By Beatrice Trum Hunter
From Consumer Research Magazine
In 1994 the U.S Department of agriculture proposed to limit sodium in school feeding programs. The Salt Institute, a trade organization, promptly protested. The group contended that removal of high-sodium foods, such as fluid milk and other dairy products, inevitably denies children other important nutrients such as calcium and potassium, present in such foods.
This challenge deserves scrutiny. The USDA's proposal, which forms public policy, must be based solidly on scientific evidence. Correct? Incorrect!
Contrary to popular perception, universal sodium restriction is unnecessary, and possibly undesirable. A common notion is that sodium induces hypertension (high blood pressure) and lowering sodium intake will prevent hypertension. Unfortunately, this scientific notion has no scientific basis. Instead, many recent medical studies have brought into question the effectiveness and even the safety of universal sodium restriction.
There is a relationship between sodium and blood pressure, which is important for about 10% of the population that is sodium-sensitive. For this group, sodium restriction is an important feature, along with other measures, for treatment. However, for about 90% of the population, there is no convincing scientific basis for the idea that sodium restriction will prevent hypertension.
Treatment Differs from Prevention. In earlier times, medically supervised sodium restriction therapy was common with hypertensives, For the general public, however, the Food and Nutrition Board of the National Academy of Sciences warned in 1954 that "harmful results may follow the restriction of sodium intake... when the diet is severely restricted in sodium for long periods,...reduction of intake of essential nutrients, especially vitamins, may occur...(in studies) calcium, riboflavin, and protein were the principal nutrients in short supply. These dietary deficiencies were occasioned chiefly by the omission of milk....Metabolic studies on patients with hypertension treated with sodium-restricted diets have revealed a number of changes....these changes are potentially dangerous, perhaps leading to... reduced renal (kidney) function."
At that time, there was a medical consensus regarding the treatment of hypertension. In terms of prevention, one doctor warned the public against self-imposed sodium restriction that "affords no benefit to the normal individual....self restriction will not prevent disease."
Another doctor noted that "thousands of misguided enthusiasts have eaten unpalatable food on a mistaken assumption that....high blood pressure would be prevented. The facts are simple. There is no evidence that excessive salt intake produces high blood pressure in humans."
Treatment focuses on an individual's medical problems, with all the unique characteristics that shape the person. Prevention focuses on entire populations and improvement of their average conditions. The medical and public health models differ. Physicians dealing with a patient follow the rule of "do no harm", whereas public health doctors hope to "do some good."
The Sodium Hypothesis. In the late 1950s, the difference between treatment and prevention of high blood pressure became blurred. Lewis K. Dahl, M.D. promoted the hypothesis that there was a direct correlation between sodium intake of populations and hypertensive incidence.
Dahl's sodium hypothesis was viewed by critics as being "packaged as a panacea." A few strategically placed advocates popularized the hypothesis. Over time, and with endless repetition, the hypothesis gradually was viewed as gospel.
There were skeptics. In a 1979 report, the National Institutes of Health Hypertension Task Force noted that the brevity of the section on prevention"is indicative of the lack of knowledge concerning basic mechanisms of hypertension. Research must supply new knowledge before confident statements concerning prevention can be made."
John H. Larach, M.D., a prominent hypertension researcher, commented in 1983 on the popular anti-sodium policy:
"Now, what can I possibly have against these well-intended efforts? Nothing except the fact that they are not supported by scientific evidence. They are based on assumptions that are either entirely false or entirely unproven. Let us review some of these. First assumption: Everyone who has high blood pressure should cut back on salt to bring the pressure down. This is wrong...... Second assumption: Hypertension can be prevented in normal people if they cut down on their salt intake while they're still healthy.
This theory sounds good and conforms to the attractive idea of preventing disease by changing our diets and life-styles. The trouble is, there is not a shred of evidence to support it where high blood pressure is concerned. Not even a badly designed, poorly executed scientific study.
In 1984, a group of 13 scientists wrote on the subject in The Lancet:: "The usual scientific standards for weighing evidence and for giving advice which are now well established in drug development and prescribing seemed to have been forgotten in an evangelical crusade to present a simplistic view of the evidence which will prove attractive to the media."
Larach, joined by Michael H. Alderman, M.D. assessed the impact of sodium intake on cardiovascular health among healthy people over the course of eight years. In 1991 they reported their finding. People on low-sodium diets had dramatically higher numbers of heart attacks.
Another skeptic of the sodium hypothesis was David A McCarron, M.D. at the Oregon Health Sciences University. He argued that governmental concern about high-sodium diets was misplaced. Not an excess of nutrients such as sodium is the problem, but rather a deficiency of nutrients, especially calcium, is responsible for hypertension.
McCarron's "calcium hypothesis" reflected a renewed interest in the interaction of electrolytes-- electronically charged particles that play an important role in regulating body processes--mainly the interrelationships of sodium with calcium and potassium. Numerous articles in medical journals noted that calcium and potassium deficiencies were implicated in sodium's blood pressure effects. Some studies found them to be even more important than sodium.
Researchers began to question, too, the lack of proven safety for universal sodium restriction. Studies began to identify unanticipated risks of low-sodium diets, resulting in elevated blood pressure in some individuals, and increases in serum creatinine (a waste product from a substance found in muscles, blood, and urine). Also,there was a rise in undesirable low-density lipoprotein cholesterol, uric acid and significantly higher fasting insulin levels. All of these features are disease risk factors.
In addition, low-sodium diets might lead to a reduced capacity to absorb other nutrients and a lowered resistance to problems such as diarrhea, hyperthermia, and bleeding. Low sodium diets also seem to be related to sleep disturbances.
By 1986, INTERSALT researchers had examined numerous population studies purported to link sodium and hypertension. The studies encompassed more than 10,000 individuals, at 52 centers, in 32 countries. Most of the studies, when evaluated, were found to be flawed, and were discarded. The number of quality studies was reduced to 13, of which 10 failed to demonstrate any sodium-hypertension association. The results of the evaluation were summarized succinctly in the British Medical Journal: "Salt has only small importance in hypertension."
Thomas J. Moore, a medical writer, wrote that the INTERSALT results were "as clean an outright refutation as can be found in science, yet the findings of the INTERSALT study passed virtually unnoticed in the media and scientific journals in the United States."
According to Moore, John Larosa, then head of the American Heart Association's Nutrition Committee, a group which regularly endorsed sodium restriction, admitted that " we're trying to figure out how to back away from the salt recommendation without looking like fools."
William Ira Bennett, M.D., editor of the Harvard medical School Health letter, explained that the deafening silence by officials was because they had invested their credibility in promoting the sodium hypothesis. Bennett wrote that"little was said about the INTERSALT study because it was a kind of humiliation when you have a nutrition recommendation that you have to abandon."
Despite the lack of any confirmation of the sodium hypothesis from the INTERSALT study, federal officials continue to retain the recommendation that everyone should reduce dietary sodium. The 1988 Surgeon General's Report admitted that whether universal sodium restriction would lower population blood pressure or not had never been tested.
Recognizing that the public policy was at odds with scientific findings, the National Heart, Lung, and Blood Institute convened a Salt and High Blood Pressure Workshop in 1989. The experts could reach no consensus.
The leaders of the INTERSALT project tightly controlled the release of analyses of the data base for publication. They used meta-analysis, a technique of compiling all previous studies to gain the statistical power of large numbers of observations. However, the poor quality of many of the early studies, as already noted, was ignored, and the meta-analysis by sheer numbers was used to confirm the sodium hypothesis.
The advice for hypertensives to decrease sodium intake remains sound. However, the same advice for the general public lacks a scientific basis. There is no proof, to date, that excess sodium intake will prevent hypertension from developing.
Even when findings are positive about sodium intake, the firmly entrenched sodium hypothesis overrides other considerations. In recent studies with the elderly, sodium intake had a small beneficial effect on bones (the ultra distal radius and total hip) in men. Nevertheless, the researchers felt obliged to caution that "there are many overriding public health reasons not to increase sodium intake."
Support of the sodium hypothesis is based on population studies, which ignore the confounding variables that may determine sodium's role in hypertension. Precisely how sodium influences blood pressure is not yet firmly established.
Many Contributing Factors
There are many determinants of hypertension. Sodium appears to be only a minor player in a highly complex field. There are environmental factors of geography, location, temperature, and poisoning from heavy metals, such as lead and cadmium.
For example, cadmium, a toxic metal, is an important contributing cause of hypertension. With age, cadmium accumulates in the body, especially in the kidneys, from contamination of this heavy metal in the environment. Cadmium in food results mainly from food processing and refining; in drinking water, from areas of "soft" water lacking in minerals such as calcium and magnesium, as well as from water piping; and in air, from industrial pollutants. Cadmium's role in hypertension can be stopped if the body's zinc supply is adequate. Unfortunately, many Americans are low in zinc.
There are lifestyle factors of obesity, lack of exercise, mental stress, smoking, alcohol, coffee and tea. Hypertension is far more common among overweight adults than among those with normal weight. Studies have shown that weight loss can reduce blood pressure significantly in obese adults. Heavy drinking is known to increase hypertensive risks. Even moderate drinking may be a risk factor, according to the findings of Jacqueline Witteman and colleagues at Harvard University. They found that women who consume two mixed alcoholic drinks daily may be 40% more likely than others to develop hypertension. Milk drinkers may lower this risk, possibly due to the calcium and other protective nutrients in the milk.
There are factors of genetics, race, gender, hormones and age. A hormone has been identified and studied that is believed to be related to hypertension development. A sodium-pump inhibiting hormone appears to slow the activity of a protein that moves sodium out of the cells, according to Mordecai P. Blaustein, M.D. and John Hamlyn, Ph.D. at the Maryland School of Medicine.
There are nutritional effects of certain dietary components, and potable water quality. Studies that examine only sodium or any other single dietary component as a factor in inducing hypertension give too limited a view. Many components may be interrelated. Also, not all sodium compounds affect blood pressure as does sodium chloride (table salt). Nor do we eat sodium, per se, but rather as sodium compounds in foods.
Nutritional Factors. Hypertension is associated with certain nutritional deficiencies, especially with low intake of specific minerals, vitamins, proteins, fatty acids, carbohydrates, and calories. Excessive sodium intake is related to some of these nutrients.
Dr. McCarron and his colleagues suggest that nutritional deficiencies, not excesses, distinguish hypertensive and overweight Americans in studies, individuals on low-sodium diets with low intake of dairy products were at two to three times greater hypertensive risk than those with high intake of dairy products. McCarron concluded that the standard weight-reduction diets actually may exacerbate conditions that lead to hypertension by further reducing nutrients that are essential to maintain normal blood pressure. By recommending sodium reduction, McCarron said, "we're setting up the dietetic community for failure."
Many Americans do not get enough calcium. McCarron believes that a lack of adequate calcium may be as important a factor in hypertension as is excessive sodium and that sodium-sensitive individuals may benefit the most by increasing calcium intake.
The long held belief that sodium is the sole salt component responsible for increasing blood pressure has been challenged. Studies suggested that the chloride component in sodium chloride (table salt) might also be a factor. In rat studies, blood pressure increased far more following ingestion of sodium chloride than with other sodium-containing compounds. Chloride might enhance sodium's effects on blood pressure.
Although table salt may increase blood pressure in hypertensives, many other sodium-containing compounds may not. In a study conducted by Dr. Theodore W. Kurtz and his colleagues at the General Clinical Research Center, University of California, men with high blood pressure were given table salt supplements for a week. As anticipated, their blood pressure rose sharply. But, when they received the same amount of sodium in other sodium-containing compounds, such as sodium citrate (a common additive in many foods and beverages) their blood pressure remained constant.
A clearer designation would be "sodium chloride-dependant hypertension" rather than "sodium-dependant hypertension."
Many Americans have diets low in magnesium. Burton M. Altura, M.D. at SUNY, Downtown Medical Center (Brooklyn) reported that low magnesium levels may be related to hypertension. A group of normal rats, fed a magnesium-deficient diet for 12 weeks, developed hypertension. The interior of the fine branches of their veins and arteries had constricted in size, which caused the blood pressure rise. The lower their intake of magnesium, the smaller their blood vessels became, and the more their blood pressure rose.
In human studies conducted in The Netherlands, 91 middle-aged and elderly women with untreated mild to moderate hypertension were given magnesium supplements at levels difficult to achieve solely by dietary changes. After 6 months, they showed beneficial blood pressure reduction.
Some segments of the American population may be severely magnesium depleted, including chronic alcoholics, and individuals taking diuretics-widely used prescription drugs. The diuretics, used by hypertensives to expel sodium, also expel magnesium. A Swedish study found patients given a magnesium supplement along with the diuretic avoided this problem.
Tin may be a factor, not yet well recognized, in hypertension. The animal model used most frequently used to study hypertension is a spontaneously hypertensive rat (SHR). In tests, a tin compound (stannous chloride) was found to keep blood pressure normal in the young SHR during a 14 week study, but had no similar beneficial effect on SHR adults. Selenium deficiency has been found to accelerate the development of hypertension in SHR.
In epidemiological studies, as well as in animal experiments, an adequate intake of high-quality protein food has been shown to be beneficial for sodium excretion, improvement of arterial walls, and lowering of blood pressure.
The type of fat in the diet may be related to hypertension. In a review of non-drug therapies for hypertension, reduction of saturated fat intake was recommended in the American Journal of Hypertension (February 1989). This dietary change causes a modest lowering of blood pressure, as well as counteracting the cholesterol-raising effect of some commonly used hypertensive drugs. Vegetarians and others whose fat intake consist mainly of polyunsaturated fats have lower blood pressure levels than those whose fat intake consists mainly of saturated fats.
The American diet is low in omega-3 fatty acids, found in fish and in fish oil supplements. Increased fish consumption may reduce the risk of pregnancy-induced hypertension. Results have been inconsistent with many studies using a high fish diet or fish oil supplements to reduce high blood pressure. However, data from studies of more than 1,300 subjects, analyzed by scientists under the auspices of the national Institute of Environmental Health Science of the National Institutes of Health, suggested overwhelmingly that fish oil lowered blood pressure moderately in the majority of hypertensive subjects. Generally larger amounts of fish oil produced greater declines in blood pressure than did smaller amounts. Very low supplemental dosages had virtually no effect. Nor did it produce changes in the blood pressure level of healthy subjects. The effects of fish oils, however, might be harmful for hypertensives with impaired kidney function or poor blood clotting ability.
Sugar is a food component that, at high intake, is known to enhance the increase of blood pressure caused by salt in sodium-sensitive rats. In a study involving monkeys, larger amounts of sugar as well as salt in the diet, induced high blood pressure. The animals fed a diet containing 3% salt and 38% sugar developed higher blood pressure than those on a high salt, but sugarless, diet. Both groups developed higher blood pressure than animals fed their normal monkey chow. The study demonstrated that a diet high in both sugar and salt--much like a typical American diet-- also could raise the cholesterol level in the animals' blood.
Deficiencies of certain nutrients and food components may be additional factors in hypertension. These constituents include some vitamins (A, B3, C, and biflavonoids);certain amino acids (tyrosine and tryptophan); and inadequate intake of water and dietary fibers. Food allergy, especially gluten sensitivity to certain grains (wheat, rye, oat and barley) has been suggested by Lloyd Rosenvold, M.D. of Loma Linda University Medical School as an unrecognized factor in some cases of hypertension. There may be other nutritional factors, as yet unrecognized, that play a role in hypertension.
Continuing A misguided Policy?
The national High Blood pressure education Program Coordinating Committee met late in 1994 to formulate "prevention" strategies in the national campaign against hypertension. Some participants raised doubts about the initiative. Mary C. Winston of the American Heart Association noted the mounting opposition, "by a lot of good scientists," to sodium restriction as a preventative measure.
At the committee meeting, H. Mitchell Perry, Jr. of Washington University in St. Louis said, "I don't think the scientific evidence supports a public health campaign of this type."
James R. Sowers, M.D. of Wayne State University urged the committee to recognize that "we are not just making progress on salt." Sowers urged that more attention be given to the multiple risk factors involved in hypertension.
Despite such criticisms, the Coordinating Committee staff reported that an extensive media campaign is already under way.
In conclusion, the evidence suggests that for 90% of the population, with blood pressure within normal range, sodium intake does not cause hypertension. As with all nutrients, "moderation" is a key concept. Also, sodium intake must be balanced by intake of foods with adequate amounts of potassium, calcium, and other nutrients related to it. People are most likely to achieve both moderation and balance by selecting basic foods - fruits, vegetables,meat, fish, eggs, and dairy foods. Public health policy aiming at narrow dietary recommendations tend to obscure this sound advice. When the policy lacks scientific basis, it may actually undermine it.
The author, Beatrice Trum Hunter, MA, has written more than 30 books on food and environmental issues, frequently before widespread public awareness. She was food editor of Consumer's Research Magazine for more than two decades. She is an honorary member of The Price Pottenger Nutrition Foundation, as well as an honorary fellow of The International Academy of Preventative Medicine and an honorary member of The American Academy of Environmental Medicine. She has been the recipient of many awards, including The Jonathan Forman Award of The Society for Clinical Ecology, The New Hampshire Society for Preventative Dentistry, and The Donnon Pepper Humanitarian Award. She can be reached at 243 Falls Road, Deering, N.H. 03244