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Carbohydrate sensitivity
TIBS - October 1976
N 225
LETTERS
TOTHE EDITOR References Kaufmann,N. A., Poznanski, R., Blondheim, S. H.
Sweet truth Carbohydrate sensitivity I would like to comment on an aspect of the controversy over dietary sucrose not raised by either of the discussants (see TIBS, June 1976, p. N 126). There appears to be strong experimental evidence to indicate that dietary sucrose is a very important etiological factor in heart disease and diabetes in that segment of the population described as ‘carbohydrate sensitive’. In patients with carbohydrate-induced lipemia, sucrose produced much larger increases in blood triglycerides than did starch [l-4]. An elevated level of blood triglyceride is considered to be a risk factor in the occurrence of heart disease [5,6]. Carbohydrate-induced hyperlipemia has also been shown to be associated with abnormal glucose tolerance [7]. It is estimated that about 9 “/, of free-living volunteers in California, aged 25-79, showed the lipoproteinemia pattern associated with carbohydrate sensitivity [S]. Dietary sucrose in combination with a genetic predisposition has also been implicated in the etiology of diabetes in rats [9]. Clinical symptoms of diabetes were observed after feeding genetically selected rats diets containing as little as 25”< sucrose. In contrast, rats fed the same diet containing starch did not develop the diabetic symptoms. On the basis of these results, it is apparent that certain individuals through their genetic characteristics are more sucrose-sensitive than are others and recommendations pertaining to the level of sucrose intake considered to be safe will not apply uniformly to the population. One of the main thrusts of carbohydrate nutrition research should be directed toward establishing a characteristic pattern of defects in the regulation of carbohydrate metabolism that can be used to identify carbohydrate-sensitive individuals early in life. SIR :
SHELDON REISER
Carbohydrate Nuuition Laboratory, Nutrition Institute, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, Maryland, U.S.A.
and Stein, Y. (1966) Amer. J. Clin. NW. 18, 261269 Kuo, P.T., Feng, L., Cohen, N.N., Fitts, W.T., Jr. and Miller, L. D. (1967) Amer. J. Clin. Nutr. 20, 116-125 Little, J. A., Birchwood, B. L., Simmons, D.A., Antar, M.A., Kallos, A., Buckley, G.C. and Csima, A. (1970) Atherosclerosis 11, 17%181 Antar, M.A., Little, J.A., Lucas, C., Buckley, G.C. andCsima,A. (1970) Atherosclerosis 11,191201 Nutr. Rev. (1972) 30,223-225 Carlson, L. A. and Bottiger, L. E. (1972) Lancer I, 865-868 Fredrickson, D.S., Levy, R.I. and Lees, R.S. (1967) New Eng. J. Med. 276,273-281 Wood, P. D.S., Stern, M. P., Silver, A., Reaven, G. M. and von der Groeben, J. (1972) Circulation 45, 114126 Cohen, A.M. (1973) Hearings Before the Select Committee on Nutrition and Human Needs of the United States Senate, Part 2 - Sugar in Diet, Diabetes and Heart Diseases, pp. 167-198
Sugar and diabetes It should be clear that over the question of sugar and diabetes, discussions must deal with experimental data pertaining only to the diabetogenic effect of sucrose versus starch consumption in equal amounts and not with small or large amounts of starchy carbohydrates. Fredrick Stare discusses (see TIBS, June, p. N 126) the role of ‘sugar and other carbohydrates’ in diabetes in a single paragraph. In this paragraph he quotes a part of the statement issued by the American Diabetes Association in 1971 [l], ‘that there no longer appears to be any need to restrict disproportionately the intake of carbohydrates in the diet of most diabetic patients’ and leaves it to the readers to draw their own conclusions. In the above recommendation of the American Diabetes Association there is no mention or any hint whatsoever concerning sucrose or any other refined sugar - and no restriction of carbohydrates de& nitely does not mean sugar. Furthermore, in an article by E. L. Bierman, ‘Carbohydrates, Diabetes and Blood Lipids’ [2] in which he also discusses the recommendation of the American Diabetes AssociaSIR:
tion, Bierman makes a special point of saying that in diabetes ‘Simple sugars should still bo avoided since disaccharides and monosaccharides are rapidly absorbed and can produce hyperglycemic peaks and transient increase in glucosuria’. So one does not see why the recommendation of the American Diabetes Association which deals with the amount of carbohydrates and has nothing to do with the kind of carbohydrates, that is sugar or starch, should be brought into the discussion dealing with the effect of sugar on the development of diabetes. It only confuses the reader which definitely was not Stare’s intention. On the other hand, there is experimental, proof in man [34] and in the experimental animal [5-71 that when high amounts of sucrose substitute equal amounts of starch in the diet a deleterious effect on the glucose tolerance is noted. When dealing with the metabolic effect of high sugar intake compared to that of starch both Stare and Yudkin overlooked the role of genetics in the response of the individual. We have shown that this response varies according to the genetic build up [8]. In genetically susceptible experimental animals, high sugar intake leads to the development of diabetes mellitus and all the vascular diabetic complications, retinopathy and nephropathy while the unsusceptible population, with no such genetic trait, exposed to the same high sucrose diet remains normal. Moreover the genetically susceptible population when fed starch will not develop diabetes nor the diabetic vascular complications [9]. These experiments duplicate the observations in the epidemiological studies of populations that have changed their food habits and in whom an increased prevalence of diabetes on transition from a limited sucrose intake to high sucrose rich diet was observed [lO-111. This explains also why only a part of the population developed diabetes on a high intake of relined sugars while the rest of the population did not. The role of genetics in the development of hyperlipemias on high sucrose intake was also observed [ 121. Thus there is definite experimental proof that high amounts of sucrose substituting equal amounts of starch in the diet in man and in the experimental animal have a deleterious effect on the glucose tolerance. Moreover, in the sensitive individual a high sucrose diet will lead to the development of diabetes and all its vascular complications while an equal amount of starch will not. The issue under discussion is of paramount importance as the prevalence of diabetes in the adult population (40 years and over) is more than 10 %. Diabetes is complicated by retinal and renal angio-
N 225
LETTERS
TOTHE EDITOR References Kaufmann,N. A., Poznanski, R., Blondheim, S. H.
Sweet truth Carbohydrate sensitivity I would like to comment on an aspect of the controversy over dietary sucrose not raised by either of the discussants (see TIBS, June 1976, p. N 126). There appears to be strong experimental evidence to indicate that dietary sucrose is a very important etiological factor in heart disease and diabetes in that segment of the population described as ‘carbohydrate sensitive’. In patients with carbohydrate-induced lipemia, sucrose produced much larger increases in blood triglycerides than did starch [l-4]. An elevated level of blood triglyceride is considered to be a risk factor in the occurrence of heart disease [5,6]. Carbohydrate-induced hyperlipemia has also been shown to be associated with abnormal glucose tolerance [7]. It is estimated that about 9 “/, of free-living volunteers in California, aged 25-79, showed the lipoproteinemia pattern associated with carbohydrate sensitivity [S]. Dietary sucrose in combination with a genetic predisposition has also been implicated in the etiology of diabetes in rats [9]. Clinical symptoms of diabetes were observed after feeding genetically selected rats diets containing as little as 25”< sucrose. In contrast, rats fed the same diet containing starch did not develop the diabetic symptoms. On the basis of these results, it is apparent that certain individuals through their genetic characteristics are more sucrose-sensitive than are others and recommendations pertaining to the level of sucrose intake considered to be safe will not apply uniformly to the population. One of the main thrusts of carbohydrate nutrition research should be directed toward establishing a characteristic pattern of defects in the regulation of carbohydrate metabolism that can be used to identify carbohydrate-sensitive individuals early in life. SIR :
SHELDON REISER
Carbohydrate Nuuition Laboratory, Nutrition Institute, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, Maryland, U.S.A.
and Stein, Y. (1966) Amer. J. Clin. NW. 18, 261269 Kuo, P.T., Feng, L., Cohen, N.N., Fitts, W.T., Jr. and Miller, L. D. (1967) Amer. J. Clin. Nutr. 20, 116-125 Little, J. A., Birchwood, B. L., Simmons, D.A., Antar, M.A., Kallos, A., Buckley, G.C. and Csima, A. (1970) Atherosclerosis 11, 17%181 Antar, M.A., Little, J.A., Lucas, C., Buckley, G.C. andCsima,A. (1970) Atherosclerosis 11,191201 Nutr. Rev. (1972) 30,223-225 Carlson, L. A. and Bottiger, L. E. (1972) Lancer I, 865-868 Fredrickson, D.S., Levy, R.I. and Lees, R.S. (1967) New Eng. J. Med. 276,273-281 Wood, P. D.S., Stern, M. P., Silver, A., Reaven, G. M. and von der Groeben, J. (1972) Circulation 45, 114126 Cohen, A.M. (1973) Hearings Before the Select Committee on Nutrition and Human Needs of the United States Senate, Part 2 - Sugar in Diet, Diabetes and Heart Diseases, pp. 167-198
Sugar and diabetes It should be clear that over the question of sugar and diabetes, discussions must deal with experimental data pertaining only to the diabetogenic effect of sucrose versus starch consumption in equal amounts and not with small or large amounts of starchy carbohydrates. Fredrick Stare discusses (see TIBS, June, p. N 126) the role of ‘sugar and other carbohydrates’ in diabetes in a single paragraph. In this paragraph he quotes a part of the statement issued by the American Diabetes Association in 1971 [l], ‘that there no longer appears to be any need to restrict disproportionately the intake of carbohydrates in the diet of most diabetic patients’ and leaves it to the readers to draw their own conclusions. In the above recommendation of the American Diabetes Association there is no mention or any hint whatsoever concerning sucrose or any other refined sugar - and no restriction of carbohydrates de& nitely does not mean sugar. Furthermore, in an article by E. L. Bierman, ‘Carbohydrates, Diabetes and Blood Lipids’ [2] in which he also discusses the recommendation of the American Diabetes AssociaSIR:
tion, Bierman makes a special point of saying that in diabetes ‘Simple sugars should still bo avoided since disaccharides and monosaccharides are rapidly absorbed and can produce hyperglycemic peaks and transient increase in glucosuria’. So one does not see why the recommendation of the American Diabetes Association which deals with the amount of carbohydrates and has nothing to do with the kind of carbohydrates, that is sugar or starch, should be brought into the discussion dealing with the effect of sugar on the development of diabetes. It only confuses the reader which definitely was not Stare’s intention. On the other hand, there is experimental, proof in man [34] and in the experimental animal [5-71 that when high amounts of sucrose substitute equal amounts of starch in the diet a deleterious effect on the glucose tolerance is noted. When dealing with the metabolic effect of high sugar intake compared to that of starch both Stare and Yudkin overlooked the role of genetics in the response of the individual. We have shown that this response varies according to the genetic build up [8]. In genetically susceptible experimental animals, high sugar intake leads to the development of diabetes mellitus and all the vascular diabetic complications, retinopathy and nephropathy while the unsusceptible population, with no such genetic trait, exposed to the same high sucrose diet remains normal. Moreover the genetically susceptible population when fed starch will not develop diabetes nor the diabetic vascular complications [9]. These experiments duplicate the observations in the epidemiological studies of populations that have changed their food habits and in whom an increased prevalence of diabetes on transition from a limited sucrose intake to high sucrose rich diet was observed [lO-111. This explains also why only a part of the population developed diabetes on a high intake of relined sugars while the rest of the population did not. The role of genetics in the development of hyperlipemias on high sucrose intake was also observed [ 121. Thus there is definite experimental proof that high amounts of sucrose substituting equal amounts of starch in the diet in man and in the experimental animal have a deleterious effect on the glucose tolerance. Moreover, in the sensitive individual a high sucrose diet will lead to the development of diabetes and all its vascular complications while an equal amount of starch will not. The issue under discussion is of paramount importance as the prevalence of diabetes in the adult population (40 years and over) is more than 10 %. Diabetes is complicated by retinal and renal angio-