19

Nutritional Aspects of Diabetes

Diabetes mellitus is a spectrum of inherited and acquired disorders that is characterized
by elevated circulating blood glucose levels. This condition results from an absolute or a
relative deficiency of insulin (the hormone secreted by pancreatic h cells) and/or insulin
action with a consequent deranged metabolism of carbohydrate, fat, and protein. Diabetes
is a major health problem affecting 5–6% of the U.S. population. It is a leading
cause of blindness, amputation, and renal failure (16 million in 1995), and is a major
cause of heart attacks and stroke. Diabetes can be controlled and the patients with this
disease can lead a productive life. Nutrition plays a key role in the management of
this disease.
I. CLASSIFICATION AND EPIDEMIOLOGY
Two common types of diabetes that differ in both clinical manifestations and etiology are
well recognized: Type I or insulin-dependent diabetes (IDD), formerly called juvenileonset
diabetes, and Type II or noninsulin-dependent diabetes (NIDD), formerly called
maturity-onset diabetes (Table 1).
Type I diabetes usually, but not always, begins before 20 years of age. It constitutes
about 5% of all cases of diabetes. The peak age of onset is 11–13 years, which usually
coincides with puberty. The next peak age of onset occurs at 6–8 years of age, around the
start of grade school. The frequency is similar in boys and in girls. Approximately 7.4% of
adults who are diagnosed with diabetes between 30 and 74 years of age have Type I
diabetes. Patients with this type of diabetes have virtually no capacity to secrete insulin
after the disease is established. Type I diabetes is characterized by a tendency toward
ketosis and an absolute dependence on insulin for maintenance of health and survival. The
presentation of diabetes is often acute because of a sudden reduction in insulin secretion
that is usually related to autoimmune damage to pancreatic h cells in a genetically
susceptible individual. Some patients with Type I diabetes have a strong family history of
autoimmune conditions such as autoimmune thyroid or adrenal disease.
The genetics of Type I diabetes are incompletely understood. There is concordance
in about 50% of identical twins; however, the pattern of inheritance is not complete,
implying that several genes as well as unknown environmental factors may be involved.

TABLE 1 Comparison of Two Types of Diabetes

Insulin-dependent
(Type I)
Non-insulin-dependent
(Type II)
Age of onset Usually before age 20 years Usually after age
40 years
Nutritional status
(prior to diagnosis)
Generally malnourished Mostly obese
Genetic predisposition Moderate Strong
Prevalence Less than 6% of all diabetics About 95% of all
diabetics
Plasma insulin Very low or absent Low, normal, or high
Ketosis Common in untreated patients Rare
Acute complications Ketosis
Insulin treatment Always necessary Usually not required

Type II diabetes is usually associated with an older age of onset, around 40 years of
age or more. In the United States, approximately 95% of all individuals with diabetes have
Type II diabetes, and of these, about 80% are obese. Both the incidence and the prevalence
of diabetes increase dramatically with age. For example, the prevalence of self-reported
diabetes is 1.1% among persons 20–39 years of age, and is 13.6% among persons 68–78
years of age. It is the most common of all metabolic disorders. It has a slow, insidious
course and may be present several years before diagnosis.
There is a consistent genetic predisposition for Type II diabetes; there is nearly 90%
concordance among identical twins in which one member has the condition: Individuals
who have both parents with Type II diabetes have a 50% chance of having the disease.
Recently, researchers have identified a gene that affects susceptibility to Type II diabetes in
some diabetes-prone populations. The gene encodes calpain-10, one member of the protein
family called calpains (calcium-activated neutral proteases), which are regulatory proteins
found in all human cells. Variations in the gene are associated with up to a threefold
increase in the risk of developing Type II diabetes. In humans, at least eight versions of
calpain-10 are expressed in different tissues. One form is found in pancreatic islets.
Variations in calpain-10 affect the rate of insulin-stimulated glucose oxidation.
Type II diabetes appears to start with the resistance of insulin to stimulate glucose
uptake in insulin-sensitive tissues (e.g., muscle, adipose tissue). The pancreas tries to
compensate by producing and by secreting above-normal amounts of insulin to maintain
normal blood sugar levels. During this process, the h cells slowly require higher levels of
blood sugar to signal the secretion of insulin, resulting in impaired glucose tolerance. At
some future time, the pancreas may not be able to maintain these compensatory high levels
of insulin secretion.
Conditions associated with the development of insulin resistance, especially central
obesity (as estimated clinically by a high waist-to-hip ratio), greatly increase the risk of
Type II diabetes, although some lean individuals are insulin-resistant. Even in insulinresistant
individuals, impaired insulin-secretory capacity appears to be responsible for the
diabetic state. Both genetic and environmental factors contribute to the etiology of Type II
diabetes. Although there can be limitations on secretory capacity in Type II diabetes,
together with the presence of insulin insensitivity, these patients do not have an absolute

Nutritional Aspects of Diabetes

dependence on injectable insulin for their survival in the early stages. The hyperglycemia
can often be controlled by dietary means only and physical activity, or with an oral
hypoglycemic drug. Some insulin is detectable in the plasma of nearly all patients in this
category and they are, therefore, less prone to ketosis. In this sense, the disease is less
severe than Type I diabetes, but long-term complications occur in both types. Most persons
with Type II diabetes may be insulinopenic later on and may have to inject insulin.
In addition to the two types of diabetes described above, there is a category that
constitutes a heterogeneous groupings of patients for whom a designation of either of the
traditional forms of diabetes appears inappropriate. These are all categorized as secondary
diabetes. These include carbohydrate intolerance as a result of pancreatic insufficiency
following chronic recurrent pancreatitis and secondary to the administration of certain
drugs. Pregnant women with no previous history of abnormal carbohydrate metabolism
may develop impaired glucose tolerance or overt diabetes mellitus. Most patients will
return to normal glucose tolerance in the postpartum state.
An estimated 18 million persons in the United States have diabetes. Over 600,000
persons are newly diagnosed with diabetes each year. The prevalence of the disease is
highest among Native Americans; adult Pima Indians have a prevalence of about 50%.
Relative to white people, the prevalence of Type II diabetes is higher in African Americans
(1.6 times) and Mexican Americans (1.9 times). The overall prevalence of diabetes among
women is estimated to be 7.7%, substantially higher than among men, which is estimated
at 5.51%. According to the report by the Centers for Disease Control and Prevention
(CDC), the prevalence of diagnosed cases of diabetes increased by a third (from 4.9% to
6.5%) between 1990 and 1998. As the American population becomes increasingly nonwhite
and obese, the disease spreads rapidly. The CDC predicts that the national incidence
of diabetes will rise by 37.5% by the year 2025.
Diabetes is a serious condition that places people at risk for greater morbidity and
mortality relative to the nondiabetic population. For example, compared with the general
population, the mortality rate for people with Type I diabetes is 5–12 times higher, and for
adults with Type II diabetes, it is two times higher. In 1993, approximately 400,000 deaths
from all causes were reported in individuals with diabetes. This figure represents 18% of
all deaths of individuals aged 25 years and older in the United States. According to the
National Center for Health Statistics, diabetes was the seventh leading cause of death by
disease type. Diabetes is the fourth leading cause of death in African American women,
and the third leading cause of death in Hispanic women aged 45–74 years and in Native
American women aged 65–74 years. Morbidity also is greater for people with diabetes and
is primarily related to acute and chronic complications associated with the condition.
In 1997, the annual per capita health care expenditure for people with diabetes was
approximately three times that for individuals without diabetes (US$10,071 versus
US$2699). An estimated US$77.7 billion, or approximately 8% of all U.S. healthcare
dollars, was spent on people with diabetes and hospitalization accounted for 62% of the
direct health care costs.
There is considerable geographical variation in the incidence of Type I and Type II
diabetes. For example, Scandinavia has the highest rate of Type I diabetes (in Finland, the
incidence is 35/100,000 per year); the Pacific Rim has a much lower rate (in Japan and
China, the incidence is 1–3/100,000 per year), and Northern Europe and the United States
have an intermediate rate of incidence (8–17/100,000 per year). The prevalence of Type II
diabetes is highest in certain Pacific islands, is intermediate in countries such as India and
the United States, and is relatively low in China and Russia. This variability is usually due to both genetic and
environmental factors. The prevalence of the disease is increasing
steadily in developing countries and parallels the increase in obesity. There are currently
more than 150 million patients with diabetes worldwide and this number is estimated to
increase to 220 million by the year 2010.
II. DIAGNOSIS OF DIABETES
Patients with Type I diabetes can be usually recognized by the abrupt appearance of
polyuria (frequent urination), polydipsia (excessive thirst), and polyphagia (excessive
hunger), which is often triggered by stress or illness. These symptoms are usually
accompanied by rapid weight loss and weakness, and an unequivocal elevation of blood
glucose (200 mg/dl). Fasting plasma glucose levels above 140 mg/dl on two occasions are
diagnostic for both types of diabetes.
An oral glucose tolerance test (OGTT) is indicated for those with fasting plasma
glucose close to 140 mg/dl. The patient is given 75 g of glucose orally following an
overnight fast. Plasma glucose levels are determined at 30 min and at 2 hr after glucose
ingestion. Fasting plasma glucose level is initially higher (greater than 140 mg/dl) in the
diabetic person and rises to concentrations greater than 200 mg/dl following the oral
administration of glucose. The rate of glomerular filtration of glucose exceeds that of
tubular reabsorption in the kidney (approximately 180 mg/dl) and glucose appears in the
urine. In contrast, normal individuals show a fasting plasma glucose of 70–90 mg/dl and a
rise to only about 140 mg/dl following glucose load.
The ability of glucose to react nonenzymatically with free amino groups in proteins
has led to the development of several tests that can be used to assess the level of blood
glucose over a period of days or months. Glucose condenses with the amino terminal
valine residue of the h chain of hemoglobin to form glycohemoglobin (GH). The amount
of nonenzymatic glycated protein formed is proportional to the glucose concentration and
the time of exposure. Impaired fasting glucose (IFG) refers to abnormalities in glucose
homeostasis, with glucose values intermediate between normal and overt diabetes.
Individuals with fasting plasma glucose of between 126 and 140 mg/dl and between
140 and 200 mg/dl, 2 hr after glucose load, come in the IFG category and are considered at
substantial risk for developing Type II diabetes and cardiovascular diseases in the future
although they may not meet the criteria for diabetes mellitus. Diabetics have a higher
percentage of GH than do normal individuals (6–15% compared to 3–5%). A 1% change
in the GH can represent a 25–35 mg/dl change in mean plasma glucose. The half-life of
modified hemoglobin is equal to that of erythrocytes. Thus the measurement of GH
provides an index of the average plasma glucose level over about 2 months. Tests are also
available for the assessment of glycosylated albumin (GA) and since albumin’s half-life is
shorter than that of hemoglobin, the GA value reflects plasma glucose levels over only a
few weeks. Both of these tests are extremely useful measurements of glucose control in
diabetics, but neither is as sensitive as OGTT in the diagnosis of diabetes.
III. MECHANISM OF INSULIN ACTION
Insulin activates the transport system and the enzymes involved in intracellular utilization
and storage of glucose, amino acids, and fatty acids; it also inhibits catabolic processes
such as the breakdown of glycogen, fat, and protein. The actions of insulin are initiated
by binding to cell surface receptors, which are ligand-activated tyrosine protein kinases.
Nutritional Aspects of Diabetes

The receptor is a plasma membrane glycoprotein. It consists of two a subunits and two h
subunits linked by disulfide bonds to form a h–a–a–h heterotetramer. The a subunits are
entirely extracellular and contain the insulin-binding domain while the h subunits are
transmembrane proteins that possess tyrosine-specific protein kinase activity. Insulin
binding to the a subunits stimulates the tyrosine kinase activity of the h subunits, which,
in turn, results in receptor autophosphorylation, conformational changes in the h subunit,
and activation of the receptor kinase toward other substrates. These and other adaptor
proteins initiate a complex cascade of phosphorylation reactions, ultimately resulting in
the widespread metabolic effects of insulin.
The function of insulin is to control carbohydrate metabolism. Homeostatic mechanisms
maintain plasma glucose concentrations between 55 and 140 mg/dl. A minimum
concentration of 40–60 mg/dl is required to provide adequate fuel for the central nervous
system, which uses glucose as the primary energy source and is independent of insulin for
glucose utilization. Muscles and adipose tissues also use glucose as a major source of
energy, but these tissues require insulin for glucose uptake. If glucose is unavailable, these
tissues are able to use other substrates such as amino acids and fatty acids for fuel.
Normally we experience an increased blood glucose level shortly after food is
ingested—a postprandial hyperglycemia. The h cells of the islets of Langerhans sense the
increased levels of circulating glucose and secrete insulin. This hormone lowers the
concentration of glucose in the blood by inhibiting glucose production (glycogenolysis
and gluconeogenesis) and by stimulating the uptake of glucose by muscles and adipose
tissues. The liver does not require insulin for glucose transport, but insulin inhibits
gluconeogenesis and facilitates the conversion of glucose to glycogen and free fatty acids.
The latter are esterified to triglycerides, which are transported as very low density
lipoproteins (VLDL) to adipose tissue. In muscle, insulin promotes the uptake of glucose
and its conversion to glycogen. It also stimulates the uptake of amino acids and their
conversion to protein and inhibits protein degradation in muscle and other tissues. It thus
causes a decrease in the circulating concentration of most amino acids, except for alanine.
Insulin does not lower alanine concentration because it enhances the rate of transamination
of pyruvate to alanine.
In adipose tissue, glucose is converted to free fatty acids and is stored as triglycerides.
Insulin inhibits hormone-sensitive lipase in adipose tissue and prevents the
breakdown of triglycerides stored in adipose tissue to free fatty acids that may be
transported to other tissues for utilization. This counteracts the lipolytic action of glucagon,
epinephrine, and other hormones, and also reduces the concentration of glycerol (a substrate
for gluconeogenesis) and free fatty acids (substrates for the production of ketone bodies).
As blood glucose concentration drops toward normal during fasting state, insulin
release is inhibited and, simultaneously, a number of counterregulatory hormones that
oppose the effect of insulin are released (e.g., glucagon, epinephrine). As a result, several
processes maintain normal blood glucose for the central nervous system.
IV. COMPLICATIONS OF DIABETES
In diabetes mellitus, either insufficient insulin levels or insufficient insulin action reduces
the transport of glucose into muscles and adipose tissues. As the glucose is not rapidly
taken up by these tissues in the absence of insulin, the inability to clear the blood of
glucose is a typical characteristic of diabetes. In an untreated Type I diabetic patient, the
level of insulin is too low and that of glucagon is too high relative to the needs of the patient. Under these
conditions, glycolysis is inhibited and gluconeogenesis is stimulated.
The high glucagon/insulin ratio also promotes glycogen breakdown; therefore, the
hyperglycemic state is exaggerated. The blood glucose is often elevated to such a point
that the renal threshold (about 180 mg/dl) is exceeded and the glucose spills in the urine
(glucosuria). Thus the potential energy of the excreted glucose is lost to the body, with
the consequence of hunger, weight loss, and fatigue. Excessive thirst and urination result
from body water being utilized for the excretion of glucose.
In diabetes, adipose tissue is deficient in glucose (no transport) and therefore has a
reduced supply of glycerol-3-phosphate required for the synthesis of triglycerides. In the
absence of insulin, there is no (negative) control of the hormone-sensitive lipase and there
is increased breakdown of fat and oxidation of fatty acids to acetyl CoA; however, much of
the acetyl CoA cannot enter the citric acid cycle because of the inadequate supply of
oxaloacetate required for the condensation steps. Consequently, acetyl CoA is converted to
acetoacetic and h-hydroxybutyric acids (i.e., ketone bodies). Muscle tissues may use some
ketone bodies for energy metabolism. Usually there is excessive production and loss of
these substances from the blood by way of the lungs and the kidneys. Acetoacetate readily
breaks down into acetone, which is exhaled in the breath. Hence a characteristic acute
phase of the diabetic patient is the so-called acetone breath. Urinary excretion of ketone
bodies results in the loss of sodium, and a state of acidosis occurs. Some of the metabolic
complications of diabetes are listed in Table 2.
Ordinarily, a normal person on a mixed diet excretes less than 0–1 g of ketone bodies
in 24 hr. In ketosis (excessive ketone bodies in blood), values as high as 100 g/day or even
higher have been reported. This is an acute consequence of diabetes and is treated by the
administration of insulin and the management of fluid, acid–base, and electrolyte balance.
The chronic consequences of diabetes involve tissues that do not require insulin
(e.g., ocular lens, peripheral nerves, renal glomeruli). In these tissues, the intracellular
level of glucose parallels that in plasma. Among the many complications of diabetes are
kidney disease, gangrene, cardiovascular disease, retinopathy, and damage to the blood
vessels and the nervous system. Kidney disease is 17 times more common among diabetics
than among nondiabetics; heart disease and stroke are twice as common; and blindness is
25 times as common among diabetics as among nondiabetics. The life expectancy of the
diabetic patient is about a third less than that of the general population.
TABLE 2 Metabolic Complications of Diabetes
Protein Carbohydrate Fat
Decreased synthesis Glucose availability in
muscles and fat cells
decreased
Decreased synthesis
Increased catabolism Increased lipolysis
Urinary increase in
nitrogen and
potassium
Decreased glycogenesis,
increased glycogenolysis,
increased gluconeogenesis
Increased blood lipids
Increased gluconeogenesis Hyperglycemia, glucosuria;
increased volume of
urine, dehydration
Ketonemia, ketonuria;
loss of urinary
sodium, acidosis

The most common lipid abnormality in Type II diabetes is hypertriglyceridemia with

low levels of high-density lipoprotein (HDL) cholesterol. The poor control of Type I diabetes
is associated with elevated low-density lipoprotein (LDL) cholesterol levels as well
as triglyceridemia. These abnormalities contribute to the risk for cardiovascular disease.
Hypertension occurs more frequently in patients with diabetes compared with the
nondiabetic population, but the cause is unknown. Patients with Type I diabetes usually are
normotensive in the absence of nephropathy, but the blood pressure rises 1–2 years
following the onset of nephropathy. Thus hypertension in a Type I diabetic patient usually
is of renal origin. The relationship between hypertension and Type II diabetes is more
complex and is not as closely correlated with the presence of nephropathy. Hyperinsulinemia
may contribute to the pathogenesis by decreasing the renal excretion of sodium
or some other mechanism.
Metabolic syndrome (insulin resistance syndrome), also known as syndrome X, is a
term used to describe a constellation of derangements that includes insulin resistance,
hypertension, dyslipidemia, central obesity, endothelial dysfunction, and accelerated cardiovascular
disease. Epidemiological evidence supports hyperinsulinemia as a marker of
coronary artery disease, although an etiological role has not been demonstrated.
Although the mechanisms accounting for the development of diabetic complications
are probably multifactorial, most authorities accept a correlation between the degree and
duration of hyperglycemia and the frequency of complications, but the precise pathogenic
mechanisms for the development of diabetic complications are poorly understood. The
toxic effects of hyperglycemia may be the result of: (a) nonenzymatic protein glycation; (b)
increased formation of sorbitol; and (c) decreased level of myoinositol.
Hyperglycemia may promote the condensation of glucose with cellular proteins in a
reaction analogous to the formation of GH. These glycated proteins may mediate some of
the early microvascular changes of diabetes and nerve disorders. GH may not release its
oxygen normally and this may lead to blood vessel diseases, which, in turn, may damage
the eyes, kidneys, and other organs.
Elevated intracellular glucose concentrations and an adequate supply of reduced
nicotinamide adenine dinucleotide phosphate (NADPH) cause the formation of sorbitol;
this is catalyzed by aldose reductase. Sorbitol may also be converted to fructose by NADdependent
sorbitol dehydrogenase (Fig. 1). Sorbitol (and also fructose) diffuses poorly
across cell membranes and thus accumulates inside the cell and causes osmotic-induced
disturbances. An increased concentration of sorbitol is seen in the human lens and other
tissues in diabetics. Some of the pathological alterations associated with diabetes may be
attributed to this phenomenon, including cataract formation, peripheral neuropathy, and
vascular problems. There are inhibitors of aldose reductase that prevent the accumulation of sorbitol in these
tissues. These may prove useful in the treatment of the symptoms of
nerve injury in humans.
Another metabolic disturbance in nerves is a reduction in myoinositol content.
Inositol is a component of the membrane phospholipid, phosphatidyl inositol, and of the
second messenger, inositol triphosphate. The mechanism for decreased tissue myoinositol
levels in diabetics is not known; however, aldose reductase inhibitors, which decrease the
formation of sorbitol, also increase the level of inositol in nerves. The myoinositol depletion
in diabetics may be, in part, due to the competition of glucose (and sorbitol) with
myoinositol for its intracellular transport because of their structural similarity.
V. DIETARY MANAGEMENT
Diet is the cornerstone of treatment for both forms of diabetes. In general, diabetics have
the same nutritional requirements as nondiabetic individuals of the same age, sex, height,
and activity; however, the patient’s nutritional intake must be carefully monitored in
order to minimize the load placed on the blood sugar-regulating mechanism. For this
reason, the treatment of all diabetics involves some form of dietary modification and any
of the three programs may be selected, depending on the severity of the disorder: (a) diet
alone; (b) diet and oral hypoglycemic agents; and (c) diet and insulin. Patients with Type
I diabetes are treated with insulin and diet modification, whereas those with Type II
diabetes are treated with diet alone, or with oral hypoglycemic drugs, or insulin, depending
on the severity of the disease. Persons with mild Type II diabetes can frequently
be controlled by diet therapy.
The diet should meet all the nutritional needs compatible with good health practice
in the general population. The use of special ‘‘diabetic foods’’ appears to offer no
advantage because the dietary prescription can be met with commonly used foods. The
ultimate goal of nutrition intervention is a healthy individual with normal longevity. The
nutritional therapy attempts to diminish the effects of the disease by maintaining a normal
metabolic state. This is done by normalizing blood glucose levels through enhancement of
insulin sensitivity and optimization of glucose use and glucose production. This helps
maintain normal blood levels of other fuel sources such as fatty acids, ketone bodies, and
amino acids. For patients receiving insulin, special attention needs to be given to the
timing of meals and the distribution of foods to avoid a large variation in blood glucose
levels. Hypoglycemic episodes are harmful to the brain and should be avoided at all costs
in patients receiving insulin or oral hypoglycemic agents. For all diabetic persons, meals
and snacks should be well integrated with activity and exercise, because exercise increases
insulin availability and insulin sensitivity. A readily absorbable form of carbohydrates,
such as fruit juice, candy, sugar, or glucose solution, should be readily available.
VI. DIETARY FACTORS
A. Energy
Probably the most effective dietary management for NIDD is caloric restriction for weight
reduction, because most persons with this type of diabetes are obese. It has been shown that
the higher the average body weight in the population, the greater the prevalence of diabetes.
In many patients, the disease disappears after as little as a 10% weight loss even in those who were as much as
30% overweight at the time of diagnosis; however, a program for
energy restriction must be tailored to individual needs. The diabetic person who is at, or
near, the ideal weight must still control energy intake. In this case, the goals are adequate
nutrient intake, maintenance of weight, and prevention of obesity. Children with Type I
diabetes do not require caloric limitation. The nutrients must provide sufficient energy for
normal growth and development; otherwise, growth retardation occurs. Patients with Type
II diabetes who are young should be treated as adults except that their energy intake must be
adequate for normal growth and development without gain of excess weight. Children with
good control of sugar will gain weight rapidly if they overeat beyond energy needs. Regular
exercise is a valuable adjunct to therapy. Exercise increases caloric expenditure and is of
value in achieving weight loss in overweight patients. Both diet and exercise have a major
effect in increasing insulin sensitivity in individuals with Type I or Type II diabetes.
Exercise also tends to lower plasma triglyceride levels with concomitant increases in HDL
cholesterol, both of which may be beneficial in preventing atherosclerosis.
B. Carbohydrate
Historically, the primary goal of diet therapy for diabetics has been the reduction of
carbohydrate intake. A high carbohydrate diet is known to cause higher postprandial blood
glucose levels, a temporary worsening of glycemic control, and an increase in fasting serum
triglycerides. The recent trend, however, has been to liberalize dietary carbohydrate intake in
patients with diabetes mellitus, and it appears that the plasma glucose response to a standard
oral glucose challenge is improved if patients with diabetes ingest a high carbohydrate diet
for several days. Individuals are more sensitive to insulin when consuming high-carbohydrate
diets, as opposed to high-fat diets, because they have an increased number of insulin
receptors. Of greater importance is the enhanced intracellular glucose metabolism associated
with high-carbohydrate diets. As loss of normal insulin sensitivity seems to characterize
patients with Type II diabetes, a high-carbohydrate diet would seem to be the treatment of
choice in these patients.
It is generally recommended that 55–60% of calories be supplied by carbohydrates.
This level of carbohydrate intake facilitates diabetes management in children as well as
adults with IDD and NIDD. Complex carbohydrates (found in grain products and root
vegetables) should account for a major portion of total carbohydrate calories. Sucrose and
other caloric sweeteners with high glycemic index should be limited to 10% of the calories
at each meal. The glycemic response (the ability to contribute to the concentration of blood
glucose) to 50 g of glucose, maltose, or sucrose is much higher than the response to 50 g of
starch. Fructose offers an advantage over sucrose for diabetic individuals because it is
about 1.7 times sweeter, is metabolized without insulin, and produces less hyperglycemia.
It produces only 20% of the glycemic response of glucose and 33% of the response of
sucrose. Fructose is present in fruits, honey, and corn syrup.
Inositol is a six-carbon sugar that is configuratively related to glucose. It is widely
distributed in foods of both plant and animal origin as part of the phosphatidyl inositol of
the cell membrane and as free inositol. It can be endogenously synthesized from glucose.
Diabetics have an intracellular deficiency of inositol, especially in the nerves. The
deficiency is attributed to: (a) increased urinary excretion; (b) decreased formation,
because less glucose is available inside the cell and one of the enzymes involved in
synthesis, glucokinase, is insulin-dependent; and (c) competition of glucose (and sorbitol)
for the intracellular transport of inositol.

There are reports suggesting that the secondary complications of diabetes (i.e.,
renal disease) can be ameliorated by dietary inositol supplementation. Some investigators
have shown a reversal of the diabetes-induced increased glomerular filtration rate with a
7- to 10-fold increase in dietary levels of inositol. Thus diabetics may have a significantly
greater need for inositol than nondiabetics. There may be a broad range of inositol
requirements as there is a range of severity of diabetes. There is an increased interest to
learn more about the role of inositol in cell function and on dietary requirements of this
sugar in diabetics.
Alternative sweeteners such as sorbitol, aspartame, saccharin, and acesulfame K
have been advocated as substitutes for sucrose to provide sweetness without hyperglycemia
or increased calories for persons with diabetes. Sorbitol, a sugar alcohol, is used
as a sweetener because it is poorly absorbed from the gastrointestinal tract and thus reduces
the prompt increase in plasma glucose characteristic of dietary carbohydrate. Sorbitol is
half as sweet as sucrose and provides calories equal to those of sucrose.
The artificial sweeteners presently available for use in the United States include
aspartame (Nutrasweet), saccharin, sucralose, and acesulfame K. Aspartame is a dipeptide,
aspartyl-phenylalanyl methyl ester. It is about 200 times sweeter than sugar. Technically, it
is a nutritive sweetener that provides 4 Cal/g, but compared to the sweetness of sucrose, the
amount required would only supply about 0.5% of the calories provided by sugar.
Saccharin is 300 times sweeter, sucralose is 500 times sweeter and acesulfame K is 200
times sweeter than sugar. The risks, benefits, and effects of these sweeteners in individuals
with diabetes have not been fully tested. Because diabetics are likely to ingest greater
quantities of these sweeteners than the general population, there is a need for extensive
research to determine the long-term effect of these sweeteners on appetite, weight gain,
blood glucose, and insulin levels in diabetic individuals.
C. Fat
High-fat diets have metabolic disadvantages. They cause insulin resistance and impair
intracellular glucose metabolism in several tissues, thus decreasing glucose transport into
muscle and adipose tissue and decreasing the activity of insulin-stimulated processes. A
high-fat diet increases the risk of atherosclerosis. Because diabetic persons are much
more likely to develop atherosclerosis at an early age and more severely than nondiabetic
persons, the restriction of dietary fat and cholesterol by substituting carbohydrate
seems to be wise. The fat intake, therefore, should represent no more than 30% of
calories and should contain a good ratio (1:1:1) of polyunsaturated to monounsaturated
to saturated fatty acids, in order, to delay the development of atherosclerosis. Cholesterol
intake must be restricted to less than 300 mg/day. Vegetable fats are preferred over fats
of animal origin. The recommended cholesterol intake is <300 mg/day for diabetic
patients with normal plasma cholesterol concentrations. For patients with elevated LDL,
<7% of total calories should be from saturated fat, and cholesterol intake should be
restricted to <200 mg/day.
D. Protein
The amount of protein required by the average person with diabetes is similar to that for
the normal person. Proteins should be of reasonably high quality and should provide all the
amino acids necessary for adequate nutrition. Proteins should provide about 15% of the
total calories, or 0.8 g/kg desirable body weight for adults. Protein consumption should be
about 20% of the total calories, or 1.5 g/kg body weight daily in children and in pregnant and lactating
women.With the onset of nephropathy, a lower protein intake of 0.6 g/kg/day
is considered sufficiently restrictive.
E. Alcohol
The metabolism of alcohol does not require insulin and it would appear to offer some
theoretical advantages; however, alcohol is high in calories (7 Cal/g) and is of no other
nutritive value. It tends to promote hypertriglyceridemia. In a small minority of patients
who have high blood sulfonylurea (hypoglycemic drug) levels, alcohol produces distressing
symptoms. Even so, in most patients, an occasional drink can be permitted. A
convenient way is to trade fat calories for alcohol calories. Excess alcohol should be
avoided because it inhibits gluconeogenesis.
F. Fiber
Dietary fiber influences glucose assimilation and reduces serum cholesterol. Research
has shown that certain plant fibers delay the absorption of carbohydrate and result in less
postprandial hyperglycemia. Increased fiber in the diet is associated with reduced insulin
resistance. An increase in fiber from whole grains, legumes, and vegetables may appear
to be beneficial for the diabetic. It is recommended that adult diabetics consume about
40 g/day of dietary fiber.
G. Vitamins and Minerals
Special vitamin and mineral supplementation is ordinarily not required by diabetics. These
nutrients should be provided at the recommended dietary allowance (RDA) levels. Recent
studies have shown that people with diabetes mellitus have at least 30% lower vitamin C
concentration in the blood than persons without diabetes. Vitamin C supplementation
(1 g/day) for 3 months has little effect on blood glucose concentration, but does lower
glycosylated hemoglobin by 18%. Vitamin C may inhibit the glycosylation of proteins
in vivo by a competitive mechanism. Vitamin C supplementation (2 g/day) for 3 weeks
lowers erythrocyte sorbitol levels by 44.5% and reduces capillary fragility. Vitamin C
supplementation may provide a simple means of preventing and ameliorating the
complications of diabetes without the use of drugs.
Chromium reportedly affects insulin secretion and glucose metabolism. Chromium
or Brewer’s yeast (which contains a high concentration of chromium complex) has been
given to adults having NIDD with variable results. Some investigators found an
improvement in glucose tolerance, but in others, no change in glucose metabolism was
noted. These data suggest that in some patients, chromium deficiency may be a factor in
impaired glucose metabolism, but there is as yet no clinical indication for the use of
chromium in the treatment of diabetes.
VII. PHYSICAL ACTIVITY
Exercise is an integral component of comprehensive diabetes care that can have positive
benefits particularly in Type II diabetes because obesity and inactivity contribute to the
development of glucose intolerance in genetically predisposed individuals. A regular
program of physical activity contributes to body fat reduction, improves blood lipids, and
lowers blood pressure. For individuals with Type I and Type II diabetes, exercise is also
useful for lowering plasma glucose (during and following exercise) and for increasing
insulin sensitivity.

Despite these benefits, exercise presents severe challenges for individuals with
diabetes because they lack glucose regulatory mechanisms. The skeletal muscle is a major
site for metabolic fuel consumption during resting states, and increased muscle activity
during moderate to heavy exercise greatly increases glucose requirements. Muscle glycogen
stores are depleted quite rapidly, after which glucose is derived from the peripheral
circulation. To meet the increased glucose demands, hepatic glycogenolysis and
gluconeogenesis increase. This is mediated primarily through the suppression of insulin
secretion and the increased secretion of counterregulatory hormones such as glucagon.
Low permissive levels of insulin are required for glucose uptake by the muscle.
Peripheral glucose utilization remains high after exercise has been discontinued; this is
thought to be related to the replenishment of glycogen stores in the liver and muscle.
In nondiabetic individuals, hepatic glucose output and peripheral utilization are balanced
such that normal plasma glucose level is maintained during and after exercise.
In Type I diabetic individuals, exercise may cause hyperglycemia or hypoglycemia,
depending on the pre-exercise plasma glucose concentration, the circulating insulin level,
and the levels of exercise-induced counterregulatory hormones. If the insulin level is low
when the individual starts the exercise, hepatic glucose output will increase and peripheral
glucose utilization will decrease, and hyperglycemia will ensue. This can promote ketone
body formation and possibly lead to ketoacidosis. Patients whose plasma glucose
concentrations are more than 250 mg/dl should delay exercise because these levels
indicate insulin deficiency. Conversely, if the circulating insulin level is excessive, this
relative hyperinsulinimia may reduce hepatic glucose production (decreased glycogenolysis
and gluconeogenesis) and increase glucose entry into muscles, leading to hypoglycemia.
Hypoglycemia is more likely to occur if the blood glucose is 100 mg/dl or lower
just before exercise. Thus the individual should eat a carbohydrate snack or decrease the
dose of insulin.
To avoid exercise-related hyperglycemia or hypoglycemia, individuals with Type I
diabetes should monitor plasma glucose before, during, and after exercise and adjust
insulin dose and food intake accordingly. In general, exercise should be avoided at times
corresponding to peek insulin action because high insulin levels can suppress the action of
counterregulatory hormones.
For patients with Type II diabetes who are treated with diet alone, exercise is
unlikely to cause hypoglycemia. Individuals who take oral hypoglycemic agents or insulin
may become hypoglycemic if plasma insulin levels are high enough to increase peripheral
utilization of glucose and to suppress hepatic glucose output. Individuals whose plasma
glucose is less than 100 mg/dl before exercise should consider increasing their carbohydrate
intake. Because patients with Type II diabetes do not have absolute lack of insulin,
they are less likely to become hyperglycemic in response to exercise.
A light regular exercise routine such as walking or stationary cycling is safe
and effective.
VIII. LIFESTYLE MODIFICATION TO REDUCE RISK
OF TYPE II DIABETES
Nutrition can also reduce the incidence of diabetes. Two randomized controlled trials—
one in the United States and the other in Finland—have recently been completed.
Individuals with impaired glucose tolerance were randomly allocated to an intensive
lifestyle intervention program or a standard control group. The intervention programs were aimed to achieve a
weight reduction of 5% or more, an intake of total and saturated
fat of less than 30% and 10% of total energy intakes, respectively, an increase in fiber
intake of at least 15 g/1000 Cal, and moderate exercise for at least 30 min/day. Frequent
ingestion of whole grain products, fruits, vegetables, low-fat milk, and vegetable oils rich
in monounsaturated fatty acids were recommended. Moderate intakes of fish (some oily)
and lean meats (and for vegetarians vegetable sources of proteins) were also encouraged.
In Finland, these lifestyle programs were associated with a 58% reduction in risk of
developing diabetes, and the 4-year cumulative incidence of diabetes was 11% in the
intervention group and 23% in the control group. The results in the United States were
similar, with 29% of the control group developing diabetes during the 3-year average
follow-up period compared with 14% in the intervention group. To reduce the risk of
diabetes, people of all ages should avoid excess wieght gain, and those who are overweight
should lose weight. This lifestyle management also applies to treatment for people who
have already developed coronary heart disease and diabetes.