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Salt Toxicity: Is It A Major Threat To Public Health?

Good through December 2018.

By James J. Kenney, PhD, RD, FACN
Communicating Food for Health Newsletter April 1999-June 1999
3 CPE Hours as approved by the ADA, DMA, AAFCS

Salt is perhaps the oldest and most commonly used food additive. It improves the taste of many foods without adding calories. In larger amounts it also inhibits the growth of many microorganisms and has been used to preserve food throughout much of mans recorded history. So important was salt for preserving foods that it was often part of the pay Roman soldiers received - hence the word salary. Today, refrigeration, modern canning and other food processing techniques have made this once essential preservative role of salt largely superfluous. Most people have retained a taste for salt so its consumption has remained rather high. The average American consumes about 4,000 to 5,000 mg (174-217 mmol) of sodium per day or about 10 - 12.5 grams of salt. Ten grams of salt is about 2 teaspoons Sodium chloride is 40% sodium and 60% chloride by weight. In modern Westernized societies only about 10% of dietary salt comes naturally from the foods consumed. Another 15-25% comes from the salt shaker. About 75% of the salt in the typical Western diet comes from processed foods and meals eaten away from home [1].

What is the RDA or DV for Salt? Both sodium and chloride are essential nutrients for humans and all other animals. Nutrition researchers have known about the need for salt much longer than most other nutrients. Oddly enough there is no RDA for sodium or chloride although the 10th edition of the Recommended Dietary Allowances states "the minimum average requirement for adults ... [is]... 115 mg of Sodium...per day. In consideration of the wide variation of patterns of physical activity and climate exposure, a safe minimum intake might be set at 500 mg/day."[p. 253]. Researchers have estimated that the diet of early man contained about 600 mg of sodium on average [2].

The American Heart Association, the National Heart Lung and Blood Institute, the U.S. Dietary Guidelines, and most other public health organizations have recommended reducing dietary sodium intake to less than 2400 or less than 2,000 mg/d. It is clear that human beings evolved consuming far less salt than is customary in modern industrial countries. There is little doubt that nearly all Americans are consuming far more salt than their bodies need but whether or not this causes health problems seems to be a matter of scientific debate. So would most Americans be better off if they consumed a lot less salt as most public health organizations suggests? Not if you believe the Salt Institute.

The Salt Institute has long maintained that "Healthy persons with normal blood pressure have no problems with sodium or salt intake" [3]. If you listen to the Salt Institute it is easy to come away with the impression that only about 1/3 to 1/2 of those who already have hypertension (HTN) need cut back on dietary salt because they are "salt sensitive". They argue that since 75% of the U.S. population does not have HTN (currently defined as a blood pressure (BP) of more than 140/90 mmHg) only a small minority of Americans should be concerned about their salt intake. Of course, largely those who profit directly or indirectly from the use of excessive dietary salt fund the Salt Institute.

Is the Salt Institute a reliable source of information about salt? The now defunct Tobacco Institute was hardly a credible source for the health problems caused by cigarette smoking because they had an obvious conflict of interests. Over time even the news media (which seems wedded to the notion that there are two sides to every issue) came to dismiss the veracity of claims coming from the Tobacco Institute and this is what eventually doomed that institution. However, the Salt Institutes press releases and pronouncements about the safety of dietary salt or even the dangers of too little salt often escape much critical commentary in the news media. At best, the news media will present the Salt Institutes position as if it warrants as much credibility as that of scientific researchers. Given the economic incentives of those that support and speak on behalf of the Salt Institute it would be wise to take everything they say with a grain of salt.

Those interested in how the Salt Institute attempts to distort and misinterpret scientific data in an obvious attempt to conceal the harm caused by excessive dietary salt may want to review an article written by Richard L. Hanneman (president of the Salt Institute) and the critical commentaries that follow it [4]. The Salt Institute may be losing the scientific debate about the role of salt in promoting HTN and other health problems but it is still winning the public relations battle in the media. A recent survey found that only about 10% of Americans are concerned about their salt intake.

Mr. Hanneman, whose academic training consists of a bachelors degree in history/ government and a masters degree in history has testified as an expert on salt before the FDA, HHSs Nutrition Policy Board, and the USDAs Human Nutrition Subcommittee. He claims that the "evidence now shows clearly that only a small minority of the population really benefits from restricting salt [5]. Lets review some of the evidence that perhaps Mr. Hanneman may have overlooked or perhaps (given his academic training) may have misinterpreted. We will start with some of the basic research.

Does Dietary Salt Cause HTN in Animals? It was shown long ago that increasing dietary salt causes a progressive rise in blood pressure (BP) in rats [6]. Rats fed a diet with only 0.15% salt (dry weight of food) live significantly longer than rats fed greater amounts of dietary salt. The average Americans diet is about 2.5% salt on a dry weight basis. A diet with 0.15% salt would provide an average man consuming 2500 kcal with about 300 mg of sodium/day or about 750 mg of NaCl/day.

Chimpanzees in the wild consume a diet not dissimilar to that of our ancient ancestors. Of all animals, chimpanzees are genetically the closest to human beings. A study of a colony of chimpanzees found that the progressive addition of salt to their largely natural diet resulted in a gradual rise in their BP over 20 months. The amount of salt in the chimps diets was similar to that found in a typical American diet. This significant rise in BP was then completely reversed within 6 months after being returned to their more natural diet [7]. The evidence in animals is conclusive that simply increasing dietary salt is sufficient to cause increased BP and decreased life expectancy in virtually all mammals studied. Of course, animal studies alone cannot prove that excessive dietary salt is the primary cause of essential hypertension (HTN) in humans.

The Case Against Adding Salt to the Diet The most compelling reason for encouraging people to consume less salt is its probable role in the etiology of essential HTN (a.k.a. primary HTN). The vast majority of the scientific evidence indites excess dietary salt as the single most important factor contributing to the development of HTN. For example, when Dr. Malcolm Law was interviewed about a comprehensive review article he had recently published linking excess dietary salt with the development of HTN, he stated, "the effect of universal moderate dietary salt reduction on mortality from stroke and ischaemic heart disease would be substantial - larger, indeed, than could be achieved by fully implementing recommended policy for treating high blood pressure with drugs." Dr. Law also claimed that if salt in processed foods was moderately reduced this could "prevent some 70,000 deaths a year in Britain as well as much disability [8]. This estimate was based on only a 50 mmol (or about 1,150mg of sodium per day) reduction in daily salt intake [9].

According to Dr. Law, "Everyone should reduce their salt intake by at least 3 grams a day." He estimated that this would result in about 250,000 fewer deaths each year in the United States. Dr. Laws predictions were confirmed in a study of older people in Britain whose salt intake was cut by about 80 mmol and the fall in their BP was similar to that achieved by thiazide diuretics [10]. But would even greater reductions in salt intake be safe and more effective for preventing the rise in BP with age that occurs in all modern industrial societies?

HTN Afflicts Most Americans Sooner or Later Even though the Salt Institute likes to point out that only about 1 in four American adults has HTN, the fact is that most people will develop essential HTN in their lifetime and more than half of adult Americans have a BP > 120/80 mmHg [11]. HTN is usually due to increased peripheral resistance to the flow of blood. This resistance to the flow of blood is similar to what would happen if one was to stand on or squeeze the end of a garden hose creating backpressure. This resistance occurs primarily at the arteriole level. Table 1. below shows the prevalence of HTN in the U.S. for various age and gender groups.

Table 1. The Prevalence of HTN in Americans

  Men Women Men Women
Age %BP>140/90 %BP>140/90 %BP>150/100 %BP>150/100
18-24 13.3 2.5 2.5 0.6
25-34 17.0 6.3 5.1 2.3`
35-44 28.3 25.2 13.1 16.0
45-54 37.6 34.0 20.3 19.5
55-64 52.9 57.2 30.8 36.5


Table 2 The current medical classifications of BP:

Classification Diastolic BP (mmHg) Systolic BP (mmHg)
Normal <85 <130
High Normal 85-89 130-139
Stage 1 (mild) 90-99 140-159
Stage 2 (moderate) 100-109 160-179
Stage 3 (severe) 110-119 180-209
Stage 4 (very severe) 120 and over 210 and over
*optimal BP is less than 110/70 mmHG

By the age of 60y the majority of men and women in America have developed HTN and the vast majority of these have essential HTN [12]. The risk of HTN continues to increase with age. About 70% of women age 65-75y have developed HTN, and by age 65 almost 80% of black women have HTN [13]. But is this rise in BP primarily the result of excess salt or simply a normal part of growing older?

Population Studies Point to Excess Salt as the Main Cause of HTN Studies of human populations which add little or no salt to their food have found little or no rise in BP with age and a virtual absence of essential HTN [14]. For example, Kenyan farmers who consumed a diet with little or no added salt were found to have virtually no essential HTN [15]. However, when young Kenyan men joined the military and began consuming a diet with added salt, their BP started to rise and by the second year it was significantly higher. Kenyan farmers who migrated to urban areas (where the diet is more Westernized) were found to have had their BP rise. The elevation grew greater the longer they consumed the higher salt diet [16].

Figure 1 below shows that BP rises in populations that add significant amounts of salt to their food but changes little with age in populations that add little or no salt to their food.

Figure 1. The Relationship Between Systolic BP and Age in Various Populations:


This immunity to rising BP with age was true for Eskimos and Masai whose diets are high in fat and protein and low in carbohydrate. It was also true for the New Guinea Highlanders and Tarahumara Indians whose nearly vegetarian diets were both very high in carbohydrate [17] [18]. Given the wide ranges of climates, genetic diversity and extremely varied diet compositions among these populations it is hard to imagine what factor other than the lack of added salt could be protecting them from HTN. Clearly then the rise in BP in all Westernized populations cannot be simply a normal consequence of aging and it appears that excessive dietary salt may play an important role in the development of HTN.

Could Stress and Noise Be More Important than Salt in the Etiology of HTN? Claims that a stressful environment with a lot of noise, rather than added dietary salt, is primarily responsible for the rise in BP with age in modern industrial societies conflict with the fact the Qash qai pastoral nomads in Iran experience a marked rise in BP with age despite a fairly peaceful and quiet environment and a lifestyle that has changed little in the past 500 years [19]. However, unlike most other unacculturated populations the Quashqai nomads do add salt to their food. It also conflicts with observational studies in the Solomon Islands. The fairly unacculturated Lau tribe, who cook their food in sea water had a high incidence of HTN despite a fairly tranquil existence in the South Pacific [20]. Another Solomon Island tribe with a similar lifestyle except for using fresh water to cook their food instead of sea water does not develop HTN or experience a rise in BP with age.

Could weight gain be more important than excess salt in causing HTN? Claims that the rise in BP in Americans is due primarily to weight gain rather than excess salt intake conflict with studies of the Japanese. The Japanese diet is considerably higher in salt than that of Americans but their body weight is fairly stable throughout adult life and obesity is very uncommon in Japan. Nevertheless, the Japanese experience an even greater rise in BP with age than do Americans who, on average, gain much more weight with age [21].

By contrast, many Kuna Indians of Panama who were moderately obese but ate a diet that was low in salt have a very low incidence of HTN. In this population less than 1% of adults had HTN and BP did not rise significantly with age [22]. Today, many Kuna Indians have adopted a more Westernized diet higher in salt and now experience a significant rise in BP with age. However, among Kuna Indians the incidence of HTN still remains lower than that seen in populations who have consumed a high-salt diet throughout life [23].

There are two ways to increase the pressure of water in a garden hose. One is to increase the flow of water through the hose and the second way is to squeeze the end of the hose creating backpressure. Obesity raises BP in part due to an increase in cardiac output, which means the heart is pumping a greater volume of blood. In the long run, dietary salt creates a rise in BP primarily by causing constriction of the arterioles, which then resist the flow of blood and create backpressure. Essential HTN is usually characterized primarily by this backpressure which is also called peripheral resistance. This means that if an obese person and a lean person have the same BP, the lean person will generally have more peripheral resistance. Since increased peripheral resistance may reduce the flow of blood at the capillary level it may be more damaging to the body. This may be one reason why lean HTN subjects were found to have a higher risk of dying from cardiovascular disease than obese individuals with the same BP [24].

The point here is not that obesity has no effect on BP or health. Weight gain causes an increase in cardiac output and this is like turning up the spigot of a garden house which increases water pressure in the house. Obesity, particularly central adiposity, is associated with the development of HTN [25][26]. Both salt restriction and weight loss independently lower BP in individuals with borderline HTN [27]. When obese native Hawaiians were placed on a very-low- fat, low-sodium diet, similar to what their ancestors consumed, they lost 17lbs and reduced both SBP and DBP by more than 10% in just 21 days [28].

Weight gain, especially intra-abdominal fat, leads to insulin resistance and increased serum insulin levels [29]. Higher insulin levels have been shown to make it more difficult for the human kidney to get rid of excess salt [30]. Regular aerobic exercise is also helpful in lowering BP in HTN patients [31]. This should not be surprising since aerobic exercise promotes weight loss, reduces insulin resistance and lowers serum insulin levels. In addition, with sweating some excess salt is excreted by the sweat glands which reduces the nutritional stress on the kidney to rid the body of excessive salt.

Too Much Salt Appears to Be The #1 Cause of Essential HTN. We have seen that excessive salt intake is the only viable explanation for the rise in BP with age that occurs in all populations that add significant amounts of salt to food. Obesity and excessive alcohol consumption can certainly raise BP, but their effect is more modest compared to that of too much salt. Other factors, including stress and a noisy environment, may temporarily raise BP but there is little reason to believe they play a major role in the rise in BP with age seen in all populations that add salt to their food.

Epidemiological studies clearly indicate that reducing dietary salt to less than about 30 mEq [or about 700mg of sodium from salt] would virtually eliminate essential HTN in any population [32]. Indeed, when comparing populations that add salt to their food to population that do not add salt, the average difference in systolic blood pressure is about 50 mmHg in people above age 60y [33]. See also Figure 1.

Short-term Clinical Trials Miss Long-Term Effects This huge difference (about 50mmHg) in the average SBP of populations consuming very little salt compared to populations consuming a high-salt diet takes 5-6 decades to appear. It is much greater than the modest drop in SBP observed in most short-term clinical trials even in those few in which very large differences in dietary salt intake were achieved. Nevertheless, the authors of two recent reviews using a meta-analysis of just such short-term studies concluded that the very small drops in BP observed in clinical trials in normotensive persons on reduced sodium diets "does not justify a general recommendation for reduced sodium intake"[34]. The Salt Institute, as you may have guessed, made sure the media focused on this conclusion.

The second and similar meta-analysis of short-term clinical trials of reduced sodium intake funded by an "unrestricted grant" from the Campbell Soup company (perhaps not surprisingly) also concluded that the evidence does not support current recommendations for sodium restriction in people without HTN [35]. It may not be too cynical to suggest that it was not just a coincidence that these two questionable review articles appeared in JAMA, a journal that carries many ads for anti-HTN meds. However, despite these shortsighted and limited reviews, the bulk of the scientific evidence suggests that it takes many years to see the full hypertensive effects of excess dietary salt.

It is likely that it takes many years for excessive dietary salt to do its damage. Some of these adverse effects may be only partially reversible and/or may take many years on a very low-salt diet to reverse. Of course, most clinical trials do not reduce dietary sodium to less than 30 mEq or even 70 mEq (about 1600 mg Na) per day. Neither of these highly publicized reviews looked at the big picture. In a sense, these reviewers could not see the forest through the trees. Let us now examine some of the evidence these reviewers overlooked that suggest that waiting for HTN to develop before reducing salt intake may be courting disaster.

If BP is "normal" why not wait for HTN to develop before reducing salt intake? The Salt Institute would have people believe that if their doctor hasnt told them they have HTN then the amount of dietary salt they consume is of no consequence. Most people and many clinicians subscribe to this position and assume the only way too much salt can harm the body is by causing HTN. There are three problems with this "theory". First, the risk of dying from an increase in BP does not begin with the diagnosis of HTN and a BP > 140/90 mmHg. Figure 2 shows that people are more likely to die the higher the BP goes and that this increased death rate begins well below a DBP of 90 mmHg. It is estimated that 1/3 of cardiovascular disease that results from increased BP occurs within the "normal" range of BP [36].

Figure 2 below shows the relationship of the risk of premature death with increasing diastolic blood pressure.

Figure 2 - The risk of premature death with increasing diastolic blood pressure:

HTN, Like Atherosclerosis, May Begin Early in Life A second reason not to wait for HTN to develop is that HTN, like atherosclerosis, may begin early in life and may do serious harm before any symptoms show up. Pregnant rats fed a higher salt diet have offspring with higher BP [37]. Human infants, unlike adults, do not appear to have a taste for salt [38]. Nevertheless, baby food manufacturers had for many years routinely added salt to baby foods (to please their mothers palate). Human milk, despite the high-salt intake of most mothers is surprisingly low in sodium (only 39 mg/cup) having only about 1/3 the sodium content of cows milk (122 mg/cup).

The results from a double-blind controlled study of newborn human infants suggest that BP responds to the amount of salt in the diet. Half the infants were fed a formula diet containing the amount of sodium (and potassium) found in cows milk, the other half were fed a similar formula with the amount of sodium and potassium reduced to the level found in human breast milk. The researchers found that after 6 months, the average BP of the infants fed the higher sodium formula was already significantly higher than that of those fed the lower sodium formula [39]. The rise in BP in the infants fed the higher sodium formula did not occur in the first few weeks but just increased gradually and became significant after several months. This type of evidence has led pediatricians to conclude that the requirement for sodium in human infants is less than 9 mEq/day or no more than about 200 mg daily [40].

The Harm From Excess Salt May Not Be Due Entirely To Increased BP A third reason* to be concerned about excessive dietary salt, even in people with "normal" BP, is that HTN may simply be a symptom of more serious underlying adverse biochemical and physiological changes. Rats, like people vary in their susceptibility to develop HTN in response to a high-salt diet. Indeed, rats have been bred to be especially "salt sensitive". Other strains of rats (like some people) are more resistant to the BP raising effects of a high-salt diet. A study compared the effects of a moderate (1%) or high (8%) salt diet in genetically "salt sensitive" and "normotensive" rats. On the high-salt diet, even the "normotensive" rats showed widespread fibrosis in their hearts, kidneys and arterioles compared to the "salt sensitive" rats fed the moderate salt diet even though the BP of the "normotensive" rats was much lower. The authors "suggest that excessive salt intake may be an important direct pathogenic factor for cardiovascular disease" [41]. These results suggest that an excessive salt intake promotes the overgrowth of fibrous tissue in the arteries, arterioles and other tissues and this fibrosis gradually over time makes the blood vessels increasingly stiff and eventually makes them more resistant to the flow of blood. In "salt-resistant" individuals this damage may have to become more severe before BP rises to the point where HTN is diagnosed.

*Note: There are other reasons for people without HTN to avoid excessive dietary salt, the most serious of which are stomach cancer, osteoporosis, and kidney stones. These will be the subjects of future articles.

Why do low-salt diets often fail to sufficiently lower BP? Some doctors are led to believe salt is not a major cause of HTN based on their clinical experience. When doctors encourage their patients to reduce dietary salt they often find that most of their patients experience little or no drop in BP. Of course, most patients who are told by their doctors to reduce salt intake do not actually reduce their salt intake very much because many high-salt foods do not taste particularly salty and they are not given sufficient dietary counseling to achieve a significant drop in salt intake. For example, bread has about double, and corn flakes about triple the salt content of potato chips [on a Na/kcal basis] but most people would guess that the chips are higher in salt than the bread or cereal. In addition, since no more 15 to 25% of the salt in a typical patients diet is added at home, even patients who try hard to comply often are not successful in cutting salt intake by even 30%. This type of modest reduction in salt intake alone is generally not enough to have much effect on BP over a period of just a few weeks.

However, some primary HTN patients will not see their BP return to normal even if a low-salt diet is achieved and in a few BP does not fall at all. Nevertheless, it would be a mistake to assume that just because salt reduction doesnt always reverse HTN that it didnt cause it in the first place. Afterall, do doctors assume smoking didnt cause enphysema because it doesnt go away when patients stop smoking? It would also be a mistake to assume that if BP does not fall that a low sodium (high potassium) diet is of no clinical value. Studies in animals have shown that some rats remain hypertensive even after their salt intake is reduced to a low level while their littermates, which were continually fed the same low-salt diet for life never develop HTN [42].

Even though HTN often takes decades to develop, many clinicians expect to see complete reversal of HTN in a week or two on a low-salt diet. In fact, in patients with severe or malignant HTN, restricting salt to very low levels has been shown to cause a substantial fall in BP in most patients [43] [44]. At the Pritikin Longevity Center, it was shown that even more modest restriction of sodium intake to less than 1600 mg per day lowers BP in most HTN people within about 4 weeks if other diet and lifestyle changes are also made [45]. There are other reasons the Pritikin Program lowers BP besides the low salt content of the diet and these will be discussed later on.

Unfortunately, the long-term effects of a low-salt diet have received little attention. After an initial drop in BP that can be fairly large in some individuals, the fall in BP often continues for many months or years, provided the salt restriction is maintained. For example, one group of researchers found that BP was still declining after two years on a diet with about 70 mEq (1600 mg of sodium)[46]. Given that the BP raising effects of excessive dietary salt take years to develop it is curious that more long-term clinical trials have not taken place.

Excess salt may be the real culprit: HTN may just be a symptom. There is growing evidence that HTN is merely a symptom of an underlying nutritional imbalance caused largely by an excessive intake of salt. Salt intake was found to correlate more closely with left ventricular hypertrophy (LVH), cerebrovasular disease, microproteinuria (an early sign of kidney disease), and reduced arterial compliance than BP. A recent review found that "there is clinical and experimental evidence... that salt intake directly affects hypertensive renal disease, cerebrovascular disease, and compliance of the large arteries. The close and partially independent correlation between salt intake and hypertensive target organ disease suggests dietary sodium to be a direct perpetrator of cardiovascular disease." [47]

In simple terms this means that excessive salt intake is damaging the heart, brain, kidneys and arteries directly and a symptom of this damage that doctors can easily measure is higher BP. However, the absence of one symptom of a disease does not mean that the disease is absent - it may only mean that it is not being diagnosed because doctors are mistaking a symptom (high BP) for the underlying disease (salt toxicity) and assuming that as long as the symptom is not present there is no disease. This would be like assuming a patient has no atherosclerosis if they have not had a heart attack, stroke or developed angina. This also means that drugs, which are primarily designed to treat a symptom (in this case HTN) may be far less effective at correcting the real disease than a healthier diet and lifestyle. This is because essential HTN increasingly appears to be the result of a nutritional imbalance.

A high intake of dietary salt was shown to increase the cardiac preload to the left venticule even without increasing BP in normotensive subjects [48]. Over time this increased workload on the heart may lead to LVH. Other researchers examining people with HTN and LVH were able to "identify dietary salt as a strong determinant of cardiac structural adaptation to a persistent increase in arterial pressure." These authors went on to say that "a high salt intake might aggravate and, conversely, dietary salt restriction might prevent (or at least mitigate) the development of left ventricular hypertrophy in patients with essential hypertension." [49]

When researchers put 91 men and women with HTN and LVH on either a moderately low-sodium diet [the goal was 70 mmol Na/d or less] or "normal"-sodium diet for one year, they found a significant reduction in LVH on the low-sodium diet and concluded "that long-term non-pharmacological treatment with moderate sodium restriction decreases LVH" [50]. Since the sodium restriction achieved was closer to 2200 to 2500 mg sodium/d it is likely that even more dramatic reduction in LVH would have occurred if their therapeutic goal had been achieved.

The difference between the systolic and diastolic BP is known as the pulse pressure. In all populations that add significant salt to their diets the pulse pressure tends to increase with age. Over 2500 years ago a Chinese doctor described a hardening of the pulses as a symptom of too much salt in the diet. Today, an increased pulse pressure is an established risk factor for congestive heart failure (CHF)[51]. CHF is the only serious cardiovascular disease that has been increasing in America and is currently the leading hospital diagnosis in those over the age of 65y [51a].

Since this increase in pulse pressure does not occur in populations that add little or no salt to their diet it seems likely that increasing arterial stiffness with age is not a natural part of the aging process. Indeed, when normotensive people were maintained on a low-salt diet (average of 44 mmol Na/d or about 1000 mg/d) for an average 24.8 months they experienced a 22% reduction in arterial stiffness in the experimental group. There was no change in arterial distensibility in age-matched controls who maintained their normal diet. The authors of this study conclude, "This is prima facie evidence that reduced salt intake has a beneficial effect in improving distensibility of the central aorta and large peripheral arteries, which is independent of its antihypertensive action" [52].

The evidence continues to mount implicating a diet high in salt with changes in the cardiovascular system that lead LVH and CHF, kidney damage, and arterial and arteriole damage that can lead to HTN. But even in the absence of HTN, a high-salt and low potassium diet appears to increase risk of CHD and both hemorrhagic and ischemic strokes. In-creasingly, HTN appears to be more a symptom of salt toxicity than the direct cause of these associated serious medical problems.

Other electrolytes besides sodium affect BP and vascular disease Not only did the human Paleolithic diet have only about 1/5 to 1/10 as much salt (NaCl) as the typical American diet, but it was also about 2-3 times higher in potassium (K), calcium (Ca) and magnesium (Mg)[53]. The ratio of K/Na was probably at least 10 to 1 in our ancient ancestors diet but only about 0.6 to 1 in the typical American diet today. In rats, it has been shown that increasing K reduces deaths, cerebrovascular disease and increases life expectancy independently of its effects on BP [54].

Even though the ratio of salt to potassium in the diet is very important, one should not conclude that the absolute amount of salt is irrelevant. In animals, it was shown that increasing the amount of both sodium and chloride 3-fold resulted in a substantial 15-20 mmHg rise in BP [55]. Recall also the 6 month study of human infants in which BP rose significantly where with both Na and K increased. In patients with essential HTN a low dietary K intake results in sodium retention and increases Ca excretion which exacerbates HTN [56].

Yi farmers from southeast China have a low average BP and experience only a modest rise in BP with age despite a moderate salt intake. Like the Kenyan farmers discussed earlier, the Yi farmers also experience a rise in BP when they migrate to urban centers for work. But unlike the Kenyan farmers, the Yi farmers do add a modest amount of salt to their food in their rural setting. However, the Yi farmers diet is exceptionally high in K (even for a relatively unacculturated population) and part of the reason their BP starts to rise when they migrate to the cities appears to due as much to the decrease in K, as it is the increased NaCl. Based on the amounts and ratio of K/Na in their urine the researchers concluded that the rise in BP was due as much to decreased K (and perhaps also Mg) as it was to increased salt [57].

Epidemiological evidence has found a decreased risk of stroke in US men who consume diets higher in K, Mg and fiber [58]. Studies of vegetarians have often found that they have lower BP than non-vegetarians and attribute this, at least in part, to their higher K intake [59]. Other epidemiological studies have found that men who eat more fruits and vegetable have fewer strokes [60].

Simply substituting a mixture of NaCl plus salts of K and Mg for regular table salt for 24 week was found to lower the BP in a group of older HTN patients by 7.6/3.3 mmHg [61]. The now famous DASH study found that a low-fat diet with more fruits and vegetables and low-fat dairy products can "substantially lower blood pressure" even though dietary salt intake was a modest 7.5 g/d (or 3000mg of Na or 128 mmol). The authors concluded that "this diet offers an additional nutritional approach to preventing and treating hypertension." [62]

The recent TONE study demonstrated that reducing salt and weight loss are clearly a safe and effective treatment for HTN in older people [63]. It now appears that a low-salt diet coupled with plenty of fruits, vegetables, whole grains, and nonfat dairy products and perhaps a little fish is best for treating and preventing essential HTN because it promotes weight loss without hunger and increases the ratio of K, Ca and Mg to Na and this is more consistent with the nutritional needs of man.

Does Dietary Fat Influence Blood Pressure? There is some evidence that an increase in omega 3 fatty acids may have small hypotensive effect [64] [65]. There is also some evidence that very large changes in the ratio of polyunsaturated to saturated fat may also have a modest tendency to lower BP [66]. But suggestions that dietary fat or the type of dietary fat are more important than dietary salt and/or the ratio of salt to potassium in the diet are not supported by credible research.

Epidemiological studies have linked increased total fat and saturated fat intake with an increased incidence of HTN. These studies are usually confounded by the tendency for dietary fat and saturated fat intake to rise in conjunction with increased dietary salt and body weight as populations come to rely more on manufactured foods and animal products. One exception to this may prove instructive. In the Samoan Islands, saturated fat intake has actually dropped precipitously (from 30% to 16% of calories) as their diet has become more Westernized, due largely to a reduction in coconuts. However, their sodium intake increased by about 1/3 (from 622 mg to 884 mg/1000 kcal) and the ratio of K/Na was cut nearly in half (from 2.5 to 1.3) as the Somoan diet Westernized and these are more typical changes associated with a more modern diet. Despite the much higher total fat (46% vs 36%) and saturated fat intake in Western Samoa compared to American Somoa (the latter is more Westernized), the incidence of HTN (defined as SBP>160mmHg or DBP>95mmHg or on anti-HTN meds) was 44% and 32% for men and women, respectively in American Somoa and only 17% and 15% for men and women in the less acculturated Western Somoa [67].

These data strongly suggests that the effect of dietary salt and potassium are far more important in the etiology of HTN than are the percent fat or saturated fat content of the diet. However, there may be some benefit in including one or two servings of a high omega-3 fatty acid fish each week in the diet of HTN patients. More research is needed to establish the ideal ratio of Na, K, Ca, and Mg for treating and preventing HTN. A reasonable target for the ratio of K/Na would be at least 4 or 5 with a sodium intake (from salt) of no more than 1200 to 1600 mg daily. The current RDIs for Ca and Mg are reasonable targets.

What affect do alcohol and smoking have on BP? One or two drinks a day have little effect on BP. Alcohol in excess of two drinks a day tends to increase cardiac output, which mainly increases SBP [68]. When alcohol consumption is discontinued, the drop in SBP can take at most several weeks to be complete. Unlike excessive dietary salt, alcohol does not increase peripheral resistance (the hallmark of essential HTN) and its effects are more easily reversed so it is unlikely to play a significant causal role in the development of essential HTN. Alcohols effects on BP are generally greater in older people whose arterioles and arteries are less pliant due (at least in part) to chronic overconsumption of excess salt and/or too little dietary potassium. The Tarahumara Indians of Northern Mexico have a fairly high consumption of alcohol and yet HTN is very uncommon - no doubt due largely to the low salt content of their diet [69] [70].

Smoking also increases heart rate and cardiac output with elevations of SBP of about 5-10 mmHg occurring shortly after lighting up a cigarette. However, this very transient rise in BP does not appear to lead to the development of essential HTN. Quitting smoking for 6 weeks was not found to have any significant effect on BP [71].

What about studies showing more deaths in people with lower BP? Given the known risk of serious health problems associated with higher BP, body weight, and serum cholesterol it is somewhat surprising that in several studies of older people those with the lowest levels of cholesterol, BP and body fat are actually more likely to die than those with more moderate levels. This results in what epidemiologist call the J-shaped curve with the lowest risk of dying in the moderately low range but with risk of dying rising at the very low range. This has led some to speculate that we should not aggressively lower these known risk factors for cardiovascular disease, at least in older people.

However, these studies are always confounded by ill health at the start of the study of many of those with the lowest BP, cholesterol level and body weights. People in poor health often have poor appetites and eat less. They gradually lose weight, their cholesterol level and BP fall and then they die. For example, people who suffer a heart attack often have lower BP afterwards because their heart is weaker and cant pump as hard. People with long standing poorly controlled HTN often develop congestive heart failure and as they do their BP falls. People with cirrhosis often have very low cholesterol levels and poor appetites. People with cancer and long-standing diabetes often lose weight and experience a fall in BP. So there are a lot of ways an older person can end up with a lower BP, body weight and/or cholesterol level and yet still be more likely to die.

In the long-term, lower BP in old age is associated with better survival and short-term studies may differ because of co-morbidity and frailty with a lower BP near death. Overall, most research suggests that lowering BP in the aged is still efficacious [72]. There is no plausible theoretical basis to explain how a lower BP, body weight and/or cholesterol level can promote disease and increase the risk of dying in the elderly and yet be protective in younger people. A 6 year follow-up study of 18,022 Norwegians (age 65y+) found that the J-shaped curve for mortality and BP was indeed "indirect, possibly caused by serious underlying disease" [73].

Could reducing dietary salt intake by 1/3 be dangerous? On Jan. 21,1999, Salt Institute president Dick Hanneman wrote to NHLBIs director Dr. Claude Lenfant and suggested that the NHLBIs Workshop on Sodium and Blood Pressure focus on the "safety" of reducing dietary salt intake by 1/3. Mr. Hanneman wanted the assembled experts (on very short notice as the conference was to be held on Jan. 29th+30th) to alter their agenda to "identify published data demonstrating that that [reducing dietary salt by 1/3] would not impair mental function, disturb sleep, produce deficiency-level intakes of other electrolytes and,he stressed, would health outcomes be improved (sic)" [74]. Of course, most scientists know you cannot prove a negative assertion [a.k.a. the "null hypothesis"]. Even the suggestion that moderately reducing the already high-salt intake of Americans could result in a "deficiency-level" or somehow be harmful seems beyond the pale.

Even wackier than the questionable interpretation of the association between very low levels of BP and increased mortality are "studies" which purport to show an increased risk of dying in people who eat less salt. For example, Michael Alderman (a former consultant to the Salt Institute) published a study that purported to show that people who ate less salt were more likely to have high BP and were more likely to die [75]. Their salt and calorie intake were estimated based on a single 24-hour diet recall back in the early 1970s. In Dr. Aldermans study, the people consuming the "lower sodium" diets were actually consuming more sodium per calorie than those consuming the "higher sodium" diets. The only reason they were on a "low sodium" diet was that they had reported eating less than 1000 kcal in the past 24 hrs. When asked to comment on this study Dr. Lawrence Appel of John Hopkins University stated: "No good researcher would even publish the unadjusted data" and "I dont know how this study got published. Its outrageous" [76].

The timing of Dr. Aldermans study is also suspect. It was released at about the same time as Dr. Wheltons TONE study, which clearly established the efficacy of a low-salt diet (<1800 mg/d) in treating HTN patients. One wonders how Dr. Aldermans bogus study ever garnered so much favorable media attention last year. Could the massive press releases by the Salt Institute been a factor? Mr. Hanneman admitted to being "distressed" by the withdrawal of Dr. Alderman from the recent NHLBI Workshop [Jan. 29&30, 1999]. Perhaps Dr. Alderman simply hoped to avoid further personal embarrassment regarding his bogus "study" which will probably only be cited as an example of poor science like the "cold fusion" fiasco a few years back.

Doesnt a low-sodium diet lead to hyponatremia in athletes? Sweat typically contains about 1 gram of salt or 400 mg of sodium per liter and there have been cases of sodium depletion or hyponatremia in endurance athletes even consuming a fairly high salt intake (10-15 gm/day). This has led some to speculate that a low-salt diet could be dangerous for athletes or anyone who is sweating profusely in a hot, humid environment. Although it is not well recognized, the human sweat glands are quite capable of conserving sodium and chloride when the diet is low in salt. A study at the University of Michigan found that men who lost an average of 7 liters of sweat daily, doing several hours of intense exercise in a hot, humid environment were, nonetheless, able to maintain normal sodium levels on just .75 gm of salt (300 mg of sodium) per day [77]. The historian Michael Hanneman (Salt Institute president) apparently overlooked this historic study when he suggested that a low-salt diet could be dangerous.

The human body adapts to a low-salt intake by reducing salt in sweat and in the urine. In Dr. Conns study the men acclimatized to a very low-salt diet had sweat that contained only 40 mg of Na/L and their kidneys excreted just 20 mg Na/day. The Yanomamo Indians of the tropical rain forest of South America do not develop hyponatremia despite a sodium intake of less than 200 mg/day, an active lifestyle, and an average daily temperature of 100+ degrees Fahrenheit [78]. This suggests that hyponatremia in athletes could be due in part to a high-salt intake. This is because it takes a week or more for the body to fully adapt to a very-low-salt intake. If athletes consume large quantities of fluid without salt but are not adapted to a low salt intake their sweat will still contain a lot of salt and after several hours of profuse sweating they can become salt depleted to the point where hyponatremia develops. The irritation of dried salt on the skin of athletes could be significantly reduced if they consumed a very-low-salt diet.

But arent drugs the most effective treatment for HTN? A natural ally of the Salt Institute are the big pharmaceutical companies who rake in billions of dollars every year from the sale of their numerous antihypertensive drugs. In the words of Dr. Laragh (a long-time critic of the salt causes HTN hypothesis), a well paid consultant for the pharmaceutical industry, "existing drugs are potent enough to render the misery of effective life long salt restriction unnecessary" [79]. Mr. Hanneman also found it "distressing" that Dr. Laragh withdrew from the recent NHLBI Workshop. One might suspect that the CEOs at some big pharmaceutical companies were also distressed. Americans spend billions of dollars each year on drugs, doctor visits, hospitalization, dialysis treatment and nursing care for those disabled by strokes, heart failure, and other cardiovascular diseases due to HTN. Some would argue that treating HTN with drugs is still cost effective because it is the safest and most effective way to treat HTN. Does the research bear this out?

To the surprise of many, the MRFIT trial found that when the men judged to be at high-risk for CHD were treated more aggressively with drugs to lower their BP, they did not fair better unless their initial DBP was greater than 100 mmHg. In those with an initial DBP of 90-94 mmHg those treated aggressively with drugs in the "Stepped Care" model were actually more likely to die [80].

An even bigger challenge to the notion that drug therapy is the best way to treat "mild" to "moderate" HTN was the even larger study conducted by the British Medical Research Council. In this study over 17,000 HTN patients with initial DBP between 90 and 109 mmHg were either given a placebo or an anti-HTN drug (either a thiazide diuretic or a beta-blocker) or a placebo. In those receiving the drugs the dosage was gradually increased and additional drugs added (if need be) to get the DBP below 90 mmHg. The results showed a decreased risk of strokes, but the overall mortality of women in the drug treatment was increased by 25%, while in men the overall mortality rate in those taking anti-HTN meds did drop but only 13%. The authors of this study concluded that "treatment did not appear to save lives or substantially alter the overall risk of coronary heart disease." The results of this study suggest that no treatment is nearly as effective as drug treatment for those with "mild" to "moderate" HTN! And the one proven benefit of reduced strokes came at a high cost. In addition to the adverse effects of the drugs this study pointed out that treating 850 HTN patients with drugs will prevent about one stroke per year.

The good news is that the use of anti-HTN medication is of some value in reducing strokes in those with "mild" to" moderate" HTN and in reducing overall mortality in those with very high BP (i.e. 180/110 mmHg or higher). However, the 1993 Report of the Working Group of the NHLBI pointed out that "Even in those who derive optimal benefit from their antihypertensive treatment, they are likely to have a higher risk of morbidity and mortality than their untreated "normotensive" counterparts with a similar level of blood pressure" [81].

More recently the HOT study found no evidence that decreasing SBP below 140 mmHg with drugs reduced overall mortality even though epidemiological evidence clearly shows mortality rising with any SBP above 110 mmHg [82]. Currently only about 5 million of 50 million HTN people in the US have their BP reduced below 140/90 mmHg. The good news from the HOT study is that physicians can now use higher dosages and/or more drugs to lower their hypertensive patients BP to even lower levels without worrying about this killing them more quickly. This may make the CEOs at the big pharmaceutical companies happy. The not so hot interpretation of the HOT study is that spending more money on drugs to more aggressively lower BP in HTN patients is not likely to reduce overall mortality much either. Theyll have to hope the HMOs and the government (Medicare and Medicaid) dont bother to do a cost/benefit analysis on drug therapy for HTN.

Does the scientific evidence support Dr. Laraghs claim that anti-HTN drugs are now so "effective" that "the misery of effective life long salt restriction" is "unnecessary"? Or does it appear that anti-HTN drugs are far from the perfect treatment? Drugs are far too dangerous to be used life-long to prevent HTN from developing in the first place. Even when restricted to those with established HTN their overall effect on mortality is questionable unless the HTN is severe. Aside from their cost, drugs have many adverse side effects that make a lot of people miserable such as impotence, dry mouth, dizziness and reduced eyesight capacity. But would they be even more miserable eating a low-salt diet?

Must a low-salt diet be unpalatable? When test subjects were fed a diet with only 70 mmol (about 1600 mg Na) per day and given free access to a salt shaker, researchers found that they compensated by adding only an additional 300 mg of sodium as salt. This resulted in a greater than 50 mmol reduction in salt intake, even though the test subjects were free to add as much additional salt to their food as they desired. The authors concluded that "a substantial reduction in dietary sodium is possible if lowered sodium foods are consumed in conjunction with ad libitum table salt" [83]. Recall that 75% of the average Americans salt intake comes from manufactured foods. If the food industry would cut their use of salt by 50% it is unlikely that many people would be miserable. However, according to Dr. Laws extensive review of the scientific literature even a 50 mmol reduction in salt intake would save about 250,000 lives in America each year as well as prevent many nonfatal strokes, heart attacks and other health problems that lead to real misery.

In addition to this, researchers have shown that moderate reductions in dietary salt for 2 months reduces the concentration of salt in food judged most pleasant [84]. A controlled study of young adults on a self-maintained low sodium diet for 5 months found that they came to enjoy lower sodium content foods [85]. Another study found that after 24 weeks of a low sodium diet the subjects most pre-ferred level of salt in food declined from .72% to .33% (wet weight basis) [86].

It has also been shown that one can mask a reduction of salt in bread and water by adding acetic or lactic acid [87]. Sodium compounds other than salt such as MSG or sodium citrate can also enhance the flavor of food without causing a rise in BP [88]. It seems likely that with a little creativity the food scientists and chefs could develop food products that are as palatable or nearly as palatable as current high salt products but which will not lead the development of essential HTN.

One should not use salt substitutes containing chloride (Cl) and should avoid significant amounts of other Cl containing compounds if one elects to use baking powder (sodium bicarbonate), monosodium glutamate, sodium citrate and other sodium compounds in foods. It appears to be too much of both Na and Cl together in the body that leads to the release of endogenous digitalis-like substance (EDLS). This oubain-like hormone or EDLS is released from the brain and helps the kidney get rid of excess NaCl by blocking the re-uptake of NaCl from the collecting tubules of the kidney. Unfortunately, it blocks the Na/K pump in the smooth muscle cells of the arterioles and other tissues leading to increased intracellar Na and Ca. By disrupting normal cell chemistry this hormone may be behind much of the damage seen in essential HTN [89] [90] [91].

The Bottom Line Excessive dietary salt is almost certainly the major causal agent in the development of essential HTN in the US and other modern societies. The food industry is largely responsible for most of the excessive salt consumed by Americans. Medical doctors and the pharmaceutical industry are not fully informing patients with HTN about minimal proven benefits of drugs for treating "mild" to "moderate" HTN. Many doctors are also negligent in fully informing their patients about the likely long-term benefits of reducing salt intake. Nor do many doctors strongly encourage their patients to consume a more natural foods diet high in fiber, potassium, calcium, magnesium and other potentially useful chemicals that may help reverse the biochemical and physiological damage due to a typical American diet. Salt appears to be a serial killer which has escaped indictment and prosecution thanks in large part to a well orchestrated PR campaign by the Salt Institute. As the nutrition experts, registered dietitians have a duty to inform their clients about the dangers of too much salt and the likely health benefits of reducing excessive salt intake.

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