perspectives
goals-a
progressive
view1
D. M. Hegsted,2 Ph.D.
The Dietary Goals for the United States published by the Senate Select Committee on Nutrition and Human Needs (1, 2) recommend that Americans should eat less food and specifically that they should eat less fat, particularly saturated fat, less cholesterol, less sugar, and less salt, and that they should increase their consumption of fruits, vegetables, grain products, and unsaturated oils. It is not surprising that various segments of the food-producing and manufacturing community fmd fault with these guidelines. Of more significance, perhaps, are the adverse comments of some of the current leaders of the nutrition community (3) such as the recent editorial by Harper (4). These opponents fmd the report either premature or unjustified on the basis of current knowledge. We should be very clear what is being said. Dr. Harper is either saying that the intake of fat, cholesterol, salt, and sugar has no nutritional significance and, therefore, does not deserve attention by serious nutritionists or the public, or that, having reviewed all of the evidence, the current American diet estimated to provide about 40% of the calories as fat, about 20% of the calories as sugar, 500 to 700 mg of cholesterol per day, and 8 to 10 g of salt is the best diet that can be recommended for Americans. We should note that these are estimates of average intake so that half of the population is consuming larger amounts. Frankly, I fmd it inconceivable that anyone familiar with the literature can arrive at either conclusion. The Dietary Goals have been criticized that they were not a complete prescription for health-that there was inadequate discussion of obesity, fluoridation, alcohol, exercise, etc. The legitimacy of this argument depends entirely upon one’s point of view. It is perfectly clear to everyone, however, that the Goals were not intended and do not pretend to be 1504
The American
Journal
of Clinical
Nutrition
a substitute for other well established information and other legitimate goals. What they were intended to do was to call forceful attention to issues that the nutrition and biochemical community have so far failed to deal with in adequate fashion. The Goals have been criticized on the basis that they did not provide adequate supporting evidence. This is true but the nature of a document depends upon the audience. It is equally valid to criticize the report of the Committee on Recommended Dietary Allowances (RDA) as not being interpretable to the general public (5). In either case, the reports require further interpretation-the first by the scientific community; the second by those dealing with the public. Rather invidious comparisons have been drawn between the RDA and the Dietary Goals with the implication that whereas the RDA are obviously justified, the Dietary Goals are not. The change in the Goals on salt intake in the second edition (2) is said to demonstrate that the recommendations are premature. We should compare what has happened to the RDA. In the 1948 edition (6) the recommended intake of riboflavin and vitamin C were much higher than they are currently and the recommended intake of iron was the same for men and women. The last edition (5) dropped the recommendation of vitamin C for men from 60 to 45 mg. Does this mean we never knew anything about desirable vitamin C intakes and possibly still do not? It has always been understood that dietary recommendations should be continuously reviewed and will inevitably change. Otherwise, research is useless. It should also be emphasized that the RDA From the Department of Nutrition, of Public Health, Boston, Massachusetts 2 Professor of Nutrition.
31: SEPTEMBER
1978, pp. 1504-1509.
Harvard 02115.
Printed
School
in U.S.A.
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/9/1504/4650709 by California Digital Library user on 01 January 2019
Dietary
in nutrition
DIETARY
GOALS-PROGRESSIVE
1505
large proportion of Americans are at risk from excessive intakes. The Food and Nutrition Board recently recommended an expanded fortification program (10). No demonstration of benefit from such a program was thought necessary as a prelude to implementation and it is doubtful that this should be required. Much has been made of the fact that iron deficiency is a problem in the United States and that decreased consumption of meat might exacerbate this problem. It is somewhat curious that the Food and Nutrition Board can recommend a protein intake that could be easily achieved without the consumption of any meat and object to a modest reduction in meat intake. Apart from this, there is a curious inconsistency in the way the American Medical Association (11) and Dr. Harper and others consider the major chronic diseases and iron deficiency. They argue that dietary recommendation for coronary artery disease, diabetes, etc. should be reserved as therapy after susceptibles have been identified while prevention of iron deficiency is a high priority item. Most nutritionists, I think, agree that iron deficiency ought to be prevented. Yet this is a disease that is easily identified, easily treated and, as far as we know, has no residual effects. Furthermore, the actual impairment in health of the modest degrees of iron deficiency which occur have been difficult to document (12). In contrast, coronary heart disease (CHD), stroke, diabetes, hypertension, etc. are devastating diseases and dietary or other forms of treatment are relatively ineffective. Any major health gains to be made in the United States must be aimed at prevention or amelioration of these diseases. A variety of critics have read more into the Dietary Goals than is there. Dr. Harper interprets them to say that obesity would disappear if the Goals were adopted! I do not fmd this in the document. He favors the advice to eat less food to which most of us will agree. He ignores the dismal record of failure associated with this advice (13). It is likely that the recommendation to modify the diet to a leaner, bulkier diet will assist in the control of food intake and, in fact, this is what many who treat obesity do recommend. The discussion of obesity points up another inconsistency in the way we view different
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/9/1504/4650709 by California Digital Library user on 01 January 2019
have always been derived from informed judgment based upon all possible sources of information-epidemiology, metabolic studies with human subjects, and studies with experimental animals being the primary sources of information. If this procedure is valid for establishing “best estimates of nutrient need,” it is equally valid for establishing best estimates of desirable intakes of fat, sugar, salt, or any other dietary constituent. A major criticism of the Dietary Goals has been that there is no proof that adoption of the dietary pattern recommended will benefit the public. More will be said of this later but it is a somewhat strange argument for nutritionists to make. Where is the proof that an intake of 45 mg of vitamin C is better or worse than an intake of 60 or 70 mg? The FAO/ WHO group (7) recommends a calcium intake of 400 to 500 mg for adults whereas the RDA is 800 mg. There is no proof that an intake of either level is better or worse than the other. While I am critical of the 800 mg (8), it is obvious that recommendations do have to be made before all of the desired evidence is available and this has always been accepted. We should note that the RDA have always been set (at least in theory) at relatively high levels to minimize “risk” of deficiency. The nutrient needs of individuals do vary although we do not know by how much. Clearly, the recommended intake cannot be set at the estimated average need. While this leads us to the somewhat incongruous conclusion that practically everyone can consume less than the recommended intake and still be well fed (9), the basic argument must be valid. Obviously, in any field trial to demonstrate the validity of a RDA, it would be unlikely that one could demonstrate that the specified level was justified. If the RDA is correctly estimated, it follows that very few individuals would benefit from an intake that high. Similarly, it is perfectly clear that some individuals are more adversely affected by diets high in fat, cholesterol, salt, and sugar than others. A few will have little or nothing to gain from a lower intake in the same way that an individual with a vitamin A requirement of 2500 IU per day will have nothing to gain from an intake of 5000 IU. This, however, cannot mean that no advice about intake can be given to the public, particularly when a very
VIEW
1506
HEGSTED
It has been repeatedly emphasized that per capita sucrose intakes have not changed much in recent years. What is not emphasized is that other forms of purified sugar have increased. More importantly, perhaps, it is not emphasized that total energy consumption in the United States is now quite low. The Bogalusa children, for example, were consuming about 2100 kcal/day on the average compared with an RDA of about 2600 kcal. Continued consumption of the same amount of sugar with lower energy intakes means a larger proportion of the diet as sugar. I agree with the FASEB report that there is, so far, relatively little evidence that sugar is really “toxic” or that it can be directly associated with chronic disease in the same way as saturated fat. I do not agree that this means that one can ignore sugar in attempting to establish total dietary patterns and that sugar consumption is of no concern, We could, of course, reduce our fat intake and replace it by sugar. I believe this would be a ridiculous recommendation. A high sugar intake has no known nutritional merit and cannot be recommended. There is another curious dichotomy in the way many appear to view materials already in the food supply and those that are new. Everyone with an understanding of the principles of statistics and toxicology agrees that if we are to evaluate the safety of a material of suspected toxicity, it must be fed or administered at levels substantially above those which will ordinarily be encountered in the environment. Many believe that an exposure of 1/100 of the demonstrated toxic dose in animals could be considered to be safe in man. Obviously, this 100:1 tolerance cannot be achieved with many of the essential nutrients. Yet if one considers the data on salt, we know that high intakes cause hypertension in animals, that an intake of 30 to 40 g in man is toxic in man (18), that recent health statistics (19)
show
a rapidly
increasing
proportion
of
the population with age who have frank hypertension reaching the amazing values of 30 to 60% of the total adult population over 55 years of age (this ignores the fact that the blood
pressure
age and that is associated
of most
any with
Americans
increase in blood an increased risk
rises
with
pressure of coro-
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/9/1504/4650709 by California Digital Library user on 01 January 2019
problems. The association of various chronic diseases with obesity is, of course, well known. Many have automatically assumed this to be a causal relationship. The best evidence (14) is that, except for gross obesity, the additional body fat itself does not impose much of a health hazard whereas the risks associated with hyperholesterolemia, hypertension, and diabetes are clear. The degree to which these risks are associated with or causally related to obesity are not yet known (15). There has been little demand for a direct demonstration that weight reducing regimes actually improve health or life expectancy and, in view of the record of such programs, it will be extremely difficult to demonstrate. Apparently, we simply know that obesity is bad. Similarly, we apparently know that exercise is good. There have been few studies aimed at demonstrating the effects of exercise upon morbidity or mortality and the current evidence is that modest exercise does not have a major positive effect. This is not to say that exercise should not be recommended but the evidence available should be weighed objectively. The recommendation to limit sugar intake has been attacked and the report of the Life Sciences Research Office of FASEB (16) is referred to as demonstrating lack of evidence to support the recommendations. In my opinion, this report is “technically correct and practically useless.” The Committee simply failed to consider the appropriate question-”How much sugar is desirable in the diet?” This question cannot be answered from a consideration of sugar alone. In the same issue of the American Journal of Clinical Nutrition in which Dr. Harper’s article appeared, there is a report on the dietary habits of Bogalusa children 10 years of age (17). The average sucrose intake was 98 g per day. This is apparently about the national per capita average and means that half of the children were consuming more than this. Approximately 37% of the sugar came from soft drinks and 25% from candy. Does anyone believe that this is the most desirable diet that can be recommended and that questions about sugar intake are not germane? Does anyone believe that unlimited intake of sugar is desirable?
DIETARY
GOALS-PROGRESSIVE
1507
year period. This study would be easy to design but impossible to execute. Whatever the outcome of some of the current trials, such as the multiple risk factor intervention trials, they will not and cannot demonstrate the true effect of diet upon CHD. It should be noted that the reverse experience is happening all over the world-in groups that gain affluence and adopt our dietary pattern-with the expected results. Fortunately, most of the well-designed trials (20-22) have shown an amelioration of CHD after dietary modification which lowered the serum cholesterol. They indicate that advice to middle-aged men is not without benefit but, as expected, younger men have more to gain than older men. This favorable result, however, is probably not explained by a reversal or amelioration of atherosclerosis. It is more likely that these dietary effects are due to changes in platelet function, modifying the thrombotic process, which are probably mediated by prostaglandins (23). No responsible individual can conclude that further research is not necessary or that it will be unproductive. Research is the only source of new knowledge. The recent demonstration that high density lipoproteins are apparently protective against CHD is a case in point (24). This fmding, however, does not change the known fact that hypercholesterolemia is a potent risk factor. It should allow a better identification of high risk individuals and, if high density lipoprotein levels can be modified by diet or other things, may offer new avenues for prevention. Lack of knowledge, however, does not absolve the scientific community from making responsible decisions with the knowledge available. We will never know all that we should know. To the best of our knowledge then, overconsumption of food but particularly fat-especially saturated fat-of cholesterol, of sugar, and salt are contributors to the most important health problems of Americans and other affluent societies. Everyone-the public, the Congress, health professionals, etc.-want to know the best advice that can be offered at this time. They deserve to know. Given current knowledge, it is inconceivable that we can conclude that these issues are not relevant or that the “best” diet available is the one the average American eats. We know
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nary disease and stroke), that low salt intakes are therapeutic in many hypertensives, that many populations with low salt intakes do not have much hypertension, and that the actal physiological need for salt is probably less than a gram or so per day. How then can one conclude that an intake of 10 to 15 g of salt per day-nearly half the toxic dose-is safe and that no advice to the American public is needed. Common sense tells even the uninitiated that it is wise to limit salt intake. Indeed, if salt were a new food additive, it is doubtful that it would be classified as safe and certainly not at the level most of us consume. Similarly, if cholesterol were a new food additive we would cite the evidence that it produced hypercholesterolemia and atherosclerosis in animals, that it produces hypercholesterolemia in man, and that hypercholesterolemia and atherosclerosis are precursors of CHD. The conclusion would almost certainly be that cholesterol could not be considered safe at any level which raises the serum cholesterol level in man. Obviously, it would be desirable to pinpoint what would happen if Americans adopted more sensible dietary patterns, but consider the evidence with regard to diet and coronary heart disease where the most is known. There is abundant evidence to support the following sequence of events although the mechanisms at each step are not yet known: Inappropriate diet-hypercholesterolemia--* atherosclerosis-*CHD It is known that hypercholesterolemia begins to develop in adolescent boys, substantial atherosclerosis has developed by the time they are in their 20’s, but CHD, although occurring in a few very early, becomes a significant public health problem about 20 years later. Given this sequence, it would seem clear that dietary modification of atherosclerotic men in their 40’s and 50’s or older should not be expected to have much effect. The atherosclerotic lesion may not be completely irreversible but is probably nearly so in man. Thus, a definitive study to demonstrate the effect of diet upon CHD would require a study starting with adolescent boys, preventing hypercholesterolemia and atherosclerosis, and following them for a 20- or 30-
VIEW
1508
HEGSTED
from
experience with the RDA that we will debate endlessly about the details-should it be 0.6, 0.7, or 0.8 g of protein per kilogram or 4, 5, or 6 g of salt, etc.
can
long
and
we obviously about the
the honest decisions
fact is that compared to
ommendations sumption. populations
that
need to improve our most desirable levels, these are rather trivial general
do
dietary
influence
food
rec-
con-
Given the heterogeneity of the we must deal with, there is no level of anyting that is best for every-
absolute one. There
are obviously
two philosophies that may be used in establishing dietary recommendations, either of which can be defended. One is to establish desirable goals regardless of whether they can be achieved or not. The
RDA have often been defmed as “goals which we should strive to meet” even though the consequences of not achieving the specific goal cannot be precisely defmed. The other approach is to develop a specific “cut-off point,” below or above which, “health cannot be assumed.” These different approaches may yield somewhat different recommendations but some goals or guidelines are necessary. Above all, we cannot assume that die-
tary
habits
are immutable.
everything
that
States during is happening
has
the past all around
discussing “The and its Relationship to nand (25) emphasizes means of establishing esses of emergence so
shall
current
is denied
by
in the United 30 to 40 years and what
In
vival,” gence
This
happened
the world. Code of the Scientist Ethics”, Andr#{233}Courthat “We must fmd a control over the procas to favor man’s sur-
dietary
habits
emergence.”
represent
Our
knowledge is now available. The total evidence related
sugar,
how
dis-
how
much
much
desirable
argue learned advice sible.
hypertension, problems
of
in
that
salt,
fat, and the
how
what
much
kind
cholesterol,
of fat, etc. are
American diet? To simply ignorant, that we have not useful, and that we have no is self-defeating and irrespon-
we are
anything to offer,
References 1. Select Committee on Nutrition and Human Needs. U.S. Senate. Dietary Goals for the United States. Washington, D.C.: U.S. Government Printing Office, February 1977. 2. Select Committee on Nutrition and Human Needs. U.S. Senate. Dietary Goals for the United States (2nd ed). Washington, D.C.: U.S. Government Printing Office, December 1977. 3. LEVEILLE. G. A. Establishing and implementing dietary
4. 5.
6.
7. 8.
9. 10.
11.
to coronary
health
It is the responsibility of the nutrition community to provide some leadership. It must answer the questions put to it-How much
an example
of “blind emergence.” They can certainly not be said to have been planned for any nutritional purpose. Although the recommendation to “eat more meat, more milk, more eggs-more of everything-but don’t get fat” has characterized our nutritional strategy for the past 50 years, and nutritionists, therefore, bear some responsibility, these recommendations were not based upon any knowledge of the ultimate effects of such a diet. Such
cancer,
major
deficiencies are not the important nutritional problems of our population and a more moderate diet will not create nutritional deficiencies. If the proper dietary recommendations are not those specified in the Dietary Goals, they are certainly something very similar.
...
to as humanizing
diabetes,
etc.-the
Americans-indicates that a more moderate diet will lessen the impact of these diseases. There are no reasons to believe that such a diet will impose nutritional risks. Nutritional
and that “Unchecked, this blind emeroverpowers its antithesis, which I refer
stroke,
goals.
Family
Economics
Rev.
(Winter-
Spring). Washington, D.C.: U.S. Department of Agriculture Publ. ARS-NE-36, 1978, p.7. HARPER. A. E. Dietary goals-a skeptical view. Am. J. Chin. Nutr. 31: 310, 1978. Food and Nutrition Board. Recommended Dietary Allowances (8th ed). Washington, D.C.: National Academy of Sciences/National Research Council, 1974. Food and Nutrition Board. Recommended Dietary Allowances (rev.). Washington, D.C.: National Academy of Sciences/National Research Council, 1948. World Health Organization. Calcium requirements. Geneva: WHO Tech. Rept. Ser. No. 230, 1962. HEGSTED. D. M. Calcium and phosphorus. In: Modern Nutrition in Health and Disease (5th ed), edited by R. S. Goodhard and M. E. Shils. Philadelphia: Lea & Febiger, 1973, p. 268. HEGSTED. D. M. On dietary standards. Nutr. Rev. 36: 33, 1978. Food and Nutrition Board. Proposed fortification policy for cereal-grain products. Washington, D.C.: National Academy of Sciences, 1974. Select Committee on Nutrition and Human Needs. U.S. Senate. Statement of the American Medical
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/9/1504/4650709 by California Digital Library user on 01 January 2019
Although knowledge
ease, obesity,
DIETARY
12.
14.
15.
16.
17.
Association. In: Dietary Goals for the United States-Supplemental Views. Washington, D.C.: U.S. Government Printing Office, 1977, p. 670. Department of Health, Education and Welfare, Food and Drug Administration. Iron fortification of flour and bread. Federal Register 42: 59513, 1977. COATES, T. J., AND C. E. THORESEN. Treating obesity in children and adolescents: a review. Am. J. Public Health 68: 143, 1978. National Heart, Lung and Blood Institute. 1977 Working Group to Review the 1971 Report of the Task Force on Arteriosclerosis. Arteriosclerosis. Bethesda, Md.: DHEW Publication No. (NIH) 78-1526, 1977. KEYS. A. Overweight and the risk of heart attack and sudden death. Bethesda, Md.: Fogarty Center Conference on Obesity, NIH, 1973. Life Sciences Research Office. Evaluation of the Health Aspects of Sucrose as a Food Ingredient. Bethesda, Md.: Federation of American Societies for Experimental Biology, 1976. FRANK, C. G., G. S. BERENSON AND L. S. WEBBER. Dietary studies and the relationship of diet to cardiovascular disease risk factor variables in 10-yearold children-the Bogalusa heart study. Am. J. Cliii.
VIEW
1509
Nutr. 31: 328, 1978. MENEELY. G. R., AND H. D. BATFARBEE. Sodium and potassium. In: Present Knowledge of Nutrition. (4th ed). Washington, D.C.: The Nutrition Foundation, 1976. 19. Health Resources Administration. Health United States 1976-77 Chart Book. Bethesda, Md.: DHEW Pulbication No. (HRA) 77-1233, 1977. 20. LEREN, P. The Oslo diet-heart study. Eleven-year report. Circulation 42: 935, 1970. 21. MIETTINEN. M.,M. J. KARVONEN. 0. TURPEINEN. R. ELoSuo AND E. PAAVILAINEN. Effect of cholesterol-lowering diet on mortality for coronary heart disease and other causes. Lancet 2:835, 1972. 22. DAYTON. S., M. L. PEARCE. S. HASHIMOTO. W. J. DIXON AND U. TOMIYASU. A controlled clinical trial of a diet high in unsaturated fat. Am. Heart Ass. Mono. 25. New York: American Heart Association, Inc., 1969. 23. VERGROESEN, A. J. Physiological effects of dietary hnoleic acid. Nutr. Rev. 35: 1, 1977. 24. Anonymous. Diabetes, blood lipids and obesity: coronary heart disease. Nutr. Rev. In press. 25. COURNAND. A. The code of the scientist and its relationship to ethics. Science 198: 699, 1977. 18.
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/9/1504/4650709 by California Digital Library user on 01 January 2019
13.
GOALS-PROGRESSIVE
goals-a
progressive
view1
D. M. Hegsted,2 Ph.D.
The Dietary Goals for the United States published by the Senate Select Committee on Nutrition and Human Needs (1, 2) recommend that Americans should eat less food and specifically that they should eat less fat, particularly saturated fat, less cholesterol, less sugar, and less salt, and that they should increase their consumption of fruits, vegetables, grain products, and unsaturated oils. It is not surprising that various segments of the food-producing and manufacturing community fmd fault with these guidelines. Of more significance, perhaps, are the adverse comments of some of the current leaders of the nutrition community (3) such as the recent editorial by Harper (4). These opponents fmd the report either premature or unjustified on the basis of current knowledge. We should be very clear what is being said. Dr. Harper is either saying that the intake of fat, cholesterol, salt, and sugar has no nutritional significance and, therefore, does not deserve attention by serious nutritionists or the public, or that, having reviewed all of the evidence, the current American diet estimated to provide about 40% of the calories as fat, about 20% of the calories as sugar, 500 to 700 mg of cholesterol per day, and 8 to 10 g of salt is the best diet that can be recommended for Americans. We should note that these are estimates of average intake so that half of the population is consuming larger amounts. Frankly, I fmd it inconceivable that anyone familiar with the literature can arrive at either conclusion. The Dietary Goals have been criticized that they were not a complete prescription for health-that there was inadequate discussion of obesity, fluoridation, alcohol, exercise, etc. The legitimacy of this argument depends entirely upon one’s point of view. It is perfectly clear to everyone, however, that the Goals were not intended and do not pretend to be 1504
The American
Journal
of Clinical
Nutrition
a substitute for other well established information and other legitimate goals. What they were intended to do was to call forceful attention to issues that the nutrition and biochemical community have so far failed to deal with in adequate fashion. The Goals have been criticized on the basis that they did not provide adequate supporting evidence. This is true but the nature of a document depends upon the audience. It is equally valid to criticize the report of the Committee on Recommended Dietary Allowances (RDA) as not being interpretable to the general public (5). In either case, the reports require further interpretation-the first by the scientific community; the second by those dealing with the public. Rather invidious comparisons have been drawn between the RDA and the Dietary Goals with the implication that whereas the RDA are obviously justified, the Dietary Goals are not. The change in the Goals on salt intake in the second edition (2) is said to demonstrate that the recommendations are premature. We should compare what has happened to the RDA. In the 1948 edition (6) the recommended intake of riboflavin and vitamin C were much higher than they are currently and the recommended intake of iron was the same for men and women. The last edition (5) dropped the recommendation of vitamin C for men from 60 to 45 mg. Does this mean we never knew anything about desirable vitamin C intakes and possibly still do not? It has always been understood that dietary recommendations should be continuously reviewed and will inevitably change. Otherwise, research is useless. It should also be emphasized that the RDA From the Department of Nutrition, of Public Health, Boston, Massachusetts 2 Professor of Nutrition.
31: SEPTEMBER
1978, pp. 1504-1509.
Harvard 02115.
Printed
School
in U.S.A.
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/9/1504/4650709 by California Digital Library user on 01 January 2019
Dietary
in nutrition
DIETARY
GOALS-PROGRESSIVE
1505
large proportion of Americans are at risk from excessive intakes. The Food and Nutrition Board recently recommended an expanded fortification program (10). No demonstration of benefit from such a program was thought necessary as a prelude to implementation and it is doubtful that this should be required. Much has been made of the fact that iron deficiency is a problem in the United States and that decreased consumption of meat might exacerbate this problem. It is somewhat curious that the Food and Nutrition Board can recommend a protein intake that could be easily achieved without the consumption of any meat and object to a modest reduction in meat intake. Apart from this, there is a curious inconsistency in the way the American Medical Association (11) and Dr. Harper and others consider the major chronic diseases and iron deficiency. They argue that dietary recommendation for coronary artery disease, diabetes, etc. should be reserved as therapy after susceptibles have been identified while prevention of iron deficiency is a high priority item. Most nutritionists, I think, agree that iron deficiency ought to be prevented. Yet this is a disease that is easily identified, easily treated and, as far as we know, has no residual effects. Furthermore, the actual impairment in health of the modest degrees of iron deficiency which occur have been difficult to document (12). In contrast, coronary heart disease (CHD), stroke, diabetes, hypertension, etc. are devastating diseases and dietary or other forms of treatment are relatively ineffective. Any major health gains to be made in the United States must be aimed at prevention or amelioration of these diseases. A variety of critics have read more into the Dietary Goals than is there. Dr. Harper interprets them to say that obesity would disappear if the Goals were adopted! I do not fmd this in the document. He favors the advice to eat less food to which most of us will agree. He ignores the dismal record of failure associated with this advice (13). It is likely that the recommendation to modify the diet to a leaner, bulkier diet will assist in the control of food intake and, in fact, this is what many who treat obesity do recommend. The discussion of obesity points up another inconsistency in the way we view different
Downloaded from https://academic.oup.com/ajcn/article-abstract/31/9/1504/4650709 by California Digital Library user on 01 January 2019
have always been derived from informed judgment based upon all possible sources of information-epidemiology, metabolic studies with human subjects, and studies with experimental animals being the primary sources of information. If this procedure is valid for establishing “best estimates of nutrient need,” it is equally valid for establishing best estimates of desirable intakes of fat, sugar, salt, or any other dietary constituent. A major criticism of the Dietary Goals has been that there is no proof that adoption of the dietary pattern recommended will benefit the public. More will be said of this later but it is a somewhat strange argument for nutritionists to make. Where is the proof that an intake of 45 mg of vitamin C is better or worse than an intake of 60 or 70 mg? The FAO/ WHO group (7) recommends a calcium intake of 400 to 500 mg for adults whereas the RDA is 800 mg. There is no proof that an intake of either level is better or worse than the other. While I am critical of the 800 mg (8), it is obvious that recommendations do have to be made before all of the desired evidence is available and this has always been accepted. We should note that the RDA have always been set (at least in theory) at relatively high levels to minimize “risk” of deficiency. The nutrient needs of individuals do vary although we do not know by how much. Clearly, the recommended intake cannot be set at the estimated average need. While this leads us to the somewhat incongruous conclusion that practically everyone can consume less than the recommended intake and still be well fed (9), the basic argument must be valid. Obviously, in any field trial to demonstrate the validity of a RDA, it would be unlikely that one could demonstrate that the specified level was justified. If the RDA is correctly estimated, it follows that very few individuals would benefit from an intake that high. Similarly, it is perfectly clear that some individuals are more adversely affected by diets high in fat, cholesterol, salt, and sugar than others. A few will have little or nothing to gain from a lower intake in the same way that an individual with a vitamin A requirement of 2500 IU per day will have nothing to gain from an intake of 5000 IU. This, however, cannot mean that no advice about intake can be given to the public, particularly when a very
VIEW
1506
HEGSTED
It has been repeatedly emphasized that per capita sucrose intakes have not changed much in recent years. What is not emphasized is that other forms of purified sugar have increased. More importantly, perhaps, it is not emphasized that total energy consumption in the United States is now quite low. The Bogalusa children, for example, were consuming about 2100 kcal/day on the average compared with an RDA of about 2600 kcal. Continued consumption of the same amount of sugar with lower energy intakes means a larger proportion of the diet as sugar. I agree with the FASEB report that there is, so far, relatively little evidence that sugar is really “toxic” or that it can be directly associated with chronic disease in the same way as saturated fat. I do not agree that this means that one can ignore sugar in attempting to establish total dietary patterns and that sugar consumption is of no concern, We could, of course, reduce our fat intake and replace it by sugar. I believe this would be a ridiculous recommendation. A high sugar intake has no known nutritional merit and cannot be recommended. There is another curious dichotomy in the way many appear to view materials already in the food supply and those that are new. Everyone with an understanding of the principles of statistics and toxicology agrees that if we are to evaluate the safety of a material of suspected toxicity, it must be fed or administered at levels substantially above those which will ordinarily be encountered in the environment. Many believe that an exposure of 1/100 of the demonstrated toxic dose in animals could be considered to be safe in man. Obviously, this 100:1 tolerance cannot be achieved with many of the essential nutrients. Yet if one considers the data on salt, we know that high intakes cause hypertension in animals, that an intake of 30 to 40 g in man is toxic in man (18), that recent health statistics (19)
show
a rapidly
increasing
proportion
of
the population with age who have frank hypertension reaching the amazing values of 30 to 60% of the total adult population over 55 years of age (this ignores the fact that the blood
pressure
age and that is associated
of most
any with
Americans
increase in blood an increased risk
rises
with
pressure of coro-
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problems. The association of various chronic diseases with obesity is, of course, well known. Many have automatically assumed this to be a causal relationship. The best evidence (14) is that, except for gross obesity, the additional body fat itself does not impose much of a health hazard whereas the risks associated with hyperholesterolemia, hypertension, and diabetes are clear. The degree to which these risks are associated with or causally related to obesity are not yet known (15). There has been little demand for a direct demonstration that weight reducing regimes actually improve health or life expectancy and, in view of the record of such programs, it will be extremely difficult to demonstrate. Apparently, we simply know that obesity is bad. Similarly, we apparently know that exercise is good. There have been few studies aimed at demonstrating the effects of exercise upon morbidity or mortality and the current evidence is that modest exercise does not have a major positive effect. This is not to say that exercise should not be recommended but the evidence available should be weighed objectively. The recommendation to limit sugar intake has been attacked and the report of the Life Sciences Research Office of FASEB (16) is referred to as demonstrating lack of evidence to support the recommendations. In my opinion, this report is “technically correct and practically useless.” The Committee simply failed to consider the appropriate question-”How much sugar is desirable in the diet?” This question cannot be answered from a consideration of sugar alone. In the same issue of the American Journal of Clinical Nutrition in which Dr. Harper’s article appeared, there is a report on the dietary habits of Bogalusa children 10 years of age (17). The average sucrose intake was 98 g per day. This is apparently about the national per capita average and means that half of the children were consuming more than this. Approximately 37% of the sugar came from soft drinks and 25% from candy. Does anyone believe that this is the most desirable diet that can be recommended and that questions about sugar intake are not germane? Does anyone believe that unlimited intake of sugar is desirable?
DIETARY
GOALS-PROGRESSIVE
1507
year period. This study would be easy to design but impossible to execute. Whatever the outcome of some of the current trials, such as the multiple risk factor intervention trials, they will not and cannot demonstrate the true effect of diet upon CHD. It should be noted that the reverse experience is happening all over the world-in groups that gain affluence and adopt our dietary pattern-with the expected results. Fortunately, most of the well-designed trials (20-22) have shown an amelioration of CHD after dietary modification which lowered the serum cholesterol. They indicate that advice to middle-aged men is not without benefit but, as expected, younger men have more to gain than older men. This favorable result, however, is probably not explained by a reversal or amelioration of atherosclerosis. It is more likely that these dietary effects are due to changes in platelet function, modifying the thrombotic process, which are probably mediated by prostaglandins (23). No responsible individual can conclude that further research is not necessary or that it will be unproductive. Research is the only source of new knowledge. The recent demonstration that high density lipoproteins are apparently protective against CHD is a case in point (24). This fmding, however, does not change the known fact that hypercholesterolemia is a potent risk factor. It should allow a better identification of high risk individuals and, if high density lipoprotein levels can be modified by diet or other things, may offer new avenues for prevention. Lack of knowledge, however, does not absolve the scientific community from making responsible decisions with the knowledge available. We will never know all that we should know. To the best of our knowledge then, overconsumption of food but particularly fat-especially saturated fat-of cholesterol, of sugar, and salt are contributors to the most important health problems of Americans and other affluent societies. Everyone-the public, the Congress, health professionals, etc.-want to know the best advice that can be offered at this time. They deserve to know. Given current knowledge, it is inconceivable that we can conclude that these issues are not relevant or that the “best” diet available is the one the average American eats. We know
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nary disease and stroke), that low salt intakes are therapeutic in many hypertensives, that many populations with low salt intakes do not have much hypertension, and that the actal physiological need for salt is probably less than a gram or so per day. How then can one conclude that an intake of 10 to 15 g of salt per day-nearly half the toxic dose-is safe and that no advice to the American public is needed. Common sense tells even the uninitiated that it is wise to limit salt intake. Indeed, if salt were a new food additive, it is doubtful that it would be classified as safe and certainly not at the level most of us consume. Similarly, if cholesterol were a new food additive we would cite the evidence that it produced hypercholesterolemia and atherosclerosis in animals, that it produces hypercholesterolemia in man, and that hypercholesterolemia and atherosclerosis are precursors of CHD. The conclusion would almost certainly be that cholesterol could not be considered safe at any level which raises the serum cholesterol level in man. Obviously, it would be desirable to pinpoint what would happen if Americans adopted more sensible dietary patterns, but consider the evidence with regard to diet and coronary heart disease where the most is known. There is abundant evidence to support the following sequence of events although the mechanisms at each step are not yet known: Inappropriate diet-hypercholesterolemia--* atherosclerosis-*CHD It is known that hypercholesterolemia begins to develop in adolescent boys, substantial atherosclerosis has developed by the time they are in their 20’s, but CHD, although occurring in a few very early, becomes a significant public health problem about 20 years later. Given this sequence, it would seem clear that dietary modification of atherosclerotic men in their 40’s and 50’s or older should not be expected to have much effect. The atherosclerotic lesion may not be completely irreversible but is probably nearly so in man. Thus, a definitive study to demonstrate the effect of diet upon CHD would require a study starting with adolescent boys, preventing hypercholesterolemia and atherosclerosis, and following them for a 20- or 30-
VIEW
1508
HEGSTED
from
experience with the RDA that we will debate endlessly about the details-should it be 0.6, 0.7, or 0.8 g of protein per kilogram or 4, 5, or 6 g of salt, etc.
can
long
and
we obviously about the
the honest decisions
fact is that compared to
ommendations sumption. populations
that
need to improve our most desirable levels, these are rather trivial general
do
dietary
influence
food
rec-
con-
Given the heterogeneity of the we must deal with, there is no level of anyting that is best for every-
absolute one. There
are obviously
two philosophies that may be used in establishing dietary recommendations, either of which can be defended. One is to establish desirable goals regardless of whether they can be achieved or not. The
RDA have often been defmed as “goals which we should strive to meet” even though the consequences of not achieving the specific goal cannot be precisely defmed. The other approach is to develop a specific “cut-off point,” below or above which, “health cannot be assumed.” These different approaches may yield somewhat different recommendations but some goals or guidelines are necessary. Above all, we cannot assume that die-
tary
habits
are immutable.
everything
that
States during is happening
has
the past all around
discussing “The and its Relationship to nand (25) emphasizes means of establishing esses of emergence so
shall
current
is denied
by
in the United 30 to 40 years and what
In
vival,” gence
This
happened
the world. Code of the Scientist Ethics”, Andr#{233}Courthat “We must fmd a control over the procas to favor man’s sur-
dietary
habits
emergence.”
represent
Our
knowledge is now available. The total evidence related
sugar,
how
dis-
how
much
much
desirable
argue learned advice sible.
hypertension, problems
of
in
that
salt,
fat, and the
how
what
much
kind
cholesterol,
of fat, etc. are
American diet? To simply ignorant, that we have not useful, and that we have no is self-defeating and irrespon-
we are
anything to offer,
References 1. Select Committee on Nutrition and Human Needs. U.S. Senate. Dietary Goals for the United States. Washington, D.C.: U.S. Government Printing Office, February 1977. 2. Select Committee on Nutrition and Human Needs. U.S. Senate. Dietary Goals for the United States (2nd ed). Washington, D.C.: U.S. Government Printing Office, December 1977. 3. LEVEILLE. G. A. Establishing and implementing dietary
4. 5.
6.
7. 8.
9. 10.
11.
to coronary
health
It is the responsibility of the nutrition community to provide some leadership. It must answer the questions put to it-How much
an example
of “blind emergence.” They can certainly not be said to have been planned for any nutritional purpose. Although the recommendation to “eat more meat, more milk, more eggs-more of everything-but don’t get fat” has characterized our nutritional strategy for the past 50 years, and nutritionists, therefore, bear some responsibility, these recommendations were not based upon any knowledge of the ultimate effects of such a diet. Such
cancer,
major
deficiencies are not the important nutritional problems of our population and a more moderate diet will not create nutritional deficiencies. If the proper dietary recommendations are not those specified in the Dietary Goals, they are certainly something very similar.
...
to as humanizing
diabetes,
etc.-the
Americans-indicates that a more moderate diet will lessen the impact of these diseases. There are no reasons to believe that such a diet will impose nutritional risks. Nutritional
and that “Unchecked, this blind emeroverpowers its antithesis, which I refer
stroke,
goals.
Family
Economics
Rev.
(Winter-
Spring). Washington, D.C.: U.S. Department of Agriculture Publ. ARS-NE-36, 1978, p.7. HARPER. A. E. Dietary goals-a skeptical view. Am. J. Chin. Nutr. 31: 310, 1978. Food and Nutrition Board. Recommended Dietary Allowances (8th ed). Washington, D.C.: National Academy of Sciences/National Research Council, 1974. Food and Nutrition Board. Recommended Dietary Allowances (rev.). Washington, D.C.: National Academy of Sciences/National Research Council, 1948. World Health Organization. Calcium requirements. Geneva: WHO Tech. Rept. Ser. No. 230, 1962. HEGSTED. D. M. Calcium and phosphorus. In: Modern Nutrition in Health and Disease (5th ed), edited by R. S. Goodhard and M. E. Shils. Philadelphia: Lea & Febiger, 1973, p. 268. HEGSTED. D. M. On dietary standards. Nutr. Rev. 36: 33, 1978. Food and Nutrition Board. Proposed fortification policy for cereal-grain products. Washington, D.C.: National Academy of Sciences, 1974. Select Committee on Nutrition and Human Needs. U.S. Senate. Statement of the American Medical
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Although knowledge
ease, obesity,
DIETARY
12.
14.
15.
16.
17.
Association. In: Dietary Goals for the United States-Supplemental Views. Washington, D.C.: U.S. Government Printing Office, 1977, p. 670. Department of Health, Education and Welfare, Food and Drug Administration. Iron fortification of flour and bread. Federal Register 42: 59513, 1977. COATES, T. J., AND C. E. THORESEN. Treating obesity in children and adolescents: a review. Am. J. Public Health 68: 143, 1978. National Heart, Lung and Blood Institute. 1977 Working Group to Review the 1971 Report of the Task Force on Arteriosclerosis. Arteriosclerosis. Bethesda, Md.: DHEW Publication No. (NIH) 78-1526, 1977. KEYS. A. Overweight and the risk of heart attack and sudden death. Bethesda, Md.: Fogarty Center Conference on Obesity, NIH, 1973. Life Sciences Research Office. Evaluation of the Health Aspects of Sucrose as a Food Ingredient. Bethesda, Md.: Federation of American Societies for Experimental Biology, 1976. FRANK, C. G., G. S. BERENSON AND L. S. WEBBER. Dietary studies and the relationship of diet to cardiovascular disease risk factor variables in 10-yearold children-the Bogalusa heart study. Am. J. Cliii.
VIEW
1509
Nutr. 31: 328, 1978. MENEELY. G. R., AND H. D. BATFARBEE. Sodium and potassium. In: Present Knowledge of Nutrition. (4th ed). Washington, D.C.: The Nutrition Foundation, 1976. 19. Health Resources Administration. Health United States 1976-77 Chart Book. Bethesda, Md.: DHEW Pulbication No. (HRA) 77-1233, 1977. 20. LEREN, P. The Oslo diet-heart study. Eleven-year report. Circulation 42: 935, 1970. 21. MIETTINEN. M.,M. J. KARVONEN. 0. TURPEINEN. R. ELoSuo AND E. PAAVILAINEN. Effect of cholesterol-lowering diet on mortality for coronary heart disease and other causes. Lancet 2:835, 1972. 22. DAYTON. S., M. L. PEARCE. S. HASHIMOTO. W. J. DIXON AND U. TOMIYASU. A controlled clinical trial of a diet high in unsaturated fat. Am. Heart Ass. Mono. 25. New York: American Heart Association, Inc., 1969. 23. VERGROESEN, A. J. Physiological effects of dietary hnoleic acid. Nutr. Rev. 35: 1, 1977. 24. Anonymous. Diabetes, blood lipids and obesity: coronary heart disease. Nutr. Rev. In press. 25. COURNAND. A. The code of the scientist and its relationship to ethics. Science 198: 699, 1977. 18.
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13.
GOALS-PROGRESSIVE
