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6 Dietary Carbohydrates: Sugars and Starches SUMMARY The primary role of carbohydrates (sugars and starches) is to provide energy to cells in the body, particularly the brain, which is the only carbohydrate-dependent organ in the body. The Recom- mended Dietary Allowance (RDA) for carbohydrate is set at 130 g/d for adults and children based on the average minimum amount of glucose utilized by the brain. This level of intake, however, is typi- cally exceeded to meet energy needs while consuming acceptable intake levels of fat and protein (see Chapter 11). The median intake of carbohydrates is approximately 220 to 330 g/d for men and 180 to 230 g/d for women. Due to a lack of sufficient evidence on the prevention of chronic diseases in generally healthy indi- viduals, no recommendations based on glycemic index are made. BACKGROUND INFORMATION Classification of Dietary Carbohydrates Carbohydrates can be subdivided into several categories based on the number of sugar units present. A monosaccharide consists of one sugar unit such as glucose or fructose. A disaccharide (e.g., sucrose, lactose, and maltose) consists of two sugar units. Oligosaccharides, containing 3 to 10 sugar units, are often breakdown products of polysaccharides, which contain more than 10 sugar units. Oligosaccharides such as raffinose and stachyose are found in small amounts in legumes. Examples of polysaccharides include starch and glycogen, which are the storage forms of carbohydrates in plants and 265
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266 DIETARY REFERENCE INTAKES animals, respectively. Finally, sugar alcohols, such as sorbitol and mannitol, are alcohol forms of glucose and fructose, respectively. Definition of Sugars The term “sugars” is traditionally used to describe mono- and disac- charides (FAO/WHO, 1998). Sugars are used as sweeteners to improve the palatability of foods and beverages and for food preservation (FAO/ WHO, 1998). In addition, sugars are used to confer certain functional attributes to foods such as viscosity, texture, body, and browning capacity. The monosaccharides include glucose, galactose, and fructose, while the disaccharides include sucrose, lactose, maltose, and trehalose. Some commonly used sweeteners contain trisaccharides and higher saccharides. Corn syrups contain large amounts of these saccharides; for example, only 33 percent or less of the carbohydrates in some corn syrups are mono- and disaccharides; the remaining 67 percent or more are trisaccharides and higher saccharides (Glinsmann et al., 1986). This may lead to an under- estimation of the intake of sugars if the trisaccharides and higher saccharides are not included in an analysis. Extrinsic and Intrinsic Sugars The terms extrinsic and intrinsic sugars originate from the United Kingdom Department of Health. Intrinsic sugars are defined as sugars that are present within the cell walls of plants (i.e., naturally occurring), while extrinsic sugars are those that are typically added to foods. An additional phrase, “non-milk extrinsic sugars,” was developed due to the lactose in milk also being an extrinsic sugar (FAO/WHO, 1998). The terms were developed to help consumers differentiate sugars inherent to foods from sugars that are not naturally occurring in foods. Added Sugars The U.S. Department of Agriculture (USDA) has defined “added sugars” for the purpose of analyzing the nutrient intake of Americans using nation- wide surveys, as well as for use in the Food Guide Pyramid. The Food Guide Pyramid, which is the food guide for the United States, translates recommendations on nutrient intakes into recommendations for food intakes (Welsh et al., 1992). Added sugars are defined as sugars and syrups that are added to foods during processing or preparation. Major sources of added sugars include soft drinks, cakes, cookies, pies, fruitades, fruit punch, dairy desserts, and candy (USDA/HHS, 2000). Specifically, added sugars include white sugar, brown sugar, raw sugar, corn syrup, corn-syrup
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267 D IETARY CARBOHYDRATES: SUGARS AND STARCHES solids, high-fructose corn syrup, malt syrup, maple syrup, pancake syrup, fructose sweetener, liquid fructose, honey, molasses, anhydrous dextrose, and crystal dextrose. Added sugars do not include naturally occurring sugars such as lactose in milk or fructose in fruits. The Food Guide Pyramid places added sugars at the tip of the pyramid and advises consumers to use them sparingly (USDA, 1996). Table 6-1 shows the amounts of added sugars that could be included in diets that meet the Food Guide Pyramid for three different calorie levels. Since USDA developed the added sugars definition, the added sugars term has been used in the scientific literature (Bowman, 1999; Britten et al., 2000; Forshee and Storey, 2001; Guthrie and Morton, 2000). The 2000 Dietary Guidelines for Americans used the term to aid consumers in identify- ing beverages and foods that are high in added sugars (USDA/HHS, 2000). Although added sugars are not chemically different from naturally occur- ring sugars, many foods and beverages that are major sources of added sugars have lower micronutrient densities compared with foods and bever- ages that are major sources of naturally occurring sugars (Guthrie and Morton, 2000). Currently, U.S. food labels contain information on total sugars per serving, but do not distinguish between sugars naturally present in foods and added sugars. Definition of Starch Starch consists of less than 1,000 to many thousands of α-linked glucose units. Amylose is the linear form of starch that consists of α-(1,4) linkages of glucose polymers. Amylopectin consists of the linear TABLE 6-1 Amount of Sugars That Can Be Added for Three Different Energy Intakes That Meet the Food Guide Pyramid Food Guide Pyramid Patterns at Three Calorie Levels Pattern A Pattern B Pattern C Kilocalories (approximate) 1,600 2,200 2,800 Bread/grain group (servings) 6 9 11 Vegetable group (servings) 3 4 5 Fruit group (servings) 2 3 4 Milk group (servings) 2–3 2–3 2–3 Meat group (oz) 5 6 7 Total fat (g) 53 73 93 Total added sugars (tsp)a 6 12 18 a 1 tsp added sugars = 4 g added sugars. SOURCE: USDA (1996).
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268 DIETARY REFERENCE INTAKES α-(1,4) glucose polymers, as well as branched 1-6 glucose polymers. The amylose starches are compact, have low solubility, and are less rapidly digested. They are prone to retrogradation (hydrogen bonding between amylose units) to form resistant starches (RS3). The amylopectin starches are digested more rapidly, presumably because of the more effective enzy- matic attack of the more open-branched structure. Definition of Glycemic Response, Glycemic Index, and Glycemic Load Foods containing carbohydrate have a wide range of effects on blood glucose concentration during the time course of digestion (glycemic response), with some resulting in a rapid rise followed by a rapid fall in blood glucose concentration, and others resulting in a slow extended rise and a slow extended fall. Prolonging the time over which glucose is avail- able for absorption in healthy individuals greatly reduces the postprandial glucose response (Jenkins et al., 1990). Holt and coworkers (1997), how- ever, reported that the insulin response to consumption of carbohydrate foods is influenced by the level of the glucose response, but varies among individuals and with the amount of carbohydrate consumed. Adults with type 1 or type 2 diabetes have been shown to have similar glycemic responses to specific foods (Wolever et al., 1987), whereas glycemic responses were shown to vary with severity of diabetes (Gannon and Nuttall, 1987). Individuals with lactose maldigestion have reduced glycemic responses to lactose-containing items (Maxwell et al., 1970). The glycemic index (GI) is a classification proposed to quantify the relative blood glucose response to foods containing carbohydrate (Jenkins et al., 1981). It is defined as the area under the curve for the increase in blood glucose after the ingestion of a set amount of carbohydrate in an individual food (e.g., 50 g) in the 2-hour postingestion period as compared with ingestion of the same amount of carbohydrate from a reference food (white bread or glucose) tested in the same individual, under the same conditions, using the initial blood glucose concentration as a baseline. The average daily dietary GI of a meal is calculated by summing the products of the carbohydrate content per serving for each food, times the average number of servings of that food per day, multiplied by the GI, and all divided by the total amount of carbohydrate (Wolever and Jenkins, 1986). Individual foods have characteristic values for GI (Foster-Powell and Brand Miller, 1995), although within-subject and between-subject vari- ability is relatively large (Wolever et al., 1991). Because GI has been deter- mined by using 50-g carbohydrate portions of food, it is possible that there is a nonlinear response between the amount of food ingested, as is the case for fructose (Nuttall et al., 1992) and the glycemic response.
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269 D IETARY CARBOHYDRATES: SUGARS AND STARCHES The average glycemic load is derived the same way as the GI, but without dividing by the total amount of carbohydrate consumed. Thus, glycemic load is an indicator of glucose response or insulin demand that is induced by total carbohydrate intake. GI is referred to throughout this chapter because many studies have used this classification system. This does not imply that it is the best or only system for classifying glycemic responses or other statistical associations. The GI approach does not consider different metabolic responses to the ingestion of sugars versus starches, even though they may have the same GI values (Jenkins et al., 1988b). Utilization of the Glycemic Index Several food characteristics that influence GI are summarized in Table 6-2. Broadly speaking, the two main factors that influence GI are carbohydrate type and physical determinants of the rate of digestion, such as whether grains are intact or ground into flour, food firmness resulting from cooking, ripeness, and soluble fiber content (Wolever, 1990). Intrin- sic factors such as amylose:amylopectin ratio, particle size and degree of gelatinization, as well as extrinsic factors such as enzyme inhibitors and food preparation and processing, affect GI in their ability to interact with digestive enzymes and the consequent production of monosaccharides. With progressive ripeness of foods, there is a decrease in starch and an increase in free sugar content. The ingestion of fat and protein has been shown to decrease the GI of foods by increasing plasma glucose disposal through the increased secretion of insulin and possibly other hormones (Gannon et al., 1993; Nuttall et al., 1984). Significantly high correlations between GI and protein, fat, and total caloric content were observed and TABLE 6-2 Factors That Reduce the Rate of Starch Digestibility and the Glycemic Index Intrinsic Extrinsic High amylose:amylopectin ratio Protective insoluble fiber seed coat as in whole intact grains Intact grain/large particle size Viscous fibers Intact starch granules Enzyme inhibitors Raw, ungelatinized or unhydrated starch Raw foods (vs. cooked foods) Physical interaction with fat or protein Minimal food processing Reduced ripeness in fruit Minimal (compared to extended) storage
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270 DIETARY REFERENCE INTAKES explained 87 percent of the variation in glycemic response among foods (Hollenbeck et al., 1986). In addition to these factors, the GI of a meal can affect the glycemic response of the subsequent meal (Ercan et al., 1994; Wolever et al., 1988). Examples of published values for the GI of pure carbohydrates and other food items are shown in Table 6-3. A number of research groups have reported a significant relationship between mixed-meal GI predicted from individual food items and either the GI measured directly (Chew et al., 1988; Collier et al., 1986; Gulliford et al., 1989; Indar-Brown et al., 1992; Järvi et al., 1995; Wolever and Jenkins, 1986; Wolever et al., 1985, 1990) or metabolic parameters such as high TABLE 6-3 Glycemic Index (GI) of Common Foods GI Food Item (White Bread = 100) Rice, white, low-amylose 126 Baked potato 121 Corn flakes 119 Rice cakes 117 Jelly beans 114 Cheerios 106 Carrots 101 White bread 101 Wheat bread 99 Soft drink 97 Angel food cake 95 Sucrose 92 Cheese pizza 86 Spaghetti (boiled) 83 Popcorn 79 Sweet corn 78 Banana 76 Orange juice 74 Rice, Uncle Ben’s converted long-grain 72 Green peas 68 Oat bran bread 68 Orange 62 All-Bran cereal 60 Apple juice 58 Pumpernickel bread 58 Apple 52 Chickpeas 47 Skim milk 46 Kidney beans 42 Fructose 32 SOURCE: Foster-Powell and Brand Miller (1995).
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271 D IETARY CARBOHYDRATES: SUGARS AND STARCHES density lipoprotein cholesterol concentration that are known to be influ- enced by GI (Liu et al., 2001). Although the glycemic response of diabetics is distinctly higher than that of healthy individuals, the relative response to different types of mixed meals is similar (Indar-Brown et al., 1992; Wolever et al., 1985). The prediction of GI in mixed meals by Wolever and Jenkins (1986) is shown in Figure 6-1. In contrast, some studies reported no such relationship between the calculated and measured GI of mixed meals (Coulston et al., 1984; Hollenbeck et al., 1986; Laine et al., 1987). There are a number of reasons why different groups have reported different findings on the calculation of GI in mixed meals. As previously discussed, there are a number of intrinsic (e.g., particle size) and extrinsic (e.g., ingestion of fat and protein, degree of food preparation) factors that can affect the glycemic response of a meal (Table 6-2), some of which are known to also affect the absorption of other nutrients such as vitamins and minerals. For instance, coingestion of dietary fat and protein can some- times have a significant influence on the glucose response of a carbohydrate- containing food, with a reduction in the glucose response generally seen with increases in fat or protein content (Gulliford et al., 1989; Holt et al., Mixed Meal GI Incremental Plasma Glucose Area (mg/dl-h) FIGURE 6-1 Correlation between calculated glycemic index (GI) of four test meals (•) and incremental blood glucose response areas. Based on data from Coulston et al. (1984). Reproduced, with permission, from Wolever and Jenkins (1986). Copy- right 1986 by the American Society for Clinical Nutrition.
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272 DIETARY REFERENCE INTAKES 1997). Palatability can have an influence on GI, independent of food type and composition (Sawaya et al., 2001). Furthermore, there are expected inherent biological variations in glucose control and carbohydrate toler- ance that are unrelated to the GI of a meal. Finally, varied experimental design and methods for calculating the area under the blood glucose curve can result in a different glycemic response to meals of a similar predicted GI (Coulston et al., 1984; Wolever and Jenkins, 1986). For instance, it is important that the incremental area, rather than the absolute area, under the blood glucose curve be measured (Wolever and Jenkins, 1986). Taken together, the results from these different studies indicate that the GI of mixed meals can usually be predicted from the GI of individual food components. Physiology of Digestion, Absorption, and Metabolism Digestion Starch. The breakdown of starch begins in the mouth where salivary amylase acts on the interior α-(1,4) linkages of amylose and amylopectin. The digestion of these linkages continues in the intestine where pancre- atic amylase is released. Amylase digestion produces large oligosaccharides (α-limit dextrins) that contain approximately eight glucose units of one or more α-(1,6) linkages. The α-(1,6) linkages are cleaved more easily than the α-(1,4) linkages. Oligosaccharides and Sugars. The microvilli of the small intestine extend into an unstirred water layer phase of the intestinal lumen. When a limit dextrin, trisaccharide, or disaccharide enters the unstirred water layer, it is rapidly hydrolyzed by enzymes bound to the brush border membrane. These limit dextrins, produced from starch digestion, are degraded by glucoamylase, which removes glucose units from the nonreducing end to yield maltose and isomaltose. Maltose and isomaltose are degraded by intestinal brush border disaccharidases (e.g., maltase and sucrase). Maltase, sucrase, and lactase digest sucrose and lactose to monosaccharides prior to absorption. Intestinal Absorption Monosaccharides first diffuse across to the enterocyte surface, followed by movement across the brush border membrane by one of two mecha- nisms: active transport or facilitated diffusion.
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273 D IETARY CARBOHYDRATES: SUGARS AND STARCHES Active Transport. The intestine is one of two organs that vectorially transports hexoses across the cell into the bloodstream. The mature enterocytes capture the hexoses directly ingested from food or produced from the digestion of di- and polysaccharides. Active transport of sugars involves sodium dependent glucose transporters (SGLTs) in the brush border membrane (Díez-Sampedro et al., 2001). Sodium is pumped from the cell to create a gradient between the interior of the cell and the lumen of the intestine, requiring the hydrolysis of adenosine triphosphate (ATP). The resultant gradient results in the cotransport of one molecule each of sodium and glucose. Glucose is then transported across the basolateral membrane of the small intestine by glucose transporter (GLUT) 2. Similar to glucose, galactose utilizes SGLT cotransporters and basolateral GLUT 2. Fructose is not transported by SGLT cotransporters. Facilitated Diffusion. There are also transporters of glucose that require neither sodium nor ATP. The driving force for glucose transport is the glucose gradient and the energy change that occurs when the unstirred water layer is replaced with glucose. In this type of transport, called facili- tated diffusion, glucose is transported down its concentration gradient (from high to low). Fructose is also transported by facilitated diffusion. One facilitated glucose transporter, GLUT 5, has been identified in the small intestine (Levin, 1999). GLUT 5 appears to transport glucose poorly and is the main transporter of fructose. Metabolism Cellular Uptake. Absorbed sugars are transported throughout the body to cells as a source of energy. The concentration of glucose in the blood is highly regulated by the release of insulin. Uptake of glucose by the adipocyte and muscle cell is dependent upon the binding of insulin to a membrane-bound insulin receptor that increases the translocation of intra- cellular glucose transporters (GLUT 4) to the cell membrane surface for uptake of glucose. GLUT 1 is the transporter of the red blood cell; how- ever, it is also present in the plasma membrane of many other tissues (Levin, 1999). Besides its involvement in the small intestine, GLUT 2 is expressed in the liver and can also transport galactose, mannose, and fruc- tose (Levin, 1999). GLUT 3 is important in the transport of glucose into the brain (Levin, 1999). Intracellular Utilization of Galactose. Absorbed galactose is primarily the result of lactose digestion. The majority of galactose is taken up by the liver where it is metabolized to galactose-1-phosphate, which is then con-
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274 DIETARY REFERENCE INTAKES verted to glucose-1-phosphate. Most of the glucose-1-phosphate derived from galactose metabolism is converted to glycogen for storage. Intracellular Utilization of Fructose. Absorbed fructose, from either direct ingestion of fructose or digestion of sucrose, is transported to the liver and phosphorylated to fructose-1-phosphate, an intermediate of the glycolytic pathway, which is further cleaved to glyceraldehyde and dihydroxyacetone phosphate (DHAP). DHAP is an intermediary metabolite in both the glycolytic and gluconeogenic pathways. The glyceraldehyde can be con- verted to glycolytic intermediary metabolites that serve as precursors for glycogen synthesis. Glyceraldehyde can also be used for triacylglycerol synthesis, provided that sufficient amounts of malonyl coenzyme A (CoA) (a precursor for fatty acid synthesis) are available. Intracellular Utilization of Glucose. Glucose is a major fuel used by most cells in the body. In muscle, glucose is metabolized anaerobically to lactate via the glycolytic pathway. Pyruvate is decarboxylated to acetyl CoA, which enters the tricarboxylic acid (TCA) cycle. Reduced coenyzmes generated in the TCA cycle pass off their electrons to the electron transport system, where it is completely oxidized to carbon dioxide and water. This results in the production of the high-energy ATP that is needed for many other metabolic reactions. After the consumption of carbohydrates, fat oxida- tion is markedly curtailed, allowing glucose oxidation to provide most of the body’s energy needs. In this manner, the body’s glucose and glycogen content can be reduced toward more normal concentrations. Gluconeogenesis. Glucose can be synthesized via gluconeogenesis, a metabolic pathway that requires energy. Gluconeogenesis in the liver and renal cortex is inhibited via insulin following the consumption of carbohy- drates and is activated during fasting, allowing the liver to continue to release glucose to maintain adequate blood glucose concentrations. Glycogen Synthesis and Utilization. Glucose can also be converted to glycogen (glycogenesis), which contains α-(1-4) and α-(1-6) linkages of glucose units. Glycogen is present in the muscle for storage and utilization and in the liver for storage, export, and maintenance of blood glucose concentrations. Glycogenesis is activated in skeletal muscle by a rise in insulin concentration following the consumption of carbohydrate. In the liver, glycogenesis is activated directly by an increase in circulating glucose, fructose, galactose, or insulin concentration. Muscle glycogen is mainly used in the muscle. Following glycogenolysis, glucose can be exported from the liver for maintenance of normal blood glucose concentrations and for use by other tissues.
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275 D IETARY CARBOHYDRATES: SUGARS AND STARCHES Formation of Amino Acids and Fatty Acids from Carbohydrates. Pyruvate and intermediates of the TCA cycle are precursors of certain nonessential amino acids. A limited amount of carbohydrate is converted to fat because de novo lipogenesis is generally quite minimal (Hellerstein, 1999; Parks and Hellerstein, 2000). This finding is true for those who are obese, indi- cating that the vast majority of deposited fat is not derived from dietary carbohydrate when consumed at moderate levels. Insulin. Based on the metabolic functions of insulin discussed above, the ingestion of carbohydrate produces an immediate increase in plasma insulin concentrations. This immediate rise in plasma insulin concentra- tion minimizes the extent of hyperglycemia after a meal. The effects of insulin deficiency (elevated blood glucose concentration) are exemplified by type 1 diabetes. Individuals who have type 2 diabetes may or may not produce insulin and insulin-dependent muscle and adipose tissue cells may or may not respond to increased insulin concentrations (insulin resis- tant); therefore, circulating glucose is not effectively taken up by these tissues and metabolized. Clinical Effects of Inadequate Intake The lower limit of dietary carbohydrate compatible with life appar- ently is zero, provided that adequate amounts of protein and fat are con- sumed. However, the amount of dietary carbohydrate that provides for optimal health in humans is unknown. There are traditional populations that ingested a high fat, high protein diet containing only a minimal amount of carbohydrate for extended periods of time (Masai), and in some cases for a lifetime after infancy (Alaska and Greenland Natives, Inuits, and Pampas indigenous people) (Du Bois, 1928; Heinbecker, 1928). There was no apparent effect on health or longevity. Caucasians eating an essentially carbohydrate-free diet, resembling that of Greenland natives, for a year tolerated the diet quite well (Du Bois, 1928). However, a detailed modern comparison with populations ingesting the majority of food energy as carbohydrate has never been done. It has been shown that rats and chickens grow and mature success- fully on a carbohydrate-free diet (Brito et al., 1992; Renner and Elcombe, 1964), but only if adequate protein and glycerol from triacylglycerols are provided in the diet as substrates for gluconeogenesis. It has also been shown that rats grow and thrive on a 70 percent protein, carbohydrate-free diet (Gannon et al., 1985). Azar and Bloom (1963) also reported that nitrogen balance in adults ingesting a carbohydrate-free diet required the ingestion of 100 to 150 g of protein daily. This, plus the glycerol obtained from triacylglycerol in the diet, presumably supplied adequate substrate
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328 DIETARY REFERENCE INTAKES Fitzsimons D, Dwyer JT, Palmer C, Boyd LD. 1998. Nutrition and oral health guide- lines for pregnant women, infants, and children. J Am Diet Assoc 98:182–189. Fomon SJ, Thomas LN, Filer LJ, Anderson TA, Nelson SE. 1976. Influence of fat and carbohydrate content of diet on food intake and growth of male infants. Acta Paediatr Scand 65:136–144. Fontvieille AM, Acosta M, Rizkalla SW, Bornet F, David P, Letanoux M, Tchobroutsky G, Slama G. 1988. A moderate switch from high to low glycaemic-index foods for 3 weeks improves the metabolic control of type I (IDDM) diabetic subjects. Diabetes Nutr Metab 1:139–143. Fontvieille AM, Rizkalla SW, Penfornis A, Acosta M, Bornet FRJ, Slama G. 1992. The use of low glycaemic index foods improves metabolic control of diabetic patients over five weeks. Diabet Med 9:444–450. Ford ES, Liu S. 2001. Glycemic index and serum high-density lipoprotein choles- terol concentration among US adults. Arch Intern Med 161:572–576. Forshee RA, Storey ML. 2001. The role of added sugars in the diet quality of children and adolescents. J Am Coll Nutr 20:32–43. Forsum E, Kabir N, Sadurskis A, Westerterp K. 1992. Total energy expenditure of healthy Swedish women during pregnancy and lactation. A m J Clin Nutr 56:334–342. Foster-Powell K, Brand Miller J. 1995. International tables of glycemic index. Am J Clin Nutr 62:871S–890S. Franceschi S, Dal Maso L, Augustin L, Negri E, Parpinel M, Boyle P, Jenkins DJA, La Vecchia C. 2001. Dietary glycemic load and colorectal cancer risk. Ann Oncol 12:173–178. Frost G, Wilding J, Beecham J. 1994. Dietary advice based on the glycaemic index improves dietary profile and metabolic control in type 2 diabetic patients. Diabet Med 11:397–401. Frost G, Leeds A, Trew G, Margara R, Dornhorst A. 1998. Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycemic diet. Metabolism 47:1245–1251. Frost G, Leeds AA, Doré CJ, Madeiros S, Brading S, Dornhorst A. 1999. Glycaemic index as a determinant of serum HDL-cholesterol concentration. L ancet 353:1045–1048. Gamble JL. 1946. Physiological information gained from studies on the life raft ration. Harvey Lect 42:247–273. Gannon MC, Nuttall FQ. 1987. Factors affecting interpretation of postprandial glucose and insulin areas. Diabetes Care 10:759–763. Gannon MC, Nuttall FQ. 1999. Protein and diabetes. In: Franz MJ, Bantle JP, eds. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association. Pp. 107–125. Gannon MC, Niewoehner CB, Nuttall FQ. 1985. Effect of insulin administration on cardiac glycogen synthase and synthase phosphatase activity in rats fed diets high in protein, fat or carbohydrate. J Nutr 115:243–251. Gannon MC, Nuttall FQ, Westphal SA, Seaquist ER. 1993. The effect of fat and carbohydrate on plasma glucose, insulin, C-peptide, and triglycerides in normal male subjects. J Am Coll Nutr 12:36–41. Gibbons A. 1998. Solving the brain’s energy crisis. Science 280:1345–1347. Gibney M, Sigman-Grant M, Stanton JL, Keast DR. 1995. Consumption of sugars. Am J Clin Nutr 62:178S–194S.
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