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CHAPTER 3

INTRODUCTION TO DIABETES

3.1 INTRODUCTION

Diabetes mellitus, often referred to simply as diabetes , is a

syndrome of disordered metabolism, usually due to a combination of
hereditary and environmental causes, resulting in abnormally high blood
sugar levels (hyperglycemia). Blood glucose levels are controlled by a
complex interaction of multiple chemicals and hormones in the body,
including the hormone insulin made in the beta cells of the pancreas.
Diabetes mellitus refers to the group of diseases that lead to high blood
glucose levels due to defects in either insulin secretion or insulin action.

Diabetes develops due to a diminished production of insulin (in

type 1) or resistance to its effects (in type 2 and gestational). Both lead to
hyperglycaemia, which largely causes acute signs of diabetes: excessive
urine production, resulting compensatory thirst and increased fluid
intake, blurred vision, unexplained weight loss, lethargy, and changes in
energy metabolism. Monogenic forms.
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All forms of diabetes are treatable since insulin became medically

available in 1921, but there is no cure. The injections by a syringe,
insulin pump, or insulin pen deliver insulin, which is a basic treatment of
type 1 diabetes. Type 2 is managed with a combination of dietary
treatment, exercise, medications and insulin supplementation.

Diabetes and its treatments can cause many complications. Acute

complications (hypoglycemia, ketoacidosis, or nonketotic hyperosmolar
coma) may occur if the disease is not adequately controlled. Serious
long-term complications include cardiovascular disease, chronic renal
failure, retinal damage (which can lead to blindness), nerve damage, and
microvascular damage, which may cause erectile dysfunction and poor
wound healing. Poor healing of wounds, particularly of the feet, can lead
to gangrene, and the danger of amputation. Adequate treatment of
diabetes, as well as increased emphasis on blood pressure control and
lifestyle factors (such as not smoking and maintaining a healthy body
weight), may improve the risk profile of most of the chronic
complications. In the developed world, diabetes is the most significant
cause of adult blindness in the non-elderly and the leading cause of non-
traumatic amputation in adults, and diabetes nephropathy is the main
illness requiring renal dialysis in the United States.

3.2 CLASSIFICATION

The term diabetes, without qualification, usually refers to diabetes

mellitus, which is associated with excessive sweet urine (known as
"glycosuria") but there are several rarer conditions also named diabetes.
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The most common of these is diabetes insipidus in which the urine is not
sweet (insipidus meaning "without taste" in Latin); it can be caused by
either kidney (nephrogenic DI) or pituitary gland (central DI) damage.
The term "type 1 diabetes" has universally replaced several former
terms, including childhood-onset diabetes, juvenile diabetes, and insulin-
dependent diabetes (IDDM). Likewise, the term "type 2 diabetes" has
replaced several former terms, including adult-onset diabetes, obesity-
related diabetes, and non-insulin-dependent diabetes (NIDDM). Beyond
these two types, there is no agreed-upon standard nomenclature. Various
sources have defined "type 3 diabetes" as, among others, gestational
diabetes, insulin-resistant type 1 diabetes (or "double diabetes"), type 2
diabetes which has progressed to require injected insulin, and latent
autoimmune diabetes of adults (or LADA or "type 1.5" diabetes. There is
also maturity onset diabetes of the young (MODY) which is a group of
several single gene (monogenic) disorders with strong family histories
that present as type 2 diabetes before 30 years of age.

3.2.1 Type 1 diabetes mellitus

Type 1 diabetes mellitus is characterized by loss of the insulin-

producing beta cells of the islets of Langerhans in the pancreas, leading
to a deficiency of insulin. This type of diabetes can be further classified
as immune mediated or idiopathic. The majority of type 1 diabetes is of
the immune mediated variety, where beta cell loss is a T-cell mediated
autoimmune attack. There is no known preventive measure which can be
taken against type 1 diabetes; it is about 10% of diabetes mellitus cases
in North America and Europe (though this varies by geographical
location), and is a higher percentage in some other areas. Most affected
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persons are otherwise healthy and of a healthy weight when the onset
occurs. Sensitivity and responsiveness to insulin are usually normal,
especially in the early stages. Type 1 diabetes can affect children or
adults but was traditionally termed "juvenile diabetes" because it
represents a majority of the diabetes cases in children.

The principal treatment of type 1 diabetes, even in its earliest

stages, is the delivery of artificial insulin via injection combined with
careful monitoring of blood glucose levels using blood testing monitors.
Without insulin, diabetes ketoacidosis often develops which may result
in coma or death. Treatment emphasis is now also placed on lifestyle
adjustments (diet and exercise) though these cannot reverse the progress
of the disease. Apart from the common subcutaneous injections, it is also
possible to deliver insulin by a pump, which allows continuous infusion
of insulin 24 hours a day at preset levels, and the ability to program
doses (a bolus) of insulin as needed at meal times. An inhaled form of
insulin was approved by the FDA in January 2006, although it was
discontinued for business reasons in October 2007. Non-insulin
treatments, such as monoclonal antibodies and stem-cell based therapies,
are effective in animal models but have not yet completed clinical trials
in humans.

Type 1 treatment must be continued indefinitely in essentially all

cases. Treatment need not significantly impair normal activities, if
sufficient patient training, awareness, appropriate care, discipline in
testing and dosage of insulin is taken. However, treatment is burdensome
for patients; insulin is replaced in a non-physiological manner, and this
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approach is therefore far from ideal. The average glucose level for the
type 1 patient should be as close to normal (80–120 mg/dl, 4–6 mmol/l)
as is safely possible. Some physicians suggest up to 140–150 mg/dl (7-
7.5 mmol/l) for those having trouble with lower values, such as frequent
hypoglycemic events. Values above 400 mg/dl (20 mmol/l) are
sometimes accompanied by discomfort and frequent urination leading to
dehydration. Values above 600 mg/dl (30 mmol/l) usually require
medical treatment and may lead to ketoacidosis, although they are not
immediately life-threatening. However, low levels of blood glucose,
called hypoglycemia, may lead to seizures or episodes of
unconsciousness and must be treated immediately, via emergency high-
glucose gel placed in the patient's mouth or an injection of glucagon.

3.2.2 Type 2 diabetes mellitus

Type 2 diabetes mellitus is characterized differently and is due to

insulin resistance or reduced insulin sensitivity, combined with relatively
reduced insulin secretion which in some cases becomes absolute. The
defective responsiveness of body tissues to insulin almost certainly
involves the insulin receptor in cell membranes. However, the specific
defects are not known. Diabetes mellitus, due to a known specific defect,
are classified separately.

In the early stage of type 2 diabetes, the predominant abnormality

is reduced insulin sensitivity, characterized by elevated levels of insulin
in the blood. At this stage, hyperglycemia can be reversed by a variety of
measures and medications that improve insulin sensitivity or reduce
glucose production by the liver. As the disease progresses, the
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impairment of insulin secretion worsens, and therapeutic replacement of

insulin often becomes necessary.
There are numerous theories as to the exact cause of and
mechanism in type 2 diabetes. Central obesity (fat concentrated around
the waist in relation to abdominal organs, but not subcutaneous fat) is
known to predispose individuals to insulin resistance. Abdominal fat is
especially active hormonally, secreting a group of hormones called
adipokines that may possibly impair glucose tolerance. Obesity is found
in approximately 55% of patients diagnosed with type 2 diabetes. Other
factors include aging (about 20% of elderly patients in North America
have diabetes) and family history (type 2 is much more common in those
with close relatives who have had it). In the last decade, type 2 diabetes
has increasingly begun to affect children and adolescents, likely in
connection with the increased prevalence of childhood obesity seen in
recent decades in some places. Environmental exposures may contribute
to recent increases in the rate of type 2 diabetes. A positive correlation
has been found between the concentration in the urine of bisphenol A, a
constituent of polycarbonate plastic, and the incidence of type 2 diabetes.

Type 2 diabetes may go unnoticed for years because visible

symptoms are typically mild, non-existent or sporadic, and usually there
are no ketoacidotic episodes. However, severe long-term complications
can result from unnoticed type 2 diabetes, including renal failure due to
diabetes nephropathy, vascular disease (including coronary artery
disease), vision damage due to diabetes retinopathy, loss of sensation or
pain due to diabetes neuropathy, liver damage from non-alcoholic
steatohepatitis and heart failure from diabetes cardiomyopathy.
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Type 2 diabetes is usually first treated by increasing physical

activity, decreasing carbohydrate intake, and loss of weight. These can
restore insulin sensitivity even when the weight loss is modest, for
example, around 5 kg (10 to 15 lb), most especially when it is in
abdominal fat deposits. It is sometimes possible to achieve long-term,
satisfactory glucose control with these measures alone. However, the
underlying tendency to insulin resistance is not lost, and so attention to
diet, exercise, and weight loss must continue. The next usual step, if
necessary, is treatment with oral antidiabetes drugs. Insulin production is
initially only moderately impaired in type 2 diabetes, so oral medication
(often used in various combinations) can be used to improve insulin
production (e.g., sulfonylureas), to regulate inappropriate release of
glucose by the liver and attenuate insulin resistance to some extent (e.g.,
metformin), and to substantially attenuate insulin resistance (e.g.,
thiazolidinediones). According to one study, overweight patients treated
with metformin compared with diet alone, had relative risk reductions of
32% for any diabetes endpoint, 42% for diabetes related death and 36%
for all causes of mortality and stroke. Oral medication may eventually
fail due to further impairment of beta cell insulin secretion. At this point,
insulin therapy is necessary to maintain normal or near normal glucose
levels.

3.2.3 Gestational diabetes

Gestational diabetes mellitus (GDM) resembles type 2 diabetes in

several respects, involving a combination of relatively inadequate insulin
secretion and responsiveness. It occurs in about 2%–5% of all
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pregnancies and may improve or disappear after delivery. Gestational

diabetes is fully treatable but requires careful medical supervision
throughout the pregnancy. About 20%–50% of affected women develop
type 2 diabetes later in life.

Even though it may be transient, untreated gestational diabetes can

damage the health of the fetus or mother. Risks to the baby include
macrosomia (high birth weight), congenital cardiac and central nervous
system anomalies, and skeletal muscle malformations. Increased fetal
insulin may inhibit fetal surfactant production and cause respiratory
distress syndrome. Hyperbilirubinemia may result from red blood cell
destruction. In severe cases, perinatal death may occur, most commonly
as a result of poor placental perfusion due to vascular impairment.
Induction may be indicated with decreased placental function. A
cesarean section may be performed if there is marked fetal distress or an
increased risk of injury associated with macrosomia, such as shoulder
dystocia.

A 2008 study completed in the U.S. found that more American

women are entering pregnancy with preexisting diabetes. In fact, the rate
of diabetes in expectant mothers has more than doubled in the past 6
years. This is particularly problematic as diabetes raises the risk of
complications during pregnancy, as well as increasing the potential that
the children of diabetic mothers will also become diabetics in the future.

3.2.4 Other types

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Most cases of diabetes mellitus fall into the two broad etiologic
categories of type 1 or type 2 diabetes. However, many types of diabetes
mellitus have known specific causes, and thus fall into separate
categories as diabetes due to a specific cause. As more research is being
done into diabetes, many patients who were previously diagnosed as type
1 or type 2 diabetes will be reclassified as diabetics due to their known
specific cause.

Some cases of diabetes are caused by the body's tissue receptors

not responding to insulin (even when insulin levels are normal, which is
what separates it from type 2 diabetes); this form is very uncommon.
Genetic mutations (autosomal or mitochondrial) can lead to defects in
beta cell function. Abnormal insulin action may also have been
genetically determined in some cases. Any disease that causes extensive
damage to the pancreas may lead to diabetes (for example, chronic
pancreatitis and cystic fibrosis). Diseases associated with excessive
secretion of insulin-antagonistic hormones can cause diabetes (which is
typically resolved once the hormone excess is removed). Many drugs
impair insulin secretion and some toxins damage pancreatic beta cells.

3.3 SIGNS AND SYMPTOMS

The classical triad of diabetes symptoms is polyuria, polydipsia

and polyphagia, which are, respectively, frequent urination, increased
thirst and consequent increased fluid intake, and increased appetite.
Symptoms may develop quite rapidly (in weeks or months) in type 1
diabetes, particularly in children. However, in type 2 diabetes, symptoms
usually develop much more slowly and may be subtle or completely
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absent. Type 1 diabetes may also cause a rapid yet significant weight
loss (despite normal or even increased eating) and irreducible fatigue.
All of these symptoms except weight loss can also manifest in type 2
diabetes in patients whose diabetes is poorly controlled.

When the glucose concentration in the blood rises beyond its

renal threshold, reabsorption of glucose in the proximal renal tubuli is
incomplete, and part of the glucose remains in the urine (glycosuria).
This increases the osmotic pressure of the urine and inhibits reabsorption
of water by the kidney, resulting in increased urine production (polyuria)
and increased fluid loss. The lost blood volume will be replaced
osmotically from water held in body cells and other body compartments,
causing dehydration and increased thirst.

Prolonged high blood glucose causes glucose absorption, which

leads to changes in the shape of the lenses of the eyes, resulting in vision
changes; sustained sensible glucose control usually returns the lens to its
original shape. Blurred vision is a common complaint leading to a
diabetes diagnosis; type 1 should always be suspected in cases of rapid
vision change, whereas, with type 2, change is generally more gradual,
but should still be suspected.

Patients (usually with type 1 diabetes) may also initially be found

to have diabetes ketoacidosis (DKA), an extreme state of metabolic
dysregulation characterized by the smell of acetone on the patient's
breath; a rapid, deep breathing known as Kussmaul breathing; polyuria;
nausea; vomiting and abdominal pain; and any of many altered states of
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consciousness or arousal (such as hostility and mania or, equally,

confusion and lethargy). In severe DKA, coma may follow, progressing
to death. Diabetes ketoacidosis is a medical emergency and requires
immediate hospitalization.

A rarer but equally severe possibility is hyperosmolar nonketotic

state, which is more common in type 2 diabetes and is mainly the result
of dehydration due to loss of body water. Often, the patient has been
drinking extreme amounts of sugar-containing drinks, leading to a
vicious circle in regard to the water loss.

3.4 GENETICS

Both type 1 and type 2 diabetes are at least partly inherited.

Type 1 diabetes appears to be triggered by some (mainly viral)
infections, or less commonly, by stress or environmental exposure (such
as exposure to certain chemicals or drugs). There is a genetic element in
individual susceptibility to some of these triggers which has been traced
to particular HLA genotypes (i.e., the genetic "self" identifiers relied
upon by the immune system). However, even in those who have
inherited the susceptibility, type 1 diabetes mellitus seems to require an
environmental trigger. A small proportion of people with type 1 diabetes
carry a mutated gene that causes maturity onset diabetes of the young
(MODY).

There is a stronger inheritance pattern for type 2 diabetes. Those

with first-degree relatives with type 2 have a much higher risk of
developing type 2, increasing with the number of those relatives.
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Concordance among monozygotic twins is close to 100%, and about

25% of those with the disease have a family history of diabetes.
Moreover, obesity (which is an independent risk factor for type 2
diabetes) is strongly inherited.

Various hereditary conditions may feature diabetes, as for

example, myotonic dystrophy and Friedreich's ataxia. Wolfram's
syndrome is an autosomal recessive neurodegenerative disorder that first
becomes evident in childhood.

3.5 PATHOPHYSIOLOGY

Insulin production is more or less constant within the beta cells,

irrespective of blood glucose levels. It is stored within vacuoles pending
release, via exocytosis, which is primarily triggered by food, chiefly food
containing absorbable glucose. The chief trigger is a rise in blood
glucose levels after eating.

Insulin is the principal hormone that regulates uptake of glucose

from the blood into most cells (primarily muscle and fat cells, but not
central nervous system cells). Therefore, a deficiency of insulin or the
insensitivity of its receptors plays a central role in all forms of diabetes
mellitus.

Most of the carbohydrates in food are converted within a few

hours to the monosaccharide glucose, the principal carbohydrate found
in blood and used by the body as fuel. The most significant exceptions
are fructose, most disaccharides (except sucrose and in some people
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lactose), and all more complex polysaccharides, with the outstanding

exception of starch. Insulin is released into the blood by beta cells (β-
cells), found in the Islets of Langerhans in the pancreas, in response to
rising levels of blood glucose, typically after eating. Insulin is used by
about two-thirds of the body's cells to absorb glucose from the blood for
use as fuel, for conversion to other needed molecules, or for storage.

Insulin is also the principal control signal for conversion of

glucose to glycogen for internal storage in liver and muscle cells.
Reduced glucose levels result both in the reduced release of insulin from
the beta cells and in the reverse conversion of glycogen to glucose when
glucose levels fall. This is mainly controlled by the hormone glucagon
which acts in an opposite manner to insulin. Glucose thus recovered by
the liver re-enters the bloodstream; muscle cells lack the necessary
export mechanism.

Higher insulin levels increase some anabolic ("building up")

processes such as cell growth and duplication, protein synthesis, and fat
storage. Insulin (or its lack) is the principal signal in converting many of
the bidirectional processes of metabolism from a catabolic to an anabolic
direction, and vice versa. In particular, a low insulin level is the trigger
for entering or leaving ketosis (the fat burning metabolic phase).

If the amount of insulin available is insufficient, if cells respond

poorly to the effects of insulin (insulin insensitivity or resistance), or if
the insulin itself is defective, then glucose will not be absorbed properly
by those body cells that require it nor will it be stored appropriately in
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the liver and muscles. The net effect is persistent high levels of blood
glucose, poor protein synthesis, and other metabolic derangements, such
as acidosis.

3.6 DIAGNOSIS

The diagnosis of type 1 diabetes, and many cases of type 2, is

usually prompted by recent-onset symptoms of excessive urination
(polyuria) and excessive thirst (polydipsia), often accompanied by
weight loss. These symptoms typically worsen over days to weeks; about
a quarter of people with new type 1 diabetes have developed some
degree of diabetes ketoacidosis by the time the diabetes is recognized.
The diagnosis of other types of diabetes is usually made in other ways.
These include ordinary health screening; detection of hyperglycemia
during other medical investigations; and secondary symptoms such as
vision changes or inexplicable fatigue. Diabetes is often detected when a
person suffers a problem that is frequently caused by diabetes, such as a
heart attack, stroke, neuropathy, poor wound healing or a foot ulcer,
certain eye problems, certain fungal infections, or deliver of a baby with
macrosomia or hypoglycemia.

Diabetes mellitus is characterized by recurrent or persistent

hyperglycemia, and is diagnosed by the demonstration of any one of the
following:

• fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/l).

• plasma glucose at or above 200 mg/dL (11.1 mmol/l) two hours
after a 75 g oral glucose load as in a glucose tolerance test.
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• symptoms of hyperglycemia and casual plasma glucose at or

above 200 mg/dL (11.1 mmol/l).

A positive result, in the absence of unequivocal hyperglycemia,

should be confirmed by a repeat of any of the above-listed methods on a
different day. Most physicians prefer to measure a fasting glucose level
because of the ease of measurement and the considerable time
commitment of formal glucose tolerance testing, which takes two hours
to complete. According to the current definition, two fasting glucose
measurements above 126 mg/dL (7.0 mmol/l) is considered diagnostic
for diabetes mellitus.

Patients with fasting glucose levels from 100 to 125 mg/dL (6.1
and 7.0 mmol/l) are considered to have impaired fasting glucose.
Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/l, but
not over 200, two hours after a 75 g oral glucose load are considered to
have impaired glucose tolerance. Of these two pre-diabetes states, the
latter in particular is a major risk factor for progression to full-blown
diabetes mellitus as well as cardiovascular disease.

While not used for diagnosis, an elevated level of glucose

irreversibly bound to hemoglobin (termed glycosylated hemoglobin or
HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered
abnormal by most labs; HbA1c is primarily used as a treatment-tracking
test reflecting average blood glucose levels over the preceding 90 days
(approximately). However, some physicians may order this test at the
time of diagnosis to track changes over time. The current recommended
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goal for HbA1c in patients with diabetes is <7.0%, which is considered

good glycemic control, although some guidelines are stricter (<6.5%).
People with diabetes who have HbA1c levels within this range have a
significantly lower incidence of complications from diabetes, including
retinopathy and diabetes nephropathy.

3.7 SCREENING

Diabetes screening is recommended for many people at various

stages of life, and for those with any of the several risk factors. The
screening test varies according to circumstances and local policy, and
may be a random blood glucose test, a fasting blood glucose test, a blood
glucose test two hours after 75 g of glucose, or an even more formal
glucose tolerance test. Many healthcare providers recommend universal
screening for adults at age 40 or 50, and often periodically thereafter.
Earlier screening is typically recommended for those with risk factors
such as obesity, family history of diabetes, high-risk ethnicity (Hispanic,
Native American, Afro-Caribbean, Pacific Islander).

Many medical conditions are associated with diabetes and warrant

screening. A partial list includes: high blood pressure, elevated
cholesterol levels, coronary artery disease, past gestational diabetes,
polycystic ovary syndrome, chronic pancreatitis, fatty liver,
hemochromatosis, cystic fibrosis, several mitochondrial neuropathies
and myopathies, myotonic dystrophy, Friedreich's ataxia, some of the
inherited forms of neonatal hyperinsulinism. The risk of diabetes is
higher with chronic use of several medications, including high-dose
glucocorticoids, some chemotherapy agents (especially L-asparaginase),
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as well as some of the antipsychotics and mood stabilizers (especially

phenothiazines and some atypical antipsychotics).

People with a confirmed diagnosis of diabetes are tested routinely

for complications. This includes annual urine testing for
microalbuminuria and examination of the retina of the eye for
retinopathy.

3.8 PREVENTION

Type 1 diabetes risk is known to depend upon a genetic

predisposition based on HLA types , an unknown environmental trigger
(suspected to be an infection, although none has proven definitive in all
cases), and an uncontrolled autoimmune response that attacks the insulin
producing beta cells. Some research has suggested that breastfeeding
decreased the risk in later life; various other nutritional risk factors are
being studied, but no firm evidence has been found. Giving children
2000 IU of Vitamin D during their first year of life is associated with a
reduced risk of type 1 diabetes, though the causal relationship is obscure.

Children with antibodies to beta cell proteins (ie, at early stages of

an immune reaction to them) but no overt diabetes, and treated with
vitamin B-3 (niacin), had less than half the diabetes onset incidence in a
7-year time span as did the general population, and an even lower
incidence relative to those with antibodies as above, but who received no
vitamin B3.
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Type 2 diabetes risk can be reduced in many cases by making

changes in diet and increasing physical activity. The American Diabetes
Association (ADA) recommends maintaining a healthy weight, getting at
least 2½ hours of exercise per week (several brisk sustained walks
appear sufficient), having a modest fat intake, and eating sufficient fiber
(eg, from whole grains). The ADA does not recommend alcohol
consumption as a preventive, but it is interesting to note that a moderate
alcohol intake may reduce the risk (though heavy consumption
absolutely and clearly increases damage to bodily systems significantly);
a similarly confused connection between low dose alcohol consumption
and heart disease is termed the French Paradox.

There is inadequate evidence to show that eating foods of low

glycemic index is clinically helpful despite recommendations and
suggested diets emphasizing this approach.

There are numerous studies which suggest connections between

some aspects of Type II diabetes with ingestion of certain foods or with
some drugs. Some studies have shown delayed progression to diabetes in
predisposed patients through prophylactic use of metformin,
rosiglitazone, or valsartan. In patients on hydroxychloroquine for
rheumatoid arthritis, incidence of diabetes was reduced by 77% though
causal mechanisms are unclear. Breastfeeding may also help prevention
of type 2 of the disease in mothers. Clear evidence for these and any of
many other connections between foods and supplements and diabetes is
sparse to date; none, despite secondary claims for (or against), is
sufficiently well established to justify as a standard clinical approach.
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3.9 TREATMENT AND MANAGEMENT

Diabetes mellitus is currently a chronic disease, without a cure,

and medical emphasis must necessarily be on managing/avoiding
possible short-term as well as long-term diabetes-related problems.
There is an exceptionally important role for patient education, dietetic
support, sensible exercise, self monitoring of blood glucose, with the
goal of keeping both short-term blood glucose levels, and long term
levels as well, within acceptable bounds. Careful control is needed to
reduce the risk of long term complications. This is theoretically
achievable with combinations of diet, exercise and weight loss (type 2),
various oral diabetes drugs (type 2 only), and insulin use (type 1 and for
type 2 not responding to oral medications, mostly those with extended
duration diabetes). In addition, given the associated higher risks of
cardiovascular disease, lifestyle modifications should be undertaken to
control blood pressure and cholesterol by exercising more, smoking less
or ideally not at all, consuming an appropriate diet, wearing diabetes
socks, wearing diabetes shoes, and if necessary, taking any of several
drugs to reduce blood pressure. Many type 1 treatments include
combination use of regular or NPH insulin, and/or synthetic insulin
analogs (eg, Humalog, Novolog or Apidra) in combinations such as
Lantus/Levemir and Humalog, Novolog or Apidra. Another type 1
treatment option is the use of the insulin pump (eg, from Deltec Cozmo,
Animas, Medtronic Minimed, Insulet Omnipod). A blood lancet is used
to pierce the skin (typically of a finger), in order to draw blood to test it
for sugar levels.