HighBeam Research


Title: Reexamining cholesterol and sodium recommendations.

Date: 9/1/1994; Publication: Nutrition Today; Author: Callaway, Wayne

What is the most healthful diet? Recommendations from organizations such as the American Heart Association (AHA) and the U.S. Department of Agriculture, and official reports such as the 1989 U.S. Surgeon General's Report on Nutrition and Health and the 1990 National Academy of Sciences' Diet and Health Report make the answer to the question seem clear: Eat a diet that provides no more than 30% of calories from fat, with no more than one-third of that from saturated fat; include at least 20 to 35 g of fiber per day, eat at least five servings of fruits and vegetables, and consume no more than 300 milligrams of cholesterol and 2,400 to 3,000 mg of sodium each day.

Now, a growing chorus of experts are asking: Are all of these guidelines applicable to everyone? Few would argue the recommendations that virtually everyone should eat more fruits, vegetables, and whole grains and that most Americans could benefit from eating less fat and more fiber. But is there justification for the recommended across-the-board ceiling on cholesterol of 300 mg and 2,400 to 3,000 mg for sodium? This is a question that the newly formed committee for the fourth edition of the 1995 Dietary Guidelines for Americans will have to wrestle with as it works to update its recommendations for the general public. It won't be an easy task. We, as health and nutrition professionals, are at a crossroads, attempting to make the not-so-subtle transition from giving one-size-fits-all dietary recommendations to individualizing them as much as is realistically possible. A look at the research and history behind the cholesterol and sodium recommendations provides a glimpse of the issues policy-making nutrition experts must deal with while developing new guidelines for healthy eating.


There is little doubt that elevated plasma cholesterol levels are related to increased risk for cardiovascular disease (CVD). Disagreement arises, however, over whether dietary cholesterol by itself is an important determinant of blood cholesterol levels. Hypercholesterolemic and erogenic effects of large amounts of dietary cholesterol have been reported in experimental animals, but experiments on animals tend to test the effects of pharmacological doses of cholesterol, not amounts comparable to those normally consumed by humans. Effects on plasma lipids in humans still remain controversial. Least is known about the independent effects of dietary cholesterol on plasma lipids in moderately hypercholesterolemic older subjects, the group for whom dietary modification is most often recommended.(1)

Recommendations were first made by the AHA in the late 1970s to limit total cholesterol intake to a maximum of 300 mg per day. Rather than being based on a specific study or studies, the 300-mg number was merely a "best guess" of an appropriate limit. That number has not been seriously challenged since then. In fact, it was the maximum recommended limit set in the much more recent 1989 Diet and Health report.

However, in a 1984 review of the science behind the AHA's dietary recommendations for preventing heart disease, Reiser(2) found that "not only are most of the references obsolete, but many of their conclusions are the antitheses of those attributed to them." In his insightful paper, Reiser pointed out that a 1965 study done by Keys,(3) which was cited as part of the basis for the cholesterol recommendation, actually concluded that "For purposes of controlling serum [cholesterol] level, dietary cholesterol should not be ignored, but attention to this factor alone accomplishes little."

In an earlier report done by Keys,(4) it was concluded that the "findings make it reasonably clear that the serum cholesterol level of 'normal' men is not significantly related to differences in the habitual cholesterol intake over a range of 250 to 800 milligrams per day" and, contrary to AHA's recommendation, "...efforts to control the serum cholesterol by alteration of the intake within this range are unlikely to succeed."

Although there is much epidemiological evidence as to the connection between blood cholesterol levels and heart disease, not all epidemiological studies show a correlation between dietary cholesterol alone and either serum cholesterol or coronary heart disease. The correlations, when present, are small and often statistically weak, and when confounding factors such as fat and saturated fat intake are accounted for, often are not significant.

Another issue affecting public recommendations to lower dietary cholesterol intake revolves around who is sensitive to dietary cholesterol in the range of normal intake. Those for whom a difference of 200 mg a day leads to a significant change in serum cholesterol are at risk for CVD.

Individualized patient responses to dietary intervention designed to lower cholesterol were reported by McGill as early as 1979.(5) Despite the well-documented, wide range of responses to dietary cholesterol, he noted that investigators had been concerned primarily with the average effects of dietary manipulations and had presented only mean values, making it impossible to detect the relative proportions of people who responded to dietary cholesterol slightly or not at all and those who responded with marked elevations. It is this frequency, he added, of distribution of responses that may be more important than average responses in determining whether dietary changes should be recommended for the whole population.

McNamara(6) confirmed McGill's findings in 1987. Since then, significant heterogeneity has been observed in terms of dietary fat and cholesterol sensitivity and the precision of regulatory responses. It has been suggested that most people are resistant to the cholesterol-raising effects of dietary cholesterol alone, especially when the diet is low in fat and saturated fat and high in fiber.

A recent study found that, when young men with normal blood cholesterol levels ate one egg per day as part of a low-fat, low-saturatedfat diet (Step I Diet with 125 mg from other sources), cholesterol levels increased only 3 mg/dl, a clinically insignificant amount.(7) It is difficult with the currently available data to predict the metabolic changes in a nonhyperlipidemic population in response to modest dietary changes, especially when considering the large degree of heterogeneity that has been demonstrated in response to more dramatic dietary interventions used in many studies.(7)

Study variables that have clouded the true relationship between dietary cholesterol and serum cholesterol include the form of dietary cholesterol, egg yolk, or crystalline; the type of diet, natural foods, or formula; the amount of supplemental cholesterol within or above the range of common intake; the fat content of the diet; whether the supplemental cholesterol was added to free-living diets or to those provided by a metabolic kitchen; and the levels of other components in the diet that might alter the rates of cholesterol absorption, such as phytosterols.(8)

In a series of human studies, McNamara(9) found no evidence to support the hypothesis that reducing dietary cholesterol intake from the current level of about 450 mg/day to the currently recommended maximum of 300 mg/day would reduce plasma cholesterol levels in the general population. He suggests that reductions in dietary cholesterol may, however, benefit an unknown percentage of people who lack precise feedback control of endogenous cholesterol synthesis. He concluded that the primary determinants of a given subject's plasma cholesterol level are:

* sensitivity to dietary saturated fat and

* the degree of precision of the feedback control responses to dietary cholesterol--responses which are highly variable from person to person.

It's also been suggested that individuals are less likely to respond to dietary cholesterol when a diet low in saturated fatty acids is consumed. Edington(10) found no significant differences in plasma lipid levels among subjects consuming zero or nine eggs per week on a diet low in saturated fat. Plasma cholesterol concentration did not consistently increase when the dietary cholesterol was increased or decrease with lower intake. There was no evidence of groups of hyporesponders or hyperresponders, even when dietary cholesterol intake varied between 90 and 410 mg/day.

Blood cholesterol levels, rather than having a direct relationship with dietary cholesterol, are more likely a reflection of the complex interactions of blood lipids with total dietary fat and saturated, monounsaturated, trans, and polyunsaturated fatty acids, as well as dietary cholesterol.(11)

Only limited data exist from studies that examine the effects of changing from a pattern similar to that of the current dietary intake to one with limited total fat, saturated fat, and cholesterol intakes. Generally, however, it appears that moderate amounts of dietary cholesterol within the range that people ordinarily consume do not affect serum cholesterol, especially among normocholesterolemic individuals. This begs the question of how effective the 300-mg daily dietary cholesterol restriction is in controlling blood cholesterol levels.

It's clear that the cholesterol message has come across to consumers as a simple one: Dietary cholesterol = high blood cholesterol. However, if only 25% to 30% of the general population lacks precise metabolic adaptation for cholesterol, a valid question is: What benefit is there to the remaining 70% to 75% of the general population from restricting dietary cholesterol? Further, if the average rise in the plasma cholesterol of individuals eating supplemental cholesterol is small, does it carry a sufficient cardiovascular risk to justify advice for everyone to restrict cholesterol consumption? Also, if a reduction in total fat and saturated fat obviates the need for a reduction in cholesterol, are we sending the wrong message to the public?

The need to limit cholesterol intake may apply more strictly to dietsensitive hypercholesterolemic individuals than the population in general. Further studies need to focus on identifying predictors for hyperresponsiveness to dietary cholesterol so that dietary counseling can be used in the most efficacious manner, rather than making broad population-based recommendations that, research suggests, benefit a minority of people.(6)(12)


In a 1979 report from the National Institutes of Health Hypertension Task Force it was stated: "The brevity of this section 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."

Rather than consider these very clearly stated reservations, the government chose to forge ahead with the Food and Drug Administration's (FDA's) Sodium Initiative, a nationwide effort to educate the public about the dangers of eating too much salt. By July 1981, the FDA had dubbed sodium restriction "a national consensus" and claimed the support of "most of the leading health and medical experts." The FDA's sodium initiative was successful--too successful, in fact, increasing consumer concern for dietary sodium far beyond what science now knows to be the scope and nature of the problem.

While the sodium hypothesis enjoyed almost unchallenged acceptance in the halls of government and on the front pages of the nation's newspapers, some scientists grumbled about the very public campaign against sodium. A group of 13 researchers wrote in The Lancet in 1984(13): "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."

Still, both the 1988 Surgeon General's Report on Nutrition and Health and the National Academy of Sciences' 1989 report, Diet and Health, retained the recommendation for a nationwide reduction in dietary sodium (or salt in the case of the Diet and Health report). The Surgeon General's report did acknowledge, however, that whether universal sodium restriction would lower population blood pressure had never been tested.

In 1989, the same year The Surgeon General's Report was published, the National Institutes of Health (NIH) had sponsored a meeting of leading hypertension researchers to discuss "salt and blood pressure."

The meeting's attendees were unable to reach a consensus as to whether a relationship between sodium and hypertension did in fact exist and whether a policy of universal sodium restriction conferred more benefits than additional risks to healthy Americans.

Two years later, a FASEB report entitled "Dietary Sodium Chloride and Blood Pressure," which reviewed available scientific evidence of a sodium/hypertension link, concluded that "studies within populations have been inconclusive or have shown low correlations."

One of the studies considered in the FASEB report was Intersalt,(14) the largest and most comprehensive study done to date on the connection between sodium intake and hypertension. The study surveyed 10,079 subjects from 52 centers in 32 countries around the world. Though the interpretation of the results, including that done by the authors themselves, has come into question, most who carefully read the study agree that it showed that in Western countries sodium intake has little to do with hypertension. Rather, the study clearly shows that within the range of economically advantaged societies' sodium intakes (roughly 2,300 mg to 4,600 mg/day), there is no association between population blood pressure and average population sodium excretion.

Even the well-known study of heart disease and stroke in Framingham, Massachusetts found no relationship between salt consumption and hypertension.(15)

Although extreme differences in sodium intake are associated with different blood pressures, there is no prospective randomized data to support the widely held belief that restriction of sodium consumption among normotensive persons prevents the subsequent appearance of hypertension. Salt-sensitive hypertension is likely to be genetically determined and there is currently no reliable genetic marker to identify those persons at risk. Based on this inability to determine the persons at risk, most public health recommendations dictate that universal sodium restriction is "prudent."

It may not be just the relationship of sodium to hypertension that is critical, however. It may be, and probably is, a complex relationship of dietary potassium, calcium, and magnesium and the interrelationships of the electrolytes which affect blood pressure--one more reason why the dietary guideline to eat a variety of foods is an important one. The problem for some people may not be getting too much of sodium, but not getting enough of other nutrients critical to the hypertension equation.

In a 1991 article published in Hypertension,(16) McCarron, who challenges the notion that dietary salt is a major contributor to the development of hypertension, stated, "Our future understanding of the effects of dietary NaCl on blood pressure will be advanced only if we approach the task from the position that salt's action on blood pressure regulation must be viewed in the context of the total diet. We must temper the notion that by simply recommending the lowering of an individual's salt intake, we will be providing the public with optimal dietary advice as to how to lower cardiovascular risk through prevention of hypertension."

Because salt restriction can, at best, produce modest change in blood pressure for only some patients, it stands to reason that its widespread application must be based on the belief that it is harmless.

However, after reviewing the literature and finding moderate sodium restriction to be helpful only for a minority of patients with mild hypertension, Alderman et al.(8) also found that moderate sodium restriction actually raised blood pressure in a certain proportion of patients. A rise in plasma renin, provoked by salt depletion, may be responsible for this effect through its vasoconstrictive function. A rise of blood pressure during moderate restriction of sodium was observed in about 15% of patients. Reporting in The American Journal of Hypertension, Alderman and Lamport(17) concluded that "There is no justification for the recommendation that salt intake be restricted in the general population to avert blood pressure rise. Moderate salt restriction can not be universally recommended as a treatmetn for hypertension. It is not a benign panacea, but merely one useful component of the antihypertensive armamentarium."

More recently, in an exhaustive review of the literature, Muntzel and Tilman(18) concluded that, "Although lower NaCl intake may improve blood pressure in some persons, we have no evidence that this will decrease the occurrence of cardiovascular disease on a population level. Thus, we should be cautious in issuing nationwide (or even hypertension-wide) recommendations to reduce dietary NaCl intake."

Also untested is the question of whether diets high in sodium are associated with elevated risks of heart attacks or shorter lifespans. The sodium/hypertension hypothesis continues to be the subject of intense debate in the scientific community.


(1.)Lichtenstein AH, Ausman LM, Carrasco W, Jenner JL, Ordovas JM, Schaefer EJ. Hypercholesterolemic effect of dietary cholesterol in diets enriched in polyunsaturated and saturated fat. Arterioscler Thromb 1994; 14:168--75.

(2.)Reiser RA. Commentary on the Rationale of the Diet-Heart Statement of the American Heart Association. Am J Clin Nutr 1984; 40:654--8.

(3.)Keys A, Anderson JT, Grande F. Serum cholesterol response to changes in the diet. II. The effects of cholesterol in the diet. Metabolism 1965; 14:759--65.

(4.)Keys A, Mickelsen O, Miller EVO, Chapman, CB. The relation in man between cholesterol levels in the diet and in blood. Science 1950; 112:79--80.

(5.)McGill, HC. The relationship of dietary cholesterol to serum cholesterol concentration and to atherosclerosis in man. Am J Clin Nutr 1979; 32:2664--702.

(6.)Ginsburg HN, Karmally W, Siddiqui M, Holleran S, Tall AR, Rumsey SC, Deckelbaum RJ, Blaner WS, Ramakrishnan RA. Dose-response study of the effects of dietary cholesterol on fasting and postprandial lipid and lipoprotein metabolism in healthy young men. Arterioscler Thromb 1994; 14:576--86.

(7.)McNamara, DJ. Effects of fat-modified diets on cholesterol and lipoprotein metabolism. Annu Rev Nutr 1987; 7:173--90.

(8.)Alderman MH, Madhavan S, Ooi WL, Cohen H, Sealey, JE, Laragh JH. Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension. N Engl J Med 1991; 324:1098--104.

(9.)McNamara DJ, Kolb R, Parker TS, Batwin H, Samuel P, Brown CD, Ahrens EH. Heterogeneity of cholesterol homeostasis in man. J Clin Invest 1987; 79:1729--39.

(10.)Edington, JD, Geekie M, Carter R, Benfield L, Ball M, Mann J. Serum lipid response to dietary cholesterol in subjects fed a low-fat, high-fiber diet. Am J Clin Nutr 1989; 50:58--62.

(11.)Gurr MI. Dietary lipids and coronary heart disease: old evidence, new perspective. Prog Lipid Res 1992; 31:195--243.

(12.)Kestin M, Clifton PM, Rouse IL, Nestel PJ. Effect of dietary cholesterol in normolipidemic subjects is not modified by nature and amount of dietary fat. Am J Clin Nutr 1989; 50:528--32.

(13.)Brown JJ, Lever AF, Robertson JIS, Semple PF, Bing RF, Heagerty AM, Swales JD, Thurston H, Ledingham JGG, Laragh JH, Hansson L, Nicholls MG, Espiner EA. Salt and Hypertension. Lancet 1984; 2:1333--4.

(14.)Intersalt Cooperative Research Group. Intersalt: an international study of electrolyte excretion and blood pressure. Br Med J 1988; 297:319--28.

(15.)Dauber TR, Kannei WB, Kagan A, et al. Environmental factors in hypertension. In: Stamler J, et al. (eds.), The epidemiology of hypertension. New York: Grune & Stratton, 1976:255--88.

(16.)McCarron, DA. A consensus approach to electrolytes and blood pressure: Could we all be right? Hypertension 1991; 17(suppl I):I170--2.

(17.)Alderman MH, Lamport B. Moderate sodium restriction: Do the benefits justify the hazards? Am J Hypertens 1990; 3:499--504.

(18.)Muntzel M, Tilman D. A comprehensive review of the salt and blood pressure relationship. Am J Hypertens 1992; 5(suppl):1S--42S

COPYRIGHT 1994 Lippincott/Williams & Wilkins

This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group.

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