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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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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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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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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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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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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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Representative terms from entire chapter:
added sugars
