a good start would be to collect and analyse further observational data linking sodium intake to subsequent morbid and fatal outcomes.'
'The important question that emerges from these papers is why the combined intellects of so many distinguished epidemiologists should maintain that the evidence incriminating salt in hypertension is so convincing when clearly it adds up to very little.'[36]
So, 'healthy' guidelines seem to leave much to be desired and, if followed, may actually place the population at increased risk.
Incidentally, only about five to ten percent of salt consumed occurs in natural foods such as meat. While more may be added during cooking or at the table, by far the greatest amount is found in processed foods. Foods normally thought of as being excessively salty (eg, potato crisps) usually contain much less salt than foods with 'hidden' salt. The worst ones seem to be the 'healthy' ones such as bread and canned vegetables and soups.
References
[1]. Spitzer S, et al. The influence of social situations on ambulatory blood pressure. Psychosom Med 1992; 54: 71.
[2]. Singer, Adam J. and Hollander, Judd E. Blood pressure — Assessment of interarm differences. Arch Int Med 1996; 156: 2005- 08
[3]. Stallones RA. The Rise and Fall of Ischaemic Heart Disease. Scientific American 1980; 243 (5): 43-9.
[4]. Nakatsuka H, et al. Effectiveness of attention to reduce salt in diet, as evidenced by reduced urinary excretion of salt. Ecol Food Nutr 1991; 26: 323-332.
[5]. Gothberg G, et al. Response to slow graded bleeding in salt depleted rats. J Hypertension 1983; 1(Suppl 2): 24.
[6]. Wassertheil-Smoller S, et al. Effect of antihypertensives on sexual function and quality of life: the TAIM Study. Ann Intern Med 1991; 114: 613-20.
[7]. Medical Research Council Working Party: MRC trial of treatment of mild hypertension: principle results. Br Med J 1985; 291: 97
[8]. — Adverse reactions to bendrofluazide and propranolol. Lancet 1981; ii: 632.
[9]. Editorial. More on hypertension labelling. Lancet 1985; i: 1138.
[10]. Milne BJ, Logan AG, Flanagan PT. Alteration in health perception and life-style in treated hypertensives. J Chronic Dis 1985; 38: 37.
[11]. Brown JJ, et al. Salt and hypertension. Lancet 1984; ii: 456.
[12]. Swales J. Salt and High Blood Pressure: A Study in Education, Persuasion and Naïveté. A Diet of Reason. Social Affairs Unit, 1986
[13]. Lichtenstein MJ, et al. Heart rate, employment status and prevalent IHD confound relationship between cereal fibre intake and blood pressure. J Epid Comm Hlth 1986; 40: 330.
[14]. Barker DJP, Godfrey KM, Osmond C, Bull A. The relation of fetal length, ponderal index and head circumference to blood pressure and the risk of hypertension in later life. Paed Perinat Epidem 1992; 6: 35.
[15]. Doyle W, Crawford MA, Wynn AHA, Wynn SW. Maternal nutrient intake and birthweight. J Hum Nutr Dietet 1989; 2: 451-22.
[16]. Alderman M N, Cohen H, Madhavan S. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet 1998; 351: 781-85
[17]. Whalley H. Salt and Hypertension: consensus or controversy? Lancet 1997; 350: 1686.
[18]. Graudal N A, Gallee A M, Garred P. Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride : A Meta-analysis. JAMA 1998; 279:1383-1391
[19]. Merlo J, et al. Incidence of myocardial infarction in elderly men being treated with antihypertensive drugs: population based cohort study. Br Med J 1996; 313: 457-61
[20]. Bloom W L. Inhibition of salt excretion by carbohydrate. Arch Int Med. 1962; 109: 26-32.
[21]. Friedman G D, et al. Precursors of essential hypertension: body weight, alcohol and salt use, and parental history of hypertension. Prev Med 1988; 17: 387-400
[22]. Appel LJ, et al. Does supplementation of diet with "fish oil" reduce blood pressure? Arch Int Med, 1993; 153: 1429-38
[23]. Connor W E. Diabetes, fish oil, and vascular disease. Ann Int Med 1995; 123: 950-52.
[24]. Kenny D. The paradoxical effects of fish oil on blood pressure. Med Hypoth 1992; 37: 97.
[25]. Moran J P, et al. Plasma ascorbic acid concentrations relate inversely to blood pressure in human subjects. Am J Clin Nutr 1993; 57: 213-17.
[26]. Witteman JCM, et al. Reduction of blood pressure with oral magnesium supplementation in women with mild to moderate hypertension. Am J Clin Nutr, 1994; 60: 129-35
[27]. Dahl L K Heine M. Effects of chronic excess salt feeding: Enhanced hypertensogenic effect of sea salt over sodium chloride. J Exp Med 1961; 113: 1067-76
[28]. Reusser M E. and McCarron, D A. Micronutrient effects on blood pressure regulation. Nutr Rev 1994; 52: 367-75.
[29]. Yen L-L, et al. Comparison of relaxation techniques, routine blood pressure measurements, and self-learning packages in hypertension control. Prev Med 1996; 25: 339-45
[30]. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;157:2413—46.
[31]. Dwyer JH, Dwyer KM, Scribner RA, et al. Dietary calcium, calcium supplementation, and blood pressure in African American adolescents. Am J Clin Nutr 1998;68:648—55.
[32]. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med 1997; 336:1117—24.
[33]. McCarron DA, Morris CD, Henry HJ, Stanton JL. Blood pressure and nutrient intake in the United States: an analysis of the Health and Nutrition Examination Survey I. Science 1984;224:1392—8.
[34]. McCarron DA, Morris C, Cole C. Dietary calcium in human hypertension. Science 1982;217:267—9.
[35]. Alderman M. Data linking sodium intake to subsequent morbid and fatal outcomes must be studied. Br Med J 1997; 315: 484-5
[36]. Le Fanu J. Cross cultural studies such as Intersalt study cannot be used to infer causality. Br Med J 1997; 315: 484
Last updated 18 June 2005
Related Articles
