Epidemiology

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, 366millions were affected in 2011, and expected to reach 530 million in 2030

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.

General Epidemiological Characteristics:

DM is an important cause of premature death and causes serious health consequences

It is important RF of CHD which 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

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

CLINICAL STAGING OF DMI. 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

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 CLASSIFICATIONI - 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 1a) 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 1a) 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-1b) 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

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 SYNDROMEWorking 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/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 Macro vascular 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
• Screening for undetected DM
• Control of hyperglycemia, and other metabolic abnormalities
• 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 PREVENTION OF 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