EPIDEMIOLOGY OF

DIABETES MELLITUS

Dr Salam Jassim
Definition:
It is a heterogeneous group of
disorders characterized by
hyperglycemia, and disturbances of
carbohydrate, fat and protein
metabolism with absolute or relative
deficiency of insulin action and or
secretion
General Epidemiological
Characteristics:
It affects large number of people of about 100
million

The number can increase to 230 million by 2010

It affects all ethnic and socioeconomic groups

Incidence and prevalence are highly varied

between and within countries 20-60 folds
difference

Considerable impact on economic and social

condition, In1992 DM cost USA 90 billion $
General Epidemiological
Characteristics:
DM is an important cause of premature death and
causes serious health consequences

It is important RF of CHD

CHD is the leading cause of death among

diabetics

In developing countries, the incidence and

prevalence of Type 2 DM are rapidly increasing
mostly due to modernization of life style

In developing countries, mortality from acute

complications is high due to lack of basic
CLINICAL STAGING OF DM
I. DM
Regardless of underlying cause is
subdivided into:

Insulin requiring for survival

Insulin requiring for control
Not Insulin requiring
II. Impaired glucose regulation
It is a metabolic state intermediate
between normal glucose homeostasis and
DM

IFG: Impaired fasting glycemia (fasting)

FPG: > 110 mg/dl- <126 mg/dl (>6.1- <7
mmol/L)
Whole blood : >100 mg/dl-<110mg/dl (>5.6-
< 6.1 mmol/L)
IGT: Impaired glucose tolerance
(postprandial)
II. Impaired glucose regulation
All those with IFG should have OGTT

Individuals with IFG or IGT may be

euglycemic in their daily life as seen
through HbA1C

IGT and IFG are not clinical entities, rather

risk categories for future DM and or CVD

They are often associated with Metabolic

Syndrome
III. Normoglycemia
FPG < 110/dl
CLINICAL STAGING OF DM

Clinical staging regardless of its etiology,

progress through several clinical staging
during its natural history

Individual subject may move from one

stage to another in either direction

Clinical staging reflect the hyperglycemia

which reflect the extent of the disease
process
Diagnosis:
Diagnosis is clear when symptoms
are severe with gross hyperglycemia

Sever hyperglycemia under stress is

not sufficient
Diagnosis:
Asymptomatic subject:

A single abnormal test is not sufficient

At least one additional result within diabetic range ,

if it fails , then surveillance with periodic retesting
taking in consideration ethnicity , family history , age
, adiposity, and concomitant risk factors

Glycated Hb had similar sensitivity and specificity

for glucose test

OGTT is indicated if casual blood test is uncertain

Diagnostic range
Fasting Plasma Glucose: 126 mg/dl
(7.0 mmol/L)

Whole blood: 110mg/dl (6.1mmol/L)

In epidemiologic studies FPG is

sufficient or 2hr after 75 gm oral
glucose load
AETIOLOGICAL
CLASSIFICATION
I - Type 1
B-cell destruction usually leading to
absolute insulin deficiency (low or
undetected c-peptide level)

Insulin is usually required for

survival

Risk of ketoacidosis
Type 1
a) Autoimmune DM
Results from autoimmune
destruction of B-cell

Destruction could be rapid especially

in children or slow especially in
adults (Latent Autoimmune Diabetes
in Adults LADA)
Markers of Immune destruction

Islet cell auto Abs

Insulin Auto Abs

Auto Abs to glutamic acid

decarboxylase (GAD)
Type 1
a) Autoimmune DM
Some individuals may be metabolically normal
before the disease become evident, but the
progress of B cell destruction can be detected
Immunological markers are present in 85-90%
of those patients
Peak incidence in childhood and adolescence
Environmental factors play a role
Genetic predisposition
Patients are usually not obese
Other autoimmune diseases may be present
Type-1
b) Idiopathic
No known etiology

Seen more in Africans and Asians

II Type 2
They have relative rather than absolute
insulin deficiency with resistance to
insulin action
They do not require insulin for survival
They may remain undetected for long time
They have increased risk of macro and
micro vascular complications
The autoimmune destruction does not
occur
Ketoacidosis is infrequent
Obesity is very common
Insulin level could be normal or elevated
II Type 2
Insulin sensitivity can be increased by decreasing
weight, increasing physical activity and or
pharmacologic treatment

The risk of this type increases with age, obesity,

lack of physical activity

It is more in women with GDM and individuals

with HT or Dyslipidemia

Genetic predisposition is common

Prevalence showed racial / ethnic variation

III Other specific types
Genetic defects of B cell function
Genetic defects of insulin action
Diseases of exocrine pancreas
Endocrinopathies
Drugs or chemical induced DM
infections
Uncommon but specific forms of
immune mediated DM
Other genetic syndromes sometimes
associated with DM
GESTATIONAL
HYPERGLYCEMIA AND
DIABETES
It is carbohydrate intolerance resulting
in various severity of hyperglycemia
with onset or first recognized during
pregnancy
GESTATIONAL HYPERGLYCEMIA
AND DIABETES
Elevated fasting or postprandial
plasma glucose level in the early
pregnancy (first trimester, and first
half of second trimester) indicates
that DM antedate pregnancy

Normal OGTT in early pregnancy

does not exclude the possibility that
GDM is not going to develop
High Risk Groups
Older women

Women with previous history of large for

gestational age baby

Women from certain ethnic group

Any women with elevated fasting or

casual blood glucose
High Risk Groups
It is better to screen such groups during the first
trimester to detect previous undiagnosed DM

Formal systematic testing for gestational DM is

usually done between 24 and 28 weeks

After the pregnancy ends, the woman should be

re-classified as having:
DM, IGT, or Normal Glucose Tolerance based on
OGTT done 6 weeks or more after delivery

Women with GDM are at increased risk for

subsequent DM
THE METABOLIC SYNDROME
Working definition:
Glucose intolerance, IGT or DM and /or insulin
resistance together with 2 or more of the
following:
Raised arterial BP (>140/90)
Raised Pl.TG =/> 150 mg/dl and/or low HDL-C
(<35mg/dl in males; < 39 mg/dl in females)
Central obesity waist: hip ratio: Males: >0.9,
Females: >0.85
And /or BMI >30
Microalbuminurea (>/= 20 ug/min or
Albumin/creatinin ratio >/= 30 mg/gm)
Other components: hyperuricemia, coagulation
disorders, raised PAI-1
THE METABOLIC SYNDROME

There is heterogeneity in the strength of

insulin resistance

Metabolic syndrome increases risk of

Macro vascular disorders

Management should include control

strategies of all the components and not
only hyperglycemia

Metabolic syndrome may be present for

up to 10 years before detection of the
PRIMARY PREVENTION OF
TYPE 1 DM
It should be done before onset of type 1
pathological process.i.e: before
development of immunological markers

It is still EXPERIMENTAL

Because of the very low prevalence, it

required screening test of high specificity
and sensitivity, inexpensive and easy to
perform
Screening include:
Family history

Genetic markers (HLA)

Immunological risk markers

(ICA, IAA, Anti GAD)

Metabolic risk factors

Screening
Screening is costly and technically
difficult

Those have these factors have 10

folds excess risk

Still 95-97% of them do not develop

the disease later
 Primary Prevention Strategy
Deprivation of caw milk protein in the neonatal and
early infancy

Administration of free radical scavenger, as

nicotinamide

Allowing B-cell rest by administration of early insulin

treatment

Encouraging the development of Antigen tolerance by

administration of early insulin treatment or oral
antigens

Immunosuppression or Immunomodulation
PRIMARY PREVENTION OF
TYPE 2 DM
No population based studies on
primary prevention of type 2 DM

Prevention should be based on

efforts to decrease insulin resistance
and promotion of insulin secretion
Life style measures that decrease
insulin resistance:
Correction and prevention of obesity

Avoidance of high fat diet

Encouraging using unrefined sugar and soluble

fibers

Avoidance or cautious use of diabetogenic

drugs

Encourage physical activity

SECONDARY PREVENTION OF
TYPE 2 DM
Aims at retarding progression of DM,
decrease risk or severity of
complications and so decrease
premature morbidity and mortality

1. Screening for undetected DM

2. Control of hyperglycemia, and other

metabolic abnormalities

3. Correction of other CV RFs (smoking,

dyslipidemias, obesity)
Screening approaches:
Population approach

Selective screening: on high risk

individuals

Opportunistic screening: most

appropriate and highly cost effective
TERTIARY PREVENTIONOF
TYPE 2 DM
Aims at decreasing morbidity and
mortality by delaying or arresting the
complications

Good glycemic control (by intensive

treatment, frequent monitoring of
blood glucose level) slow or arrest
development of early microvascular
complications
COMPLICATIONS OF DM

ACUTE COMPLICATIONS
1. Hypoglycemia
Affect the brain and the heart

The risk is more among:

1. Hypoglycemia unawareness and
counter regulatory
unresponsiveness as in autonomic
neuropathy, B-blockers and
alcoholism
2. Infants
3. Patients with IHD or TIA
Prevention:
health education

Cautious exercise

Glucagons for emergency

Caution and health education when

changing treatment
2. Diabetic ketoacidosis
10-15% mortality, 50% of them are avoidable

Precipitating factors
1. Infection
2. Acute illnesses
3. Insufficient insulin treatment

Prevention:
1. Health education
2. Early control of precipitating factors
3. Infections
Poorly controlled diabetics are at increased
risk of:

1. TB , lung and other organs

2. fungal infection of skin and mucus

membrane

3. anaerobic infection of deep tissues

4. UTI ( increasing diabetic nephropathy)

CHRONIC
COMPLICATIONS
I. Macrovascular Complications
Atherosclerosis: CAD, CVA, PVD

The most common complication

among diabetics, account for 75% of
their deaths

DM increases CAD and CVA by 2-3

folds and PVD by 4 folds

Diabetic women lose their relative

protection against CAD before
Atherosclerosis:
Role of hyperglycemia as CRF
mediated through:

1. Glycation of LDL particles

2. Glycation of arterial wall protein

3. Stimulate insulin secretion

Atherosclerosis:
Hyperinsulinemia is independently
associated with atherosclerosis through
its effect on BP, TG, PAI-1 level or arterial
wall metabolism

Obesity (especially central) increases

liability to atherosclerosis and DM
through:
Increased insulin resistance,
hyperinsulinemia, Dyslipidemia, and HT

Among diabetics the process of

atherosclerosis is accelerated with
Atherosclerosis:
Screening for RFs of macrovascular complications:
Lipid profile, BP, Ht, waist/hip ratio, smoking history, family
history, urinary albumin excretion

Presence of macro vascular complications is ascertained

through:
1. Clinical history: history of MI, TIA, and intermittent
claudication
2. Physical examination: bruit, peripheral pulses, evidence of
ischemia on ECG

The sensitivity and specificity of these measures are moderate

 CHRONIC
COMPLICATIONS
II. Microvascular complications
1. Diabetic Retinopathy
It is asymptomatic gradual process, so screening is
vital at least every 2 years

Drugs and glycemic control can not prevent it

It is responsible for 86% of blindness among Type

1diabetics, and 35% of Type 2 diabetics.

100% of Type 1 diabetics developed Diabetic

retinopathy, 75% of proliferate type

60% of Type 2 diabetics developed diabetic retinopathy,

10% pf proliferative Type
Diabetic Retinopathy
Timely laser photocoagulation can
prevent 90% of sever visual loss

Treatment of HT and avoidance of

smoking are important in its control
2. Diabetic Neuropathy
It is the commonest complication of DM

The prevalence is increased with:

1. Increased duration of DM
2. Increased glycated Hb level
3. Smoking
4. History of CVD
Types of
Neuropathy
A. Peripheral Neuropathy
Polyneuropathy:
Distal sensorimotor neuropathy,
Proximal motor neuropathy
Focal neuropathy: mononeuropathy,
entrapment neuropathy
Multifocal neuropathy
B. Autonomic Neuropathy
Types of Neuropathy
The most common is the distal sensorimotor
neuropathy which is classified into:

1. Early: asymptomatic, detectable sensory loss,

positive neurological tests

2. Symptomatic: sensory loss, frank numbness,

parasthesia+/- pain

3. Severe: motor involvement, disabling

symptoms, potential for ulceration, infection,
necrosis, and gangrene
Screening Tests
Inspection: feet: dry skin, hair or nail
abnormality, callus or infection

Vibration sensation on the dorsum

of big toe: normal, reduced, absent

Ankel Reflex: normal, reduced,

absent
Types of Neuropathy
Cardiovascular autonomic neuropathy

Serious and can precipitate death.

They have difficulty in detecting

hypoglycemia and / or spontaneous
recovery from hypoglycemia
Prevention:
Education of patients and PHC
physicians

Good glycemic control

Aldose reductase inhibitor

3. Diabetic Nephropathy
A major cause of premature
morbidity and mortality in diabetics

DM increases risk of Renal Failure by

about 17-20 folds

25% of ESRD are due to DM

Diabetic Nephropathy
Diabetic Nephropathy can be divided into:

1. Incipient (sub clinical) nephropathy

Microalbuminuria: 30-300mg/24 hours
HT may be present

2. Clinical nephropathy
Persistent proteinuria >300 mg/ 24 hours
Usually accompanied with HT
Diabetic Nephropathy
3. Advanced nephropathy

Significant reduction of GFR,

Symptoms of uremia +/- nephritic
syndrome

4. ESRD
Prevention
Tight glycemic control

Yearly urinary microalbumin test

Dietary protein restriction

Vigorous control of BP
Prevention
Other supportive measures:

Correction of lipid abnormalities, metabolic

bone diseases, and anemia

Avoidance of fluid retention

Vigorous treatment of UTI

Avoidance of nephrotoxic drugs

4. DIABETIC FOOT
It is infection, ulceration, destruction,
of deep tissues with neurological and
peripheral vascular diseases

Diabetics have 15 folds risk of

amputation than non diabetics
DIABETIC FOOT
Incidence of amputation is
associated with:

1. Duration of DM
2. Glycemic control
3. HT
4. Smoking
DIABETIC FOOT
Lower limb amputation is more in developing
countries:

1. Lack of proper foot wear

2. Inadequate hygiene

3. Poorly controlled DM
Screening
1. Abnormal vibration test
2. Presence of foot deformity
3. Past history of lower extremity
ulceration or amputation

Screening should be done by a trained

physician
Prevention
Regular attendance to health care
settings

Formal teaching sessions

Provision of appropriate written and

or audiovisual materials
The patient should be advised
Not to walk bare-footed
Daily looking to foreign bodies in the
shoes
Avoid bathroom surgery
Treat fungal disease and minor cuts
Usage of mirror to examine plantar
side of the foot
Test the degree to which pain
sensation is lost
Prevent burns
AMPUTATION IS

A PREVENTABLE

COMPLICATION
EDUCATION OF DIABETIC
PATIENTS
It is the corner stone of DM
management

It covers:
self care
changing behavior to prevent and
control of complications
encourage interaction with health
care providers
Contents of Educational Program
Nature of disease, types, clinical
presentation, diagnosis, complications,
types of treatment, side effects, exercise,
self monitoring , avoidance and recognition
of hypoglycemia, and hyperglycemia, foot
care , pregnancy and OC, avoidance of
smoking, CV RFs, need for follow up, self
management skills and attitudes
Active participation of the
family is vital in DM
management
Types of education methods
1. Individual counseling
2. Group teaching
3. Educational materials: posters,
pamphlets, books

Special educational programs are

needed for special groups as
children and pregnant women
Education of Health Professionals

Basic understanding of DM and its

managements

Training in educational methods

Training of dietetics and nurses

Education of the community
Prevention or modification of dietary
habits and other life-style
characteristics that link with DM