EPIDEMIOLOGY OF DIABETES

MELLITUS
Dr Faris Al-Lami
MB ChB PhD FFPH
 Objectives
• Define DM
• Identify types, staging and diagnosis
• Brief description of metabolic syndrome
• Identify primary and secondary preventive
strategies
 Definition:
DM 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:
• Affects large number of people from all ethnic
and socioeconomic groups
• Global prevalence raised from 4.7% in 1980 to
8.5% in 2014.
• Incidence & prevalence are highly varied
between & within countries (20-60 folds
difference)
• Diabetic nephropathy is among the leading
causes of CRF worldwide
• Other common effects of DM include:
neuropathy, retinopathy, diabetic foot
Year Million
1980 108

2011 366

2013 382

2014 422 (I in every 11)

2030 530, 7th leading cause of death

2035 592
 General Epidemiological Characteristics:
• In developing countries, the incidence and prevalence of
Type 2 DM are rapidly increasing.
• Low- and middle-income countries account for more
than 80% of all deaths related to diabetes.
Why DM becomes an epidemic in developing countries?:
• Westernized diets and available cheap sugar and fat
calories
• Transition to urban lifestyles
• Genetics: non-Caucasian populations are at increased
risk
 Economic impact of diabetes
• DM and its complications causes substantial
economic loss to the patients, their families,
the health systems and national economies
through direct medical costs and loss of work.
• Direct annual cost of diabetes globally > US$
827 billion.
• Losses in Gross Domestic Product (GDP)
worldwide estimated to be US$ 1.7 trillion
from 2010 to 2030
 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
 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

 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
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

 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
 Early detection and treatment of
complications

End-stage renal disease Blindness

• Measurement of urine • Periodic eye
protein examinations and
• Progression to kidney timely laser
failure can be slowed by photocoagulation
essential drugs Lower limb amputation
Cardiovascular diseases • Proper footwear and
• Measure and control regular examination of
cardiovascular risk feet
factors • Provide rehabilitation