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

1.
2.
3.
Precipitating factors
Infection
Acute illnesses
Insufficient insulin treatment

1.
2.
Prevention:
Health education
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.
2.
3.
4.
Increased duration of DM
Increased glycated Hb level
Smoking
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
Glycemic control
HT
Smoking
2.
3.
4.
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.
2.
3.
Abnormal vibration test
Presence of foot deformity
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.
2.
3.
Individual counseling
Group teaching
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