Prevention and Therapy of Diabetes Mellitus by Kelly M. West, M. D.
D'
iabetes mellitus is a disorder characterized by hyperglycemia, a relative or absolute deficiency of insulin, and by certain characteristic symptoms and pathologic manifestations. Classical symptoms include polyuria, polydipsia, and weight loss, but these occur only with moderate or marked elevations of the blood glucose. They are entirely reversible with treatment. A substantial percentage of untreated diabetics have mild hyperglycemia without these classic symptoms. Both mild and severe diabetics are, however, prone to develop morbid changes in small and large arteries and in nerves. Complete failure of beta-cell function if untreated or inadequately treated, leads to profound hyperglycemia, ketonemia, acidosis, negative nitrogen balance, dehydration, and other severe aberrations in the intermediary metabolism of carbohydrates, lipids, proteins, and electrolytes. Untreated severe diabetes eventually leads to coma and death. Although important nutritional deficiencies, such as muscle wasting and growth failure, occur occasionally in undiscovered or inadequately treated cases of severe diabetes, the availability of insulin therapy has made these uncommon. Today the main challenge is the prevention, miti-
Dr. West is Professor of Medicine at the Department of Medicine, University of Oklahoma Health Sciences Center, 800 N.E. 13th Street, Oklahoma Ciry, Oklahoma 73190. A limited number of reprints 01 this article may be obtained from tho author. THERE ARE NO REPRINTS OF UNSIGNED REVIEWS.
gation, or postponement of the vascular and neurologic manifestations. These include retinopathy and glomerulosclerosis, increased rates of coronary atherosclerosis, and gangrene secondary to arterial insufficiency and impaired sensation in the legs. Many different factors can produce diabetes or increase risk of the disease; the most important of these are obesity and genetic factors. Diabetes may also be caused or precipitated by any agent that d i r e c t l y impairs beta-cell function or destroys beta cells (e.g., pancreatitis) or by factors that increase peripheral resistance to insulin (e.g., acromegaly or obesity). Adult-onset diabetes is much more frequent than youth-onset diabetes. About three-fourths of adult-onset cases are obese. Only a very small percent of youth-onset cases are obese. Typically, youth-onset diabetes is severe (little or no endogenous insulin); while adult-onset diabetes is usually mild or moderate in severity because beta-cell failure is only partial. This essay will summarize present knowledge concerning three related aspects of nutrition and diabetes. Discussion will include the effects of nutritional factors on the risk of diabetes, the effect of diet on the manifestations of diabetes, and the role of diet in the treatment of this disorder including some of the specific dietary objectives and strategies in the various types of diabetes. Nutrition and Etiology
It has long been suspected that nutritional factors affect the risk of diabetes. More recent investigations elucidate further NUTRITION RNIEWSIVOL. 33, NO. 7 1 JULY 1975 193
dence was not conclusive in this respect. the nature and strength of these relationAlthough we have found among populaships. Changing dietary patterns in Japan,' tions a generally positive association Israel,* and Africa3 have been associated between rates of diabetes and consumption with a profound increase in the rates of of both sugar and fat, we have also accumudiabetes. Studies by the author with lated some epidemiologic evidence that is Kalbfleisch and other collaborators in 13 inconsistent with the hypothesis that sugar societies of 1 1 countries indicated a strong and fat are important risk factors apart relationship of diabetes prevalence and from their effects or possible effects on nutritional factor^.^-^ A recent review of levels of caloric c o n s ~ m p t i o n . ~ Hims'~ available data on past and present rates of w o r t h reviewed evidence that dietary diabet's in aboriginal populations of the carbohydrate protects against diabetes.' In New World (Indians, Eskimos, Polynesians, general, rates of diabetes are low where and Micronesians) also suggested a strong starch consumption is high.6 Trowell rerelationship of diet and a risk of diabetes7 cent ly summarized evidence suggesting Marked differences in nutritional factors that, under certain conditions, the removal and exercise levels in these populations of fiber from flour and other foods may probably account for differences in rates of enhance the risk of diabetes.' diabetes as great as t e n - f ~ l d . ~ The relative importance of sugar in The factor most strongly and condetermining the risk of obesity is also not s i stently associated with prevalence of adult-onset diabetes i s the degree and the well This may vary deduration of adiposity. Arguments have also pending on what foods are available as rebeen advanced that dietary sugar2s3 and placements when sugar intake is intenfat' are especially diabetogenic. In this t i o n a l l y limited or unavailable. Since essay, the term "sugar" refers to all monorefined sucrose is a concentrated and an and disaccharides but a substantial majority attractive source of calories, it is widely of dietary sugar i s usually sucrose in those suspected that i t s consumption would tend societies in which sugars furnish as much as to increase the risk of obesity. High rates of 10 percent of the total calories. Increased obesity have also been observed occasionally in populations in which sugar conrates of diabetes have frequently been obsumption is served in populations where sugar intake and in one society, fat people probably ate less sugar than lean has increased.2p3*5n7 It has been difficult, persons.' High rates of diabetes have not however, to determine whether this is a direct relationship of cause and e f f e ~ t . ~ . ~ , ' been reported in any society in which obesity is rare. Investigations in the laboraThis is because these dietary changes are tory give considerable support to obesity as usually temporally related to other factors a risk factor. For example, obesity is assosuch as decreasing exercise, increases in ciated with resistance t o endogenous intotal calories, and fat intake, etc. Moreover, sulin. no relationship could be found between the Cohen produced mild diabetes without risk of diabetes and the previous sugar conproducing obesity in one group of rats by sumption when small groups of those with feeding high sucrose diets.* These diets, and without diabetes were studied in each however, were much higher in sucrose (72 of four different populations.1°-13 In conpercent of calories) than those consumed trast, most intrapopulation studies showed that adiposity i s a strong risk f a ~ t o r . ~ , b~y ~ any human population. Moreover, obesity and diabetes have also been C l e a ~ e , ~with support from Cohen2 and others, argued eloquently that a main preinduced repeatedly in animals by increasing cipitating factor in diabetes is the conthe dietary fat. Under these conditions, the sumption of refined carbohydrates (both percent of calories as starch or as sugar sucrose and other "refined" carbohywere often reduced. In one experiment drates). Keen' thought that present evidiabetes was induced by a diet high in 194
NUTRITION REVIEWSIVOL. 33, NO. 7 1 JULY 1975
protein.17 Experiments of this kind are often difficult t o interpret because two or more variables are usually changed. For example, if fat is increased, it is usually also necessary t o decrease carbohydrate or increase calories. In hamsters that were prone t o diabetes, Gerritsen and Dulin reduced rates of diabetes dramatically by reducing food intake.' * This was a quantitative and not a qualitative change in diet. A review of all available laboratory and epidemiologic evidence suggests that the most important dietary factor in increasing the risk of diabetes is total calorie intake irrespective of source. This still leaves open the question of the relative importance of specific nutrients such as f a t and sugar in inducing excessive caloric consumption. Previously it was commonly believed that ingestion of refined carbohydrates might "overstrain" the beta cells. Recent physiologic evidence generally tends t o diminish this possibility. For example, it has been found that the ingestion of mixed meals containing carbohydrate, fat, and protein stimulate beta-cell function much more strongly than carbohydrate alone. Severe malnutrition in childhood (as in India and Africa) is sometimes associated with an increased risk of pancreatic calcification and diabetes later in life. Excessive iron consumption may lead to diabetes, secondary t o hemochromatosis. Under certain conditions impaired glucose tolerance has been observed with deficiencies of zinc and of chromium, but it is not yet certain whether these deficiencies are significant risk factors for clinical diabetes. Complications of Diabetes Among populations of diabetics there are sometimes substantial differences in the frequency of certain complications. In Japan, for example, coronary disease and gangrene are much less common manifestations of diabetes than in the United States. It seems quite probable that the comparatively low rates of atherosclerosis seen in the diabetics in many societies of Asia, Africa, and Latin America are attributable t o their diets which are lower in cholesterol
and saturated fat (both before and after discovery of diabetes). Caloric intake is also low in relation t o energy expenditure in most of these populations. Geographic and ethnic differences among populations in rates of small-vessel disease (glomerulosclerosis and retinopathy) are considerably less. There are, however, a few societies in which microvascular disease seems t o be less frequent in diabetics (e.g., Navajo I n d ians and Nigerian~).~ Nutritional factors may or may not contribute to these differences. Although present data are not very satisfactory it appears that there are differences among societies in rates of juvenile diabetes7 It is possible that nutritional factors are influential in this respect. In Japan, for instance, marked changes in the national diet during recent years have been associated with substantial increases in rates of juvenile diabetes.*' Rates of ketosis appear to vary among populations of diabetics, but it is not yet clear whether dietary factors play a role in these variations.' p'
v7
Diet Therapy In recent years considerable progress has been made in understanding the potentialities and priorities of diet therapy in the various types of diabetes. It is now clear that in several respects, dietary objectives and strategies should be quite different in t h e t w o main types of diabetes. In maturity-onset obese diabetics, reduction of adiposity by restricting calories or increasing exercise, or both, reduces hyperglycemia. Even more fundamental and more important, these measures also reduce the insulin resistance that attends obesity. This mitigates the "overstrain" of the beta cells and usually leads t o considerable improvement of beta-cell function. Thus, in this group, diet not only helps t o control diabetes, it reduces the severity of the disease. Return of glucose tolerance t o entirely normal levels is uncommon only because of the rarity with which weight is restored t o optimum levels and maintained a t such levels. However, even partial mitigation of adiposity is helpful. Although most NUTRITION RffIEWS/YOL. 33. NO. 7 / JULY 1975 195
experts still advise restriction or complete proscription of refined sugars, it is now the consensus that limitation of calories is usually the prime goal of therapy in this type of obese diabetic. In order to establish new eating habits and patterns it may also be desirable to encourage a certain degree of consistency in the quantity, characteristics, and timing of the feedings in obese diabetics. These latter strategies, however, are not of urgent priority in this type of diabetes. For example, a high degree of consistency is not required from day to day in amounts of dietary starch, in total calories, or in the timing of feedings, as long as long-term caloric intake remains low enough to permit control of adiposity. Between-meal snacks and bedtime feedings are usually not necessary or desirable in obese diabetics. On the other hand, lean patients with no endogenous insulin require approaches that are quite different in several respects. Calories should not be restricted below normal levels. It is usually desirable to provide smaller meals and one to three between-meal snacks in order to distribute food consumption to match roughly the time-action pattern of administered insulin. This mitigates postprandial surges of hyperglycemia and protects against hypoglycemia. In contrast to the typical situation in obese diabetics, no endogenous insulin is available in response to meals. In these lean, insulin-dependent patients it is usually desirable to provide for a considerable degree of consistency and predictability of the distribution, amounts, and characteristics of the feedings. In contrast to the therapy of obese diabetics, these patients also need considerable instruction on how to adjust the diet to contend with vagaries that may include unavoidable delay of mea Is, u n usu a I exercise, complicating illnesses, management and prevention of hypoglycemic episodes, etc. In both of the major types of diabetes there is decreasing emphasis on the priority of carbohydrate restriction.2 * There are two reasons for this. First, it is now clear that insulin requirement is, in the long run, s2
196 NUTRITION REVIEWSIVOL. 33, NO. 7 1 JULY 1975
more related to total fuel supply than to the amount of dietary carbohydrate itself. With excellent help from other elements of the body economy, the liver can make glucose readily out of a variety of sources. It is now evident that diets generous in starch are very well tolerated by both insulin-dependent and insulin-independent diabetics, provided that levels of calorie consumption are appropriate. Both plasma glucose and lipid levels usually respond quite favorably to such regimens. Even diabetics with Type I V hyperlipoproteinemia do well on liberal starch diets when levels of dietary sugar and calories are appropriately controlled. Second, i f levels of carbohydrate are sharply restricted, it is difficult to construct diets that are not high in fat and cholesterol. In the United States traditional diabetic diets of the past contained about 42 percent of calories as fat and generous amounts of cholesterol; while in Asian diabetics fat provided typically only about 15 percent of calories and levels of dietary cholesterol have been quite low. North American and Western European rates of coronary disease are exceedingly high in diabetics and coronary disease accounts for a majority of the deaths. In contrast, coronary atherosclerosis is far less common in the diabetics who consumed high starch, low fat, low cholesterol diets. These considerations have now led most Western diabetologists to prescribe diabetic diets that are lower in saturated fat and cholesterol than the previous traditional regimens. The calories derived from saturated fat can then be replaced if necessary by calories from three other sources: starch, vegetable fat, and protein. A typical "modernized" diabetic diet for a person in a Western society has the following characteristics: It contains a number of calories adequate to reach or maintain optimum weight. Refined sugars are proscribed or sharply limited, but about 10 to 15 percent of calories consist of sugars from natural sources such as fruit, vegetables, and milk. Fat is limited to about 25 to 35 percent of calories. Usually it is possible to reduce ani-
ma1 fat and cholesterol considerably without making the regimen unattractive or unfeasible. Saturated f a t makes up only about 10 t o 15 percent of calories in such a regimen (about half as much as the typical American diet), while vegetable f a t (monoand polyunsaturates) supplies about 15 t o 20 percent of calories. In most adult patients, levels of protein are not critical and may range from as low as 12 percent of calories t o as high as 24 percent depending on food preferences, food budgets, and other factors. Children, and women who are pregnant or lactating, require a t least 1.5 g per kilogram. The remainder of calories, usually 30 t o 40 percent, are derived from complex carbohydrates (mainly starches). The most difficult aspects of the implementation of these "modernized diabetic diets" has been persuading dietitians, physicians, and patients that liberal amounts of starch are not bad for diabetes. In many instances these regimens do require the patient t o eat even more starch than his family or friends. A review of the considerations discussed above, however, usually leads t o an understanding and acceptance of this approach. A considerable body of recent evidence also supports the strategy of encouraging the ingestion of starches high in fiber.3*1 Other recent publications have discussed the problems responsible for low rates of adherence t o dietary prescriptions;22 methods for formulating diet prescript i o n ~ ; ~ the~ -mechanics ~ ~ of developing and implementing prescription^;^ 3 - 2 the importance and methods of educating the ~ a t i e n t ; ~and ~ - ~the ~ limited role of special foods such as artificial sweeteners, lowcalorie and low-carbohydrate "diet" drinks and food products, fructose, sorbi. ~ texts ~ edited by tol, alcohol, e t ~ The Marble e t al. (Joslin's book)26 and by Sussman and met^^^ are good sources of information on diabetes. There is considerable evidence that only a minority of diabetics receive and follow on a long-term basis appropriate diet prescriptions.2 It is also clear that diet therapy is feasible and e f f e c t i ~ e . ~ * *0~ ~ - ~ ~
1. Diabetes Mellitus in Asia, 1970. S. Tsuji and M. Wada, Editors. Excerpta Medica, Amsterdam, 1971 2. A. M. Cohen, A. Teitelbaum, and R. Saliternik, Metabolism 21: 235-240, 1972 3. T. L. Cleave in The Saccharine Disease. John Wright & Sons, Ltd., Bristol, 1974 4. K. M.West and J. M. Kalbfleisch, Diabetes 19: 656-663, 1970 5. K. M. West and J. M. Kalbfleisch, Diabetes 20: 99-108, 1971 6. K. M. West in Is the Risk of Becoming Diabetic Affected by Sugar Consumption? S. S. Hillebrand, Editor, pp. 33-43. International Sugar Research Foundation, Bethesda, 1974 7. K. M. West, Diabetes 23: 841-855, 1974 8. H. P. Himsworth, Clin. Sci. 2: 117-148, 1935-1936 9. Is the Risk of Becoming Diabetic Affected by Sugar Consumption? S. S. Hillebrand, Editor. I n ternational Sugar Research Foundation, Bethesda, 1974 10. H. P. Himsworth and E. M. Marshall, Clin. Sci. 2: 95-115, 1935 11. J. Booyens, M. de V. Frank, V. M. de Waal, G. D. Campbell, and M. D. Goldberg, S. Afr. Med. J. 44: 271-278, 1970 12. J. D. Baird, Acta Diabetol. Lat. (Suppl.) 9: 405428, 1972 13. H. A. Kahn, J. 6. Herman, J. H. Medalie, H. N. Neufeld, E. Riss, and U. Goldbourt, J. Chron. Dis. 23: 617-629, 1971 14. K. M. West in The Regulation of the Adipose Tissue Mass. J. Vague and J. Boyer, Editors. Excerpta Medica, Amsterdam, 1973 15. H. Keen in Is the Risk of Becoming Diabetic Affected by Sugar Consumption? S. S. Hillebrand, Editor, pp. 14-27. International Sugar Research Foundation, Bethesda, 1974 16. H. Trowell, Lancet I I : 998-1002, 1974 17. K. Petersen, U. Schmitthenner, and L. Kerp, Diabetologia 10: 383, 1974 18. G. C. Gerritsen and W. E. Dulin, Diabetalogia 10: 559-565, 1974 19. K. M. West, Acta Diabetol. Lat. (Suppl.) 9: 405-428, 1972 20. E. Miki and H. Maruyarna in Diabetes Mellitus in Asia 1970. S. Tsuji and M. Wada, Editors. Excerpta Medica, Amsterdam, 1971 21. E. L. Bierman, M. J. Albrink, R. A. Arky, W. E. Connor, S. Dayton, N. Spritz, and D. Steinberg, Diabetes 20: 633634, 1971 22. K. M. West, Ann. Int. Med. 79: 425-434, 1973 NUTRITION REVIEWSIVOL. 33, NO. 7 I JULY 1975
197
23. J. K. Davidson in Current Therapy 1974. H. F . Conn, Editor, pp. 386-408. W. 6. Saunders Co., Philadelphia, 1974 24. K. M. West in Nutritional Support of Medical Practice. C. E. Anderson, D. B. Coursin, and H. A. Schneider, Editors. Harper-Row, New York, 1975 25. Experimental and Therapeutic Dietetics by M. A. Ohlson. Second edition. Burgess Publishing Co., Minneapolis, 1972 26. JoslinS Diabetes Mellitus. A. Marble, Editor. Eleventh edition. Lea & Febiger, Philadelphia, 1971 27. Diabetes Mellitus: Diagnosis and Treatment. K. Sussman and R. Metz, Editors, voi. IV.
28.
29.
30. 31. 32.
American Diabetes Association, New York, 1975 (in press) R . L. Weinsier, A. Seeman, M. G. Herrera, J. J. Simmons, and M. E. Collins, Diabetes 23: 669-673, 1974 J. K. Davidson in Epidemiologic Studies and Clinical Trials in Chronic Diseases. Pp. 44-48. Pan-American Health Organization Proceedings of Symposium, Washington, D.C., 1972 G. W. Chance, E. C. Albutt, and S. M. Edkins, Brit. Med. J. 3 : 616-618, 1969 D. B. Stone, Am. J. Med. Sci. 241: 64-70, 1961 D. B. Stone and W. E. Conner, Diabetes 12: 127-132, 1963
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198 NUTRITION REYIEWSIVOL. 33, NO. 7 1 JULY 1975
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D'
iabetes mellitus is a disorder characterized by hyperglycemia, a relative or absolute deficiency of insulin, and by certain characteristic symptoms and pathologic manifestations. Classical symptoms include polyuria, polydipsia, and weight loss, but these occur only with moderate or marked elevations of the blood glucose. They are entirely reversible with treatment. A substantial percentage of untreated diabetics have mild hyperglycemia without these classic symptoms. Both mild and severe diabetics are, however, prone to develop morbid changes in small and large arteries and in nerves. Complete failure of beta-cell function if untreated or inadequately treated, leads to profound hyperglycemia, ketonemia, acidosis, negative nitrogen balance, dehydration, and other severe aberrations in the intermediary metabolism of carbohydrates, lipids, proteins, and electrolytes. Untreated severe diabetes eventually leads to coma and death. Although important nutritional deficiencies, such as muscle wasting and growth failure, occur occasionally in undiscovered or inadequately treated cases of severe diabetes, the availability of insulin therapy has made these uncommon. Today the main challenge is the prevention, miti-
Dr. West is Professor of Medicine at the Department of Medicine, University of Oklahoma Health Sciences Center, 800 N.E. 13th Street, Oklahoma Ciry, Oklahoma 73190. A limited number of reprints 01 this article may be obtained from tho author. THERE ARE NO REPRINTS OF UNSIGNED REVIEWS.
gation, or postponement of the vascular and neurologic manifestations. These include retinopathy and glomerulosclerosis, increased rates of coronary atherosclerosis, and gangrene secondary to arterial insufficiency and impaired sensation in the legs. Many different factors can produce diabetes or increase risk of the disease; the most important of these are obesity and genetic factors. Diabetes may also be caused or precipitated by any agent that d i r e c t l y impairs beta-cell function or destroys beta cells (e.g., pancreatitis) or by factors that increase peripheral resistance to insulin (e.g., acromegaly or obesity). Adult-onset diabetes is much more frequent than youth-onset diabetes. About three-fourths of adult-onset cases are obese. Only a very small percent of youth-onset cases are obese. Typically, youth-onset diabetes is severe (little or no endogenous insulin); while adult-onset diabetes is usually mild or moderate in severity because beta-cell failure is only partial. This essay will summarize present knowledge concerning three related aspects of nutrition and diabetes. Discussion will include the effects of nutritional factors on the risk of diabetes, the effect of diet on the manifestations of diabetes, and the role of diet in the treatment of this disorder including some of the specific dietary objectives and strategies in the various types of diabetes. Nutrition and Etiology
It has long been suspected that nutritional factors affect the risk of diabetes. More recent investigations elucidate further NUTRITION RNIEWSIVOL. 33, NO. 7 1 JULY 1975 193
dence was not conclusive in this respect. the nature and strength of these relationAlthough we have found among populaships. Changing dietary patterns in Japan,' tions a generally positive association Israel,* and Africa3 have been associated between rates of diabetes and consumption with a profound increase in the rates of of both sugar and fat, we have also accumudiabetes. Studies by the author with lated some epidemiologic evidence that is Kalbfleisch and other collaborators in 13 inconsistent with the hypothesis that sugar societies of 1 1 countries indicated a strong and fat are important risk factors apart relationship of diabetes prevalence and from their effects or possible effects on nutritional factor^.^-^ A recent review of levels of caloric c o n s ~ m p t i o n . ~ Hims'~ available data on past and present rates of w o r t h reviewed evidence that dietary diabet's in aboriginal populations of the carbohydrate protects against diabetes.' In New World (Indians, Eskimos, Polynesians, general, rates of diabetes are low where and Micronesians) also suggested a strong starch consumption is high.6 Trowell rerelationship of diet and a risk of diabetes7 cent ly summarized evidence suggesting Marked differences in nutritional factors that, under certain conditions, the removal and exercise levels in these populations of fiber from flour and other foods may probably account for differences in rates of enhance the risk of diabetes.' diabetes as great as t e n - f ~ l d . ~ The relative importance of sugar in The factor most strongly and condetermining the risk of obesity is also not s i stently associated with prevalence of adult-onset diabetes i s the degree and the well This may vary deduration of adiposity. Arguments have also pending on what foods are available as rebeen advanced that dietary sugar2s3 and placements when sugar intake is intenfat' are especially diabetogenic. In this t i o n a l l y limited or unavailable. Since essay, the term "sugar" refers to all monorefined sucrose is a concentrated and an and disaccharides but a substantial majority attractive source of calories, it is widely of dietary sugar i s usually sucrose in those suspected that i t s consumption would tend societies in which sugars furnish as much as to increase the risk of obesity. High rates of 10 percent of the total calories. Increased obesity have also been observed occasionally in populations in which sugar conrates of diabetes have frequently been obsumption is served in populations where sugar intake and in one society, fat people probably ate less sugar than lean has increased.2p3*5n7 It has been difficult, persons.' High rates of diabetes have not however, to determine whether this is a direct relationship of cause and e f f e ~ t . ~ . ~ , ' been reported in any society in which obesity is rare. Investigations in the laboraThis is because these dietary changes are tory give considerable support to obesity as usually temporally related to other factors a risk factor. For example, obesity is assosuch as decreasing exercise, increases in ciated with resistance t o endogenous intotal calories, and fat intake, etc. Moreover, sulin. no relationship could be found between the Cohen produced mild diabetes without risk of diabetes and the previous sugar conproducing obesity in one group of rats by sumption when small groups of those with feeding high sucrose diets.* These diets, and without diabetes were studied in each however, were much higher in sucrose (72 of four different populations.1°-13 In conpercent of calories) than those consumed trast, most intrapopulation studies showed that adiposity i s a strong risk f a ~ t o r . ~ , b~y ~ any human population. Moreover, obesity and diabetes have also been C l e a ~ e , ~with support from Cohen2 and others, argued eloquently that a main preinduced repeatedly in animals by increasing cipitating factor in diabetes is the conthe dietary fat. Under these conditions, the sumption of refined carbohydrates (both percent of calories as starch or as sugar sucrose and other "refined" carbohywere often reduced. In one experiment drates). Keen' thought that present evidiabetes was induced by a diet high in 194
NUTRITION REVIEWSIVOL. 33, NO. 7 1 JULY 1975
protein.17 Experiments of this kind are often difficult t o interpret because two or more variables are usually changed. For example, if fat is increased, it is usually also necessary t o decrease carbohydrate or increase calories. In hamsters that were prone t o diabetes, Gerritsen and Dulin reduced rates of diabetes dramatically by reducing food intake.' * This was a quantitative and not a qualitative change in diet. A review of all available laboratory and epidemiologic evidence suggests that the most important dietary factor in increasing the risk of diabetes is total calorie intake irrespective of source. This still leaves open the question of the relative importance of specific nutrients such as f a t and sugar in inducing excessive caloric consumption. Previously it was commonly believed that ingestion of refined carbohydrates might "overstrain" the beta cells. Recent physiologic evidence generally tends t o diminish this possibility. For example, it has been found that the ingestion of mixed meals containing carbohydrate, fat, and protein stimulate beta-cell function much more strongly than carbohydrate alone. Severe malnutrition in childhood (as in India and Africa) is sometimes associated with an increased risk of pancreatic calcification and diabetes later in life. Excessive iron consumption may lead to diabetes, secondary t o hemochromatosis. Under certain conditions impaired glucose tolerance has been observed with deficiencies of zinc and of chromium, but it is not yet certain whether these deficiencies are significant risk factors for clinical diabetes. Complications of Diabetes Among populations of diabetics there are sometimes substantial differences in the frequency of certain complications. In Japan, for example, coronary disease and gangrene are much less common manifestations of diabetes than in the United States. It seems quite probable that the comparatively low rates of atherosclerosis seen in the diabetics in many societies of Asia, Africa, and Latin America are attributable t o their diets which are lower in cholesterol
and saturated fat (both before and after discovery of diabetes). Caloric intake is also low in relation t o energy expenditure in most of these populations. Geographic and ethnic differences among populations in rates of small-vessel disease (glomerulosclerosis and retinopathy) are considerably less. There are, however, a few societies in which microvascular disease seems t o be less frequent in diabetics (e.g., Navajo I n d ians and Nigerian~).~ Nutritional factors may or may not contribute to these differences. Although present data are not very satisfactory it appears that there are differences among societies in rates of juvenile diabetes7 It is possible that nutritional factors are influential in this respect. In Japan, for instance, marked changes in the national diet during recent years have been associated with substantial increases in rates of juvenile diabetes.*' Rates of ketosis appear to vary among populations of diabetics, but it is not yet clear whether dietary factors play a role in these variations.' p'
v7
Diet Therapy In recent years considerable progress has been made in understanding the potentialities and priorities of diet therapy in the various types of diabetes. It is now clear that in several respects, dietary objectives and strategies should be quite different in t h e t w o main types of diabetes. In maturity-onset obese diabetics, reduction of adiposity by restricting calories or increasing exercise, or both, reduces hyperglycemia. Even more fundamental and more important, these measures also reduce the insulin resistance that attends obesity. This mitigates the "overstrain" of the beta cells and usually leads t o considerable improvement of beta-cell function. Thus, in this group, diet not only helps t o control diabetes, it reduces the severity of the disease. Return of glucose tolerance t o entirely normal levels is uncommon only because of the rarity with which weight is restored t o optimum levels and maintained a t such levels. However, even partial mitigation of adiposity is helpful. Although most NUTRITION RffIEWS/YOL. 33. NO. 7 / JULY 1975 195
experts still advise restriction or complete proscription of refined sugars, it is now the consensus that limitation of calories is usually the prime goal of therapy in this type of obese diabetic. In order to establish new eating habits and patterns it may also be desirable to encourage a certain degree of consistency in the quantity, characteristics, and timing of the feedings in obese diabetics. These latter strategies, however, are not of urgent priority in this type of diabetes. For example, a high degree of consistency is not required from day to day in amounts of dietary starch, in total calories, or in the timing of feedings, as long as long-term caloric intake remains low enough to permit control of adiposity. Between-meal snacks and bedtime feedings are usually not necessary or desirable in obese diabetics. On the other hand, lean patients with no endogenous insulin require approaches that are quite different in several respects. Calories should not be restricted below normal levels. It is usually desirable to provide smaller meals and one to three between-meal snacks in order to distribute food consumption to match roughly the time-action pattern of administered insulin. This mitigates postprandial surges of hyperglycemia and protects against hypoglycemia. In contrast to the typical situation in obese diabetics, no endogenous insulin is available in response to meals. In these lean, insulin-dependent patients it is usually desirable to provide for a considerable degree of consistency and predictability of the distribution, amounts, and characteristics of the feedings. In contrast to the therapy of obese diabetics, these patients also need considerable instruction on how to adjust the diet to contend with vagaries that may include unavoidable delay of mea Is, u n usu a I exercise, complicating illnesses, management and prevention of hypoglycemic episodes, etc. In both of the major types of diabetes there is decreasing emphasis on the priority of carbohydrate restriction.2 * There are two reasons for this. First, it is now clear that insulin requirement is, in the long run, s2
196 NUTRITION REVIEWSIVOL. 33, NO. 7 1 JULY 1975
more related to total fuel supply than to the amount of dietary carbohydrate itself. With excellent help from other elements of the body economy, the liver can make glucose readily out of a variety of sources. It is now evident that diets generous in starch are very well tolerated by both insulin-dependent and insulin-independent diabetics, provided that levels of calorie consumption are appropriate. Both plasma glucose and lipid levels usually respond quite favorably to such regimens. Even diabetics with Type I V hyperlipoproteinemia do well on liberal starch diets when levels of dietary sugar and calories are appropriately controlled. Second, i f levels of carbohydrate are sharply restricted, it is difficult to construct diets that are not high in fat and cholesterol. In the United States traditional diabetic diets of the past contained about 42 percent of calories as fat and generous amounts of cholesterol; while in Asian diabetics fat provided typically only about 15 percent of calories and levels of dietary cholesterol have been quite low. North American and Western European rates of coronary disease are exceedingly high in diabetics and coronary disease accounts for a majority of the deaths. In contrast, coronary atherosclerosis is far less common in the diabetics who consumed high starch, low fat, low cholesterol diets. These considerations have now led most Western diabetologists to prescribe diabetic diets that are lower in saturated fat and cholesterol than the previous traditional regimens. The calories derived from saturated fat can then be replaced if necessary by calories from three other sources: starch, vegetable fat, and protein. A typical "modernized" diabetic diet for a person in a Western society has the following characteristics: It contains a number of calories adequate to reach or maintain optimum weight. Refined sugars are proscribed or sharply limited, but about 10 to 15 percent of calories consist of sugars from natural sources such as fruit, vegetables, and milk. Fat is limited to about 25 to 35 percent of calories. Usually it is possible to reduce ani-
ma1 fat and cholesterol considerably without making the regimen unattractive or unfeasible. Saturated f a t makes up only about 10 t o 15 percent of calories in such a regimen (about half as much as the typical American diet), while vegetable f a t (monoand polyunsaturates) supplies about 15 t o 20 percent of calories. In most adult patients, levels of protein are not critical and may range from as low as 12 percent of calories t o as high as 24 percent depending on food preferences, food budgets, and other factors. Children, and women who are pregnant or lactating, require a t least 1.5 g per kilogram. The remainder of calories, usually 30 t o 40 percent, are derived from complex carbohydrates (mainly starches). The most difficult aspects of the implementation of these "modernized diabetic diets" has been persuading dietitians, physicians, and patients that liberal amounts of starch are not bad for diabetes. In many instances these regimens do require the patient t o eat even more starch than his family or friends. A review of the considerations discussed above, however, usually leads t o an understanding and acceptance of this approach. A considerable body of recent evidence also supports the strategy of encouraging the ingestion of starches high in fiber.3*1 Other recent publications have discussed the problems responsible for low rates of adherence t o dietary prescriptions;22 methods for formulating diet prescript i o n ~ ; ~ the~ -mechanics ~ ~ of developing and implementing prescription^;^ 3 - 2 the importance and methods of educating the ~ a t i e n t ; ~and ~ - ~the ~ limited role of special foods such as artificial sweeteners, lowcalorie and low-carbohydrate "diet" drinks and food products, fructose, sorbi. ~ texts ~ edited by tol, alcohol, e t ~ The Marble e t al. (Joslin's book)26 and by Sussman and met^^^ are good sources of information on diabetes. There is considerable evidence that only a minority of diabetics receive and follow on a long-term basis appropriate diet prescriptions.2 It is also clear that diet therapy is feasible and e f f e c t i ~ e . ~ * *0~ ~ - ~ ~
1. Diabetes Mellitus in Asia, 1970. S. Tsuji and M. Wada, Editors. Excerpta Medica, Amsterdam, 1971 2. A. M. Cohen, A. Teitelbaum, and R. Saliternik, Metabolism 21: 235-240, 1972 3. T. L. Cleave in The Saccharine Disease. John Wright & Sons, Ltd., Bristol, 1974 4. K. M.West and J. M. Kalbfleisch, Diabetes 19: 656-663, 1970 5. K. M. West and J. M. Kalbfleisch, Diabetes 20: 99-108, 1971 6. K. M. West in Is the Risk of Becoming Diabetic Affected by Sugar Consumption? S. S. Hillebrand, Editor, pp. 33-43. International Sugar Research Foundation, Bethesda, 1974 7. K. M. West, Diabetes 23: 841-855, 1974 8. H. P. Himsworth, Clin. Sci. 2: 117-148, 1935-1936 9. Is the Risk of Becoming Diabetic Affected by Sugar Consumption? S. S. Hillebrand, Editor. I n ternational Sugar Research Foundation, Bethesda, 1974 10. H. P. Himsworth and E. M. Marshall, Clin. Sci. 2: 95-115, 1935 11. J. Booyens, M. de V. Frank, V. M. de Waal, G. D. Campbell, and M. D. Goldberg, S. Afr. Med. J. 44: 271-278, 1970 12. J. D. Baird, Acta Diabetol. Lat. (Suppl.) 9: 405428, 1972 13. H. A. Kahn, J. 6. Herman, J. H. Medalie, H. N. Neufeld, E. Riss, and U. Goldbourt, J. Chron. Dis. 23: 617-629, 1971 14. K. M. West in The Regulation of the Adipose Tissue Mass. J. Vague and J. Boyer, Editors. Excerpta Medica, Amsterdam, 1973 15. H. Keen in Is the Risk of Becoming Diabetic Affected by Sugar Consumption? S. S. Hillebrand, Editor, pp. 14-27. International Sugar Research Foundation, Bethesda, 1974 16. H. Trowell, Lancet I I : 998-1002, 1974 17. K. Petersen, U. Schmitthenner, and L. Kerp, Diabetologia 10: 383, 1974 18. G. C. Gerritsen and W. E. Dulin, Diabetalogia 10: 559-565, 1974 19. K. M. West, Acta Diabetol. Lat. (Suppl.) 9: 405-428, 1972 20. E. Miki and H. Maruyarna in Diabetes Mellitus in Asia 1970. S. Tsuji and M. Wada, Editors. Excerpta Medica, Amsterdam, 1971 21. E. L. Bierman, M. J. Albrink, R. A. Arky, W. E. Connor, S. Dayton, N. Spritz, and D. Steinberg, Diabetes 20: 633634, 1971 22. K. M. West, Ann. Int. Med. 79: 425-434, 1973 NUTRITION REVIEWSIVOL. 33, NO. 7 I JULY 1975
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23. J. K. Davidson in Current Therapy 1974. H. F . Conn, Editor, pp. 386-408. W. 6. Saunders Co., Philadelphia, 1974 24. K. M. West in Nutritional Support of Medical Practice. C. E. Anderson, D. B. Coursin, and H. A. Schneider, Editors. Harper-Row, New York, 1975 25. Experimental and Therapeutic Dietetics by M. A. Ohlson. Second edition. Burgess Publishing Co., Minneapolis, 1972 26. JoslinS Diabetes Mellitus. A. Marble, Editor. Eleventh edition. Lea & Febiger, Philadelphia, 1971 27. Diabetes Mellitus: Diagnosis and Treatment. K. Sussman and R. Metz, Editors, voi. IV.
28.
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30. 31. 32.
American Diabetes Association, New York, 1975 (in press) R . L. Weinsier, A. Seeman, M. G. Herrera, J. J. Simmons, and M. E. Collins, Diabetes 23: 669-673, 1974 J. K. Davidson in Epidemiologic Studies and Clinical Trials in Chronic Diseases. Pp. 44-48. Pan-American Health Organization Proceedings of Symposium, Washington, D.C., 1972 G. W. Chance, E. C. Albutt, and S. M. Edkins, Brit. Med. J. 3 : 616-618, 1969 D. B. Stone, Am. J. Med. Sci. 241: 64-70, 1961 D. B. Stone and W. E. Conner, Diabetes 12: 127-132, 1963
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