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166

DIETARY FIBER IN AND DISEASE*l GILBERT A. LEVEILLE Michigan State University

Nutritionists have been concerned over the past several decades with the elucidation of the qualitative and quantitative aspects of essential for and wellbeing in man under a variety of physiologicsl conditions. As a consequence we have developed a reasonably good overview of the needs of man during various stages of the cycle as well as during specific physiological stress situations such as , lactation and growth. To be sure, a great deal more research is needed in each of these areas. For example, we are only beginning to understand the essentiality of the trace elements in our . Likewise we are only beginning t:, recognize the changes in nutrient needs which occur under various physiological conditions. Thus, while our knowledge has expanded tremendously, there is obviously a need for much more research before we fully understand the qualitative and quantitative nutrient needs of under all circumstances. In this rush to ascertain the essentiality of varims nutrients, we have failed to consider those components of our diets for which we could not demonstrate an essential role. is one such component. The only physiological role which could be ascribed to the fibrous material in our diets was that of a laxative. It was recognized that a certain arnmnt of fibrous material was desirable for the maintenance of normal laxation.

As a result there has been little concern over the fact that our diets have been providing less and less fiber during the last century. Fiber is provided in our diets primarily from , fruits and vegetables. We have seen a very marked reduction in ~urconsumption 3f and in certain fruits and vegetables. In particular our consumption of potat3es has decreased markedly during the last 60-70 years. Accompanying this reduction in cereal and potat3 intake has been an increase in the proportion of our total derived from animal products which contain no fiber. These changes in our dietary pattern are readily apparent if one studies the data available relative to the disappearance of from the market place or that limited amount of information available on actual food consumption patterns. It is obvims from the data presented in table 1, that the availability and consumption of fiber has been reduced. This is certainly not a new observation, but rather one which was felt to be relatively insignificant until recent years.

* Presented at the 28th Annual Reciprocal Meat Conference of the American Meat Association, 1975. Michigan Agricultural Experiment Station Journal Article No. 7330. Table 1. Trends in Annual Per Capita Food Availability 1

Meat, poultry & fish, lbs 176 192 2 03 Eggs, lbs 47 45 39 Dairy products, qts 236 240 237 and oils, lbs 57 57 57 Fruit, lbs 208 183 160 Potatoes, lbs2 123 110 101 Other vegetables 232 2 09 208 Flour and cereals, lbs 171 148 147 and sweeteners, lbs 110 106 112

Friend, B. Am. J. Clin. Nutr. 20:907, 1967 (1). Includes sweet potatoes.

The current concern, with regard to the role of dietary fiber, stems from the astute observations of British investigators, particularly Burkitt and Trowel1 (2,3). These two physicians observed that the incidence of specific types of diseases was lower in developing countries in Africa as compared to western countries. Their initial observations lead them to conclude that some component of the environment which differed between these two cultures must be responsible for the differences in incidence of various diseases. After considerable research, they have concluded that the difference can probably be related to the decreased consumption of dietary fiber in western countries as contrasted to the very high intakes of fiber in developing countries relying on cereal grains as a staple of their diets. Their tentative conclusions are reasonable in light of available evidence and enable the development of attractive hypotheses which would explain the incidence of sane diseases of western society. However, it must be kept in mind that the associations which have been developed by and large are corre- lative and do not necessarily prove cause and effect. As I will point out later in this discussion, one can develop any number of statistically, very significant correlations; however, one must interpret these apparent associations with great caution.

Let us first examine the definition of dietary fiber. Dietary fiber is not equivalent to crude fiber. In c)ur routine analysis of and feeds, we determine what is known as crude fiber and this is the value reported €n food tables. Crude fiber is the material remaining after rather rigorous treatment of a food or feed sample with acid and alkali. The residue probably reflects the and lignin content of a food. The total of foods is generally taken to be that material remaining after moisture, ash, and have been accounted for. The difference between total carbohydrate and crude fiber is considered to be the "available" carbohydrate. A portion of the material accounted for 168 in the "available carbohydrate'' component is really unavailable carbohydrate. For most foods this represents a relatively small component; hmever, from the standpoint of the undigested residue of a food it can be quite significant. Thus, for purposes of this discussion when I refer to "dietary fiber" I will be referring to the cmbined undigested in food. Dietary fiber would encompass the cellulose and lignin found in crude fiber, but would also contain the hemicellulose, pectic substances, gums and other carbDhydrates which are not normally digested by non-ruminant organisms including man. Thus, it is important to keep in mind when we consider dietary fiber, that it is not equivalent to crude fiber. Table 2 shows the level of various dietary fiber components found in cereal products.

Table 2. Components of "Dietary Fiber" In Some Foods1

Product Cellulose Hemicellulose Pent osans Lignin B 5 k k Who le 2 *5 5 -0 6.4 0.8 Whit e bread u- * * *

Shredded wheat cereal 2 -9 7.1 7 0.8 Wheat flake cereal 2.1 4.1 6.2 0.8

* Not detectable. Adapted from Eheart and Mason. Cereal Chem. 47:715. 1970 (4).

Let us now briefly consider those diseases which have been related to low dietary fiber intake. Those which have received the greatest attention are diverticular disease, of the colon, and atherosclerosis associated with hypercholesteremia. Some of the other diseases which have been related to low intakes of dietary fiber are appendicitis, hiatal hernia, irritable bowel syndrome, and hemorrhoids. These disease entities are quite common in western cultures, but are relatively rare in developing countries where the diet supplies much greater quantities of dietary fiber. This is the relationship which investigators such as Burkitt and Trowel1 have used to imply that one could reverse the trends toward increased incidence of these conditions by increasing the fiber in our diets. I would like to consider specifically the available evidence supporting the relationship of low fiber intake to the increased incidence of diverticular disease, cancer of the colon, and atherosclerosis. Diverticular disease refers to a condition in which there is an "out- pouching" or "ballooning" of the intestinal wall. This condition is thought to be virtually endemic in western societies. The diverticula themselves do not present a specific problem unless they become inflamed and the condition known as diverticulitis develops. Until recently the standard dietetic management of patients suffering from diverticular disease has involved a low residue diet, in essence diets virtually devoid of dietary fiber. Recent work by British investigators, particularly Painter and Burkitt (5), have shown that the disease is more effectively treated by providing diets high in dietary fiber, indicating that the traditional treatment is, in fact, contraindicated. These initial studies have been supported by those of numerous other clinical investigators.

The reasons for this appear quite logical. Dietary fiber has two major effects in the intestine. It increases the weight of the stool, largely because it absorbs large amounts of . The increase in bulk also reduces the transit time, that is the length of time required for a to traverse the digestive tract is shortened and hence the residence time or the amount of time that a material is in the intestine is reduced.

Table 3. Influence of "Dietary Fiber" on Stool Weight and Intestinal Transit Time in Humans'

Control Bran A k

Transit time, hrs 66 50 -24 Stool weight, G/da 120 183 f52

Adapted from Findlay --et al., Lancet Feb. 2, 1974. p 146 (6).

It has been proposed that diverticular disease develops as a consequence of having a relatively small, hard and dry residue in the intestine. As a consequence, movement through the intestine is slowed with a resulting increase in pressure within the colon. This increased pressure results in bulging of weak spots in the intestinal wall resulting in the formation of diverticuli. The clinical evidence available is in accord with this hypothesis and supports the use of high residue diets in the treatment of diverticular disease.

Let us now turn our attention to the possible'effects of dietary fiber on hypercholesteremia and caldiovascular disease. It is well established that there is a positive correlation between elevated blood levels and the incidence of atherosclerosis. Hypercholesterolemia represents one of the major risk factors in the developnent of atherosclerosis. Numerous studies have shown that, generally, populations in developing countries have significantly lower blood cholesterol levels than do individuals from developed countries. The major working hypothesis has been that the elevation in blood cholesterol levels in the developed countries is the result of om high intake of fats, particularly animal fats. We must remember that as animal products, including animal fat, increase in our diets they do so at the expense of those food items which are high in dietary fiber, namely cereals, fruits and vegetables, particularly cereal fmds. Thus, one can demonstrate on a population basis that the correlation between blood cholesterol levels and dietary fat intake is no better than the correlation between blood cholesterol level and dietary fiber except that the latter is a negative correlation. Several studies in both experimental animals and humans have clearly shown that components of dietary fiber can significantly reduce the circulating cholesterol level.

Table 4. Effect of Cellulose on Plasma Cholesterol and Bile Acid of Rats’

Plasma Fecal Diet cholesterol bile acid

Basal 64 4 93 Basal + 1.55 chd. 147 a .2 Basal + 1.5$ chol. + 2% cell. 91 18.5 Basal + 1.5$ chol. + 2@ cell. + 1% sulfapantdine 93 18.5

Adapted from Sundaravalli et al., J. Ag. Food Chem. 19:116. 1971 (7).

For example, it has been shown (table 4) that the addition of cellulose to the diet of rats fed cholesterol would overcome the increase in plasma cholesterol produced by dietary cholesterd. Further the data suggest that this depression is not due to an alteration of the intestinal microflora. The feeding of cellulose not only reduced the plasma cholesterol level but increased the excretion of bile acids in the .

Such studies have also been conducted with native fibrous materials derived from various cereal products.

F6r example, as shown in table 5, the hypercholesteremic effect of a cholesterol containing diet for rats could be overcome by the including of barley, rolled oats or whole wheat bread in their diet.

When similar studies were extended to man (table 6) it was observed that the ingestion of rolled oats did indeed depress serum chcdesterol levels and return to the control diet, free of rolled oats, resulted in an increase in the cholesterol level. Table 5. Influence of "Dietary Fiber" on Serum Cholesterol of Rats Fed a Hypercholesterolemic Diet'

Diet Serum cholesterol

$ of control

Basal 100 Barley 50 Rolled oats 27 Whole wheat bread 41

Adapted from DeGroot et al., Lancet, Aug. 10, 1963. p 303 (8).

Table 6. Effect of 140 g/day of Rolled Oats on 1he Serum Cholesterol Level of 21 Human Subjects

Period Serum cholesterol

Control diet 251 Rolled oats-- 7 day 239 --21 day 223 Control diet-14 day 246

~~ ~ ~

Adapted from DeGroot -et a1,*, Lancet Aug. 10, 1963. p 303 (8).

Table 7. Influence of Components of Rolled Oats on Serum Cholesterol Levels of Rats 1

Diet Serum cholesterol 5 of control

Basal 100 Rolled oats 18 Defatted rolled oats 39 Oat 46 Defatted rolled oats + corn oil 20

Adapted from DeGroot -et a1,*I hncet, Aug. 10, 1963. p 303 (8). An extension of these studies to determine the component of rolled oats responsible for this response demnstrated that the lipid component was partially responsible but that another component in the defatted rolled oats also produced a significant effect (table 7).

Several other studies have been conducted to ascertain the cholesteml depressing effect of pectin substances in the diet. In both animals and man it has been clearly shown that the addition 3f pectin to diets would depress the circulating cholesterol level and increase the excretion of bile acids (table 8).

Table 8. Effect of Pectin Supplementation in Cholesterol-Fed Rats'

Additions to the diet Cholesterol (1%) Cholesterol (1%) + pectin (5%)

Plasma cholesterol, mg/lOO ml 128 +-3 116 +5 Liver lipid, mg/g 7 .UO .3 6 .&0.3 Liver cholesterol, mg/g 10.350.5 7.5k0.3 Fecal sterols, %/day 142 +5 141 28 Fecal bile acids, %/day 18 52 24 +3

Adapted from kveille and Sauberlich, J. Nutrition. 1966 (9).

Recently Bennick and Chenoweth (10) have initiated investigations of the effects of oats in the diet of chicks on circulating cholesterol levels, fecal sterol and bile acid excretion. The dietary treatments employed are depicted in table 9. Diets A through D were found to contain 3.5$, 6.4$, l6.@ and 19.88 dietary fiber, respectively.

Table 9. Composition of Experimental Diets'

Dietary Treatment component A B C D

Basal diet2 57 57 57 57 43 40 -- Oats 43 40 Cellulose -- 3

From Bennink and Chenoweth (10). Basal diet contained as a percentage of the final diet: soybean oil meal, 45; cholesterol, 0.6; mix, 6; mix, 0.9; choline cl, 0.2; D1-, 0.3; corn oil, 4. The effects of these diets on various parameters are shown in table 10. It is apparent that dietary cellulose had little effect on the para- meters studied. Oats, on the other hand, significantly reduced circulating cholesterol levels and increased total lipid and bile acid excretion.

Table 10. Effect of Diet on Serum and Liver Cholesterol, and on Sterol, Total kipid and Bile Acid Excretion in the Chick

~ ~~~ -~ ~~

Treatment group A B C D

Serum cholesterol, mg/lOO ml 27’f&1$ 303tll 232-1 io 24P13 Liver cholesterol, mg/g 172 2 2 2oi 3 20? 3 Fecal excretion, mg/day bird: 1% Neutral sterol 444+11 488t 13 367k28 47252 Total lipid 23R27 2213590 2650~43 32112 142 Bile acid 10% 4 1025 5 312t19 342+-20

1 Frcan Bennink and Chenoweth (10). Mean for 10 chicks rt SEM .

The mechanism by which these dietary components depress cholesterol is not clear, however, the available evidence suggests that this effect is brought about by the binding of bile acids to dietary fiber components in the intestine. In the case of dietary pectin and various cereal products which have been studied, it is clear that the excretion of bile acids is increased.

Thus, one can develop a plausible hypothesis for this mechanism whereby bile acids which are normally secreted into the intestine by way of the bile serve to emulsify for their and absorption and are subse- quently reabsorbed and enter the bile acid pool of the body. If dietary fiber does indeed bind with bile acids and thereby inhibit their reabsorption, the size of the bile acid pool would be reduced. This might have the effect of increasing the conversion of cholesterol to bile acids and possibly lowering the circulating level of cholesterol.

This hypothesis remeins to be proven, but on the basis of available evidence would appear to be a verly likely explanation. This would not necessarily prove that the ingestion of diets containing greater amounts of dietary fiber would reduce the incidence of . However, the available data are suggestive that this might be the case and additional studies in this area are certainly warranted. I would next like to consider the other disease entity which has been related to a low intake of dietary fiber and that is cancer of the colon. This is an area which is emotional and probably the one for which the least data are available. The evidence available suggests that the incidence of cancer of the colon is considerably lover in those countries consuming greater quantit%es of dietary fiber. Further, the incidence of cancer of the colon has been increasing over the past century in developed countries. The increased incidence can be correlated with the reduction in dietary fiber consumption or with the increased consumption of animal products.

Table 11. Correlation between Incidence of Cancer of Large Intestine In Connecticut Males and Consumption of Various Products’

Correlation coefficient

Consumption of: Beef +O .go5 Meat, poultry and fish +O .941 Cereals -0e974 Potatoes -0.g68

From Leveille, J. him. Sci. (11).

I hasten to point out that this does not prove that cancer of the colon is due to a reduced consumption of dietary fiber nor does it prove that the increased incidence is directly related to the greater consumption of animal fats and protein. However, the statistical association is suggestive and does demand further attention.

The causes of cancer of the colon are not clear, however, the epidemio- logical evidence would suggest that an envimnmental factor, probably diet, is related to the development of colonic cancer.

For example, it has been observed that Japanese residing in Japan have a very low incidence of colonic cancer, whereas Japanese residing in Hawaii have a significantly higher incidence of the disease and in males the incidence is virtually identical to that of white males in the U.S. All of the evidence available, however, is epidemiological in nature.

The reason for this is fairly obvious. We do not have adequate models to study the development of colonic cancer over a protracted period of time. Thus, in order to conduct such studies the appropriate model must be available, that is a model which does develop cancer of the colon and studies must then be conducted over an extended period of time. Keeping in mind that such studies have not been conducted, we might briefly consider the possible involvement of dietary fiber in the development of colonic cancer. The development of cancer is dependent upon the presence of a carcinogen which can interact with a tissue at an adequate concentration and for a sufficient time. We do not know the identity of the carcinogen responsible for colonic cancer. It has been speculated that some components of the diet may be converted by intestinal microorganisms to carcinogenic substances. Ammonia or some bile acids have been proposed to be carcinogenic. In any event, the carcinogenic mterial apparently results from microbiological action on diet residues in the colon. Whether the product formed is ammonia resulting from the action of microorganisms on residual protein or whether it is the conversion of a bile acid to a different compound which is carcinogenic we do not how. However, one of the current working hypotheses is that some dietary residue serves as a for microorganisms in the colon. These microorganisms produce a product which is carcinogenic if it is present at a high enough concentration and if it resides in the colon for an adequate period of time. Based on this hypothesis we might now consider how dietary fiber could overcome this effect.

It is conceivable that a diet high in dietary fiber would alter the composition of the micrsorganisms in the colon resulting in a different microflora which would possibly eliminate or inhibit the production of carcinogens, or a diet, high in fiber might contain less of the substrate which is converted by microbiological action to a carcinogen. A second possibility is that dietary fiber, by decreasing the transit time of food residues through the intestine, would reduce the exposure time of the tissue to a carcinogen. Thirdly, by increasing the water content in the colon, dietary fiber might function to reduce the concentration of potential carcinogens.

I have attempted to point out the current state of our knowledge with regard to the effects of dietary fiber as it might relate to human health. It must be kept in mind that certainly in the case of the possible relationship of dietary fiber to heart disease and to cancer of the colon we do not have experimental evidence available to demonstrate that increasing our consumption of dietary fiber would be beneficial. Hopefully, definitive evidence regarding the role of dietary fiber as it relates to these two disease entities will be forthcoming. For the moment we are faced with the question of whether, on the basis of available evidence, it is desirable to increase our consumption of dietary fiber. This is not a simple question to resolve for we do not have factual information from which to arrive at an answer.

We can partially address the question, however, by considering another nutritional problem which exists in this country, namely the problem of . In dealing with this condition, a reduction in caloric intake is essential. This could be accomplished by reducing our consumption of animal products and increasing our intake of cereal products. The net effect of such a diet would be to reduce our fat consumption and to increase our consumption of carbohydrate and of dietary fiber. Such a change in dietary pattern would have no known deliterious effect, and conceivably could have a beneficial effect. I should point out one concern which should be kept 51 mind, that is, the ability of dietary fiber to bind other nutrients in the intestine. It is known that some indigestible components, nanely phytic acid, can bind some trace elements and in experimental animals produce a deficiency of trace elements. This must certainly be considered as we grapple with the question of increasing the amount of dietary fiber in the American diet.

Decisions regarding a dietary change must be individual ones. The available evidence is certainly not adequate to warrant a major change in the diet of the tota1U.S. population, however, the need for further research is apparent and we must do a better job of informing the public of the state of our knowledge regarding the possible desirable as well as deliterious effects of the changes which are occurring in our diet.

Literature Cited

1. Friend, B. 1967. Nutrients in United States Food Supply. A review of trends, 1909-1913 to 1965. her. J. Clin. Nutr. 20:907. 2. Burkitt, D. P. 1973. Some diseases characteristic of modern Western Civilization. Brit. Med. J. 1:274. 3. Trowell, H. C . 1972. Ischemic heart disease and dietary fiber. her. J . Clin. Nutr . 25:926. 4. Eheart, J. F. and B. S, Mason. 1970. Nutrient composition of selected and wheat products. V . Carbohydrate. Cereal Chem. 47:715. 5. Painter, N. S., A. Z. Almeida and K. W. Colebourne. 1972. Unprocessed bran in treatment of diverticular disease of the colon. Brit. Med. J. 2:137.

6. Findlay, J. M., A. N. Smith, W. D. Mitchell, A.J.B. Anderson and M.A. Eastwood. 1974. Effects of unprocessed bran on colon function in normal subjects and in diverticular disease Lancet 1:146.

7. Sundaravalli, 0. E., K. S. Shurpalikar and M. Narayani Rao. 1971. Effects of dietary cellulose supplements on the body composition and cholesterol of albino rats. J. Agr. Food Chem. 19:116.

8. DeGroot, A. P., R. Lugken and N. A. Pikaar. 1963. Cholesterol-lowering effect of rolled oats. Lancet 2:303.

9. Leveille, G. A. and H. Sauberlich. 1966. Mechanism of the cholesterol- depressing effect of pectin in the cholesterol-fed rat. J. Nutrition 88:2O9

10. Bennink, M. and W. Chenoweth. 1975. Personal communication. 11. Leveille, G. A. 1975. Issues in human nutrition and their probable impact on foods of animal origin. J. Anim. Sci. (In press). P. E. McClain: If the speakers will please come up to the podium again we will open the session for questions and discussion. I am going to take the Chairman's perogative here and ask the first question. Dr. Leveille, would you care to respond to this one? What is the impact of the reduced RDA for protein going to be on our fiber problem? Is it going to eliminate itself?

G. A. Leveille: Obviously, changing the RDA in and of itself does absolutely nothing to what people consume. The RDA is simply an indi- cation of need, and the fact that it is re-evaluated and re-assessed certainly does not mean that people are going to consume any less of anything. I think it is quite apmrent that since the new RDA has come out people have not reduced their intake of protein. It is still 2 to 2 1/2 times the RDA and I expect it to stay there.

Unidentified: I would like to ask Dr. Leveille a question in regard to fiber. In the cereal fiber, one of the disadvantages you pointed out is phytic acid. Is it possible that we could use a gastric compment, say cellulose, which is used in rat feeding experiments. Here we have no phytic acid and if we added some of this to the diet we might possibly reduce enormous intakes of food and yet at the same time get some of the advantages of cholestrol reduction if we have a very high meat diet.

G. A. Leveille: I think that is possible and a number of pharma- ceutical compnies are now formulating cellulated products. However, I think it should be pointed out that most of the work that has been done to date demonstrates that cellulose per se is rather ineffective, at least in-so.-far as blood serum detection is concerned. Preliminary data that we have to date suggests that gums and hemi-cellulases are the most effective components of dietary fiber. In-so-far as the effect on diverticulosis, I think there is simply bulk in cellulose, which in pure cellulose, would be as effective as anything else. In the case of cancer of the colon we simply don't know.

E. E. Schafer: I would like to ask Dr. kveille about a couple of slides in the middle of the presentation. At one point you said that feeding rolled oats wmld reduce serum cholesterol up to about 75$. The two slides that immediately followed that showed levels of serum cholesterol after rolled oats was added to the diet, going from 251 mg per 100 ml down to about 223. That did not add up to 75%. Would you explain that please? G . A. Leveille: That is very easily explained. You were looking at data from two different laboratories. In the case of our experiments conducted with chicks, we fed a relatively low level of cholesterol simply to raise the circulating level to about 250 to 300 mg percent. Working from that level we simply do not feel that we got 75% to 8&. In the group studies they fed a very high level of cholesterol to rats, not chicks, to get a very markedly elevated level of cholesterol. In spite of the fact that they had an 86reduction, the 207h which is remaining is still well above the normal level for a rat. The variation in results is a species difference and not a difference in diets. P. V. Hegarty: Dr. Leveille, why does protein influence the fiber content of food and the activity of the fiber in the intestines?

G. A. kveille: Let me simply say that we really don't know. We know so little about the of the compounds that we are talking about here. We are certainly in need of much better analytical tools than we currently have. No one really knows how to determine "dietary fiber," whatever that is. It is a mixed bag of several chemical components obviously, and we don't have good analytical tools. Comment: I think the thing with fiber and meat is that people keep talking about meat as the bad guy all the time, and then we talk about cereal and they seem to be the good guys. Cereal seems to be fine and certainly valuable, but don't forget fruits and vegetables and foods of this type. I think you come out better with the - ratio with most of the fruits and vegetables than you do with the cereal. So rather than put down meat as the bad guy in relation to calcium-phosphorus ratio, it my be better to encourage fruits and vegetables along with it.

C. W. Gehrke: I feel that I should point out that there have been some studies in which a negative correlatim was observed between the consumption of cereals and content in the population.

G. A. kveille: The point I would like to mke is that it has never been my intent to put meat in the position of the bad guy, not at all. I certainly enjoyed the ham this morning and my steak last night, and I, like everybody else, eat probably 2 1/2 to 3 times more protein than I need. I think that the important point is that we do have some suggested correlations which we really have to get down to the root of. What are the kinds of problems we are looking at? What are the mechanisms? Indeed, is there something undesirable about a diet which is high in anlraal prcducts? Not because of the animal products themselves, but simply because we are excluding something when we increase our consumption of animal products. I think we need to recognize that people eat meat not because they need animal protein. They eat meat because they like it. And they are going to continue eating meat because they like it.

Comment: I don't think we are saying meat is the bad guy. I think what we are saying is, if you look at the average American's diet, they are getting most of their calories from meat and it is not a balanced diet. There are other things that we need to eat that do not come from meat.

J. D. Kemp: I was looking at recent information on the fats and oils situation and I noticed that the per capita consumption of fat reached an all time high (in 1973) of something over fifty pounds. However, all the increase has been in plant fats and largely done in spite of a decrease in consumption of fats from animal s3urces. So when we talk about calories from fats we are not talking about calories from meat fats. We are talking about mostly calories from plant sources. G . A. Leveille: I would like to comment on that. I think one has to be careful in looking at those statistics. It is true that in terms of our visible fat we are getting most of it from plant sources in the margarines and shortenings, no arguments about that. The point we need to keep in mind is that fully a third of our total fat calories are coming as invisible fat in animal products and a very high proportion coming from meat, highly marbled meat. I think that's the point we really are talking about when we talk about the high proportion of our calories coming from meat. It is not from the protein. It is from the fat associated therewith.

R. F. Kellx: Not very much was said about the increased consumption of sugar over the years, especially in the more highly developed countries, and its relationship to the various maladies we have been talking about.

G. A. Leveille: The per capita consumption of sugar, again, based on disappearance values has not changed since 1909. It has been around 100 to 110 lbs. Now, one can ask what has changed over that same perid of time during which we have observed an increased incidence of cardio- vascular disease and cancer? In the case of cancer of the colon we only have reliable data over the last 35 years. During that period of time, over the last 35 years, our per capita consumption of sugar has not changed. What has changed, and I think this is an important and rather subtle difference, is that the per capita caloric intake has been reduced while our sugar intake has remained constant. We are, therefore, getting a somewhat higher propurtion of our calories from sugar. Per capita consumption has not increased as suggested in mny of the things that we read. In terms of pounds per year, that has remained constant.

Comment: If you go back 150 years then we do have quite a change.

G. A. Leveille: Yes, well, one could debate this quite some time. But if you look at the per capita consumption of sugar in , for example, which is extremely high, you find a population that has a relatively low incidence of cancer of the colon and cardiovascular disease.

D. G. Topel: I would like to know Dn what basis your calculations were made when you stated that we eat 2 1/2 times the amount of protein that we need in our diet? I have seen some figures where they use meat consumption on the basis of carcass weight; which is considerably different from the amount of meat we actually consume from the carcass. I would like to know your calculations and the basis for those figures?

G. A. Leveille: These are not calculations but actual data (from the USDA Household Survey) and the only data that I am aware of that are available on a National basis. They are based on recall data and we all know the potential error that is involved there. It's not based on calculations of disappearance of types of meat. This is 1965 survey data and we do have problems there in that the data are some ten years old; but it is the only direct information that is available on a 18 0 national basis at the present time. One can look at other information and estimte that it is probably better than anything we can devise from disappearance data. For example, the MICA data where they determine what is actually consumed in a large number of households over a period of a year. Unfortunately, they just have frequency of eating. In order to make an estimate one has to estirnate what the portion size is and, of course, that leads to considerable error. I think we are still left having to say that the best data we have available is the 1965 survey data. C . E. Allen: I would like to direct this to Dr . Leveille. Yesterday, we heard about the efforts to reduce the USDA grades of beef and right now we are at a stalemate on that issue. I would like to have your comments as to what you think we need to do in the U.S.? What is wrong? Here we have research to back us up in what we think is correct from the standpoint of what is necessary for palatability, and now tday we hear about what is necessary for reducing caloric intake. It seems to me that what is really happening is that the American public is throwing aside science and listening to consumer advocates. What do we need to do to get across what we think is right for everyone?

G. A. Leveille: I think, and this is a personal opinion, if one looks at the strategy which USDA used to try to change grades y~u could have predicted frm the start that it was going to fail. It was very clear from both the processor's standpoint and the consumer's standpoint. We have traditionally used grades for beef which imply that the highest amount of fat is better. The consumer really doesn't knm whether it has more or less fat. They just associate the grade with something that is better or worse in their minds. And you are now telling them you are going to sell them what heretofore has been sold as good. You are now going to move up one grade so they will be paying, in their mind, for what has been an inferior product up until this time.

I guess if it had been my choice, I would simply drop all the words we are now using and come up with some different euphemism, which would have suggested that the best grade was the one lowest in fat.

Question: With regard to high fiber diet I would like to ask this question. Do you know of any negative or positive detrimental effects from a high fiber diet in animl or human studies?

G. A. Leveille: No, we don't know of any detrimental effects; but as I pointed out there are some suggestions in animl studies that there can be some binding. After all, the components of dietary fiber, which are effective in lowering cholesterol level, functim essentially as an ion-binding resin does. Presumably then, they could bind other kinds of ions as well. I would have some concern about trace elements.

Question: What about the possibility of ulceratative effects in the intestinal area? Do you know of anything on that? 18 1

G. A. Leveille: I am not aware of any effect here. There was some early work done in swine at Purdue on ulcerative effects of different fiber levels and fineness of grind and so forth, but I don't recall the details of that.

I would like to just add one comment to vhat Dr. Gehrke said earlier. We do need to recognize that millions of people around the world are living on cereal diets. Experiments with human populations, as well as controlled experiments in this cruntry and other countries, have shown that we really can't use an evaluation of based on the rat and apply that directly to umn. For example, cereal are generally lm in for the rat but this is not the case in the adult human. For the adult man, lysine is mrginal but adequate in most cereal proteins.

P. E. McClain: If there are no more questions, I would like to thank our guests for a very interesting and enlightening program.

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G. C . Smith: I'd like to introduce the Chairmn of the Biochemistry and Biophysics Committee. Dr. Thayne Dutson, as most of you know, is a native of Idaho, did his Bachelors Degree at Utah State University and then went to Michigan State University where he worked with Dr. Pearson on his Iksters and F'h.D., did his postdoctorate at the University of Nottingham with Ralston Lawrie and then came to Texas A&M where he heads up the Meat Chemistry group of the Meats and Meat Chemistry section at Texas AM. So, at this point, I'll turn it over to your Chairman, Dr . Dutson.

T. R. Dutson: Thank you, Gary. I'd like to start off by giving my thanks to the Biochemistry and Biophysics Committee; their names are listed in the back of the program. They did a tremendous amount of work and a lot of thought went into developing this program. We had quite a bit of correspondence from mDst of the people on the Committee and we'd like to thank them greatly for all of their input. Also, I'd like to express my thanks to Dr. Kotula who is the Coordinating Director for this Committee; his direction helped greatly in putting together this program.

Our first speaker this morning is Ron Allen from Iowa State University. Ron is to address us on the topic of Myogenesis. Ron.