EPIDEMIOLOGY OF DIABETES
MELLITUS
Dr Faris Al-Lami
MB ChB PhD FFPH
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, 366 millions
were affected in 2011, and expected to reach 530
million in 2030
•
It affects all ethnic and socioeconomic groups
•
Incidence & prevalence are highly varied between
& within countries
20-60 folds
difference
•
Considerable impact on economic and social
condition.
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 requirements
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 HbA
1
C
•
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, progresses
through several clinical staging during its natural
history
•
Individual subject may move from one stage to
another in either direction
•
Clinical staging reflects the hyperglycemia which
reflects 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
•
Relative rather than absolute insulin deficiency with
resistance to insulin action
•
Do not require insulin for survival
•
May remain undetected for long time
•
Increased risk of macro and micro vascular
complications
•
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
•
Risk increases with age, obesity, lack of physical
activity
•
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 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/ml 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
Macrovascular
disorders
•
Management should include control strategies of
all
components
and not only hyperglycemia
•
Metabolic syndrome may be present for up to 10
years before detection of the glycemic disorder
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, decreases risk or
severity of complications and so decreases 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