diabetes risk factors and prevention

1. PRESENTED BY:
Dr Pratyush Kumar

2.  It is a heterogeneous chronic metabolic disorder of
multiple aetiologies principally characterised by chronic
hyperglycaemia with disturbances of carbohydrate, fat
and protein metabolism resulting from defects in insulin
secretion, action or both.

3. EPIDEMIOLOGY
 It is an iceberg disease.
 Most common endocrine metabolic disease
in childhood and adolescents
 The number of people with diabetes has
risen from 108 million in 1980 to 422 million
in 2014
 The global prevalence of diabetes among
adults over 18 years of age has risen from
4.7% in 1980 to 8.5% in 2014
 Peaks of presentation in children occur in
two age groups: at 5-7yr of age(infectious)
and at the time of puberty (gonadal
steroids).

6. Map of prevalence of diagnosed diabetes in districts of India
Source: Journal of Social Health and Diabetes

7. 0.00%
2.00%
4.00%
6.00%
8.00%
10.00%
12.00%
14.00%
rural semiurban urban
prevalence of diabetes in India in
different habitat

8. 2.40%
7.00%
16.50%
26.30%
29.10%
25.90%
11.50%
14.60% 15.40% 14.60%
16.40%
19.30%
0.00%
5.00%
10.00%
15.00%
20.00%
25.00%
30.00%
35.00%
20-29yrs 30-39yrs 40-49yrs 50-59yrs 60-69yrs >70yrs
Diabetes
IGT
Age-specific prevalence of Diabetes and Impaired glucose
tolerance (IGT)

9. 12%
26%
7%
13%
2%
28%
12%
Proportional mortality(% of total deaths,
all ages) in India Injuries
cardiovascular
diseases
Cancers
Respiratory diseases
Diabetes
communicable
other NCDs

10. CLASSIFICATION
 Diabetes mellitus
 Type 1 or Insulin-dependent diabetes mellitus(IDDM)
 Type 2 or non-insulin dependent diabetes
mellitus(NIDDM)
 Malnutrition related diabetes mellitus(MRDM)
 Other types (secondary to pancreatic, hormonal, drug
induced, genetic and other abnormalities)
 Impaired glucose tolerance(IGT)
 Gestational diabetes mellitus(GDM)

11. TYPE 2 DM MODY LADA
Age Mostly >40
Peak 60-70 years
<25 years 35 -50 years
Mode of onset Insidious Insidious Insidious
Genetics Polygenic Monogenic
autosomal
dominant
Polygenic
Insulin secretion Variable Variable Decreased
Insulin sensitivity Grossly decreased Normal/ decreased Normal
Insulin dependence Nil Nil Later in life
Obesity Common Variable Uncommon
Acanthosis Present Nil Nil
Autoimmunity No No Yes
Family history Present Invariable Of type 1 relative
Metabolic
syndrome
Usually present Rare Nil
MODY: Maturity Onset Diabetes Mellitus
LADA: Latent Autoimmune Diabetes of Adults

12. DIABETES MELLITUS IN NEONATES
AND INFANTS
 Transient neonatal diabetes mellitus
 Observed in both preterm and term babies but more
common in preterm.
 Caused by immaturity of islets of β-cells
 Polyuria and dehydration are prominent but baby looks
well and sucks vigorously
 Highly sensitive to insulin
 Disappears in 4-6 weeks.

13.  Permanent neonatal diabetes mellitus
 A familial form of diabetes that appear shortly after birth
and continue for life.
 The usual genetic and immunologic markers of type 1
diabetes are absent.
 It is often associated with other congenital anomalies
and syndromes

14. RISK FACTORS DURING CHILDHOOD

15. MODIFIABLE
 Overweight (obesity)
 Sedentary lifestyle
 Previously identified glucose
intolerance(IGT and/or IFG)
 Metabolic syndrome
 Dietary factors
 Intrauterine environment
 Viral infections
 Stress(surgery, trauma, stress of
situations)

16. NON-MODIFIABLE
 Ethnicity(African-American, Native American, Asian-
American or Pacific islander)
 Family history of type 2 diabetes
 Age
 Gender
 History of gestational diabetes
 Immune mediated
 Polycystic ovarian syndrome

17. HIGH RISK GROUP
 Obese
 First degree relative with diabetes
 High risk ethnic group
 History of gestational diabetes mellitus
 Hypertension
 Dyslipidaemia
 Previous IFT and IGT

18. STAGES OF DIABETES IN CHILDREN
 Stage of metabolic recovery:
 10- 20% of β- cells are still producing insulin
 Insulin requirement is fairly high at the time of
diagnosis i.e. 1- 1.5 units/kg/day
 There is rapid weight gain, liver enlargement, peripheral
edema, temporary hair loss.
 There are high levels of stress hormone and
compensatory hyperphagia.

19.  Stage of partial remission:
 This is invariably a temporary phase due to regression of
inflammatory changes in the islets allowing the
remaining β-cells to function better.
 This phase lasts longer in adolescents than children.
 Insulin sensitivity increases once hyperglycemia is
controlled and levels of stress hormones decline.
 Intensive phase:
 Insulin requirements begins to rise again, 3-4 months
later as β-cell destruction progresses relentlessly.
 This may happen gradually over weeks or months or it
may be abrupt, precipitated by infection or other forms
of stress.

20.  Stage of total diabetes:
 This is the stage when endogenous insulin production is
negligible and no longer plays a significant role in
glucose haemostasis.
 It is usually reached in two years after clinical onset of
disease.

21. PREVENTION

22. PRIMARY PREVENTION
 Population strategy:
 Primordial prevention
 Maintenance of normal body weight through adoption
of healthy nutritional habits and physical exercise
 Adequate protein intake
 High intake of dietary fibre avoidance of sweet foods
 Elimination of other less well defined factors such as
protein deficiency and food toxins.
 Education of patients and their families to optimize the
effectiveness of primary health care services.

23.  High-risk strategy:
 No special high-risk strategy for type 1 diabetes
 Genetic counselling may be done but not feasible at the
present.
 Correction of sedentary lifestyle, over-nutrition and
obesity for NIDDM.
 Avoidance of alcohol, diabetogenic drugs
 Reduction of factors that promote atherosclerosis e.g.
smoking, high blood pressure, elevated cholesterol.

24. SECONDARY PREVENTION
 Early diagnosis:
 Proper screening
 Routine checking of blood sugar, urine for proteins and
ketone bodies, blood pressure, visual acuity and weight
should be done periodically
 Feet should be examined for any defective blood circulation,
loss of sensation and health of the skin.

25.  Management:
 Proper management of the diabetes is most important
to prevent complications.
 Treatment is based on:
 Diet alone - small balanced meals more frequently
 Diet and oral anti diabetic drugs
 Diet and insulin

26.  Self care:
 Adherence to diet and drug regimen
 Blood glucose monitoring
 Self administration of insulin
 Maintenance of optimum weight
 Attending periodic check-ups
 Recognition of symptoms associated
with glycosuria and hypoglycemia

27. TERTIARY PREVENTION
 Diabetes is the major cause of
disability through its complications
e.g. blindness, kidney failure,
coronary thrombosis, gangrene of
lower extremities etc
 The main objective at the tertiary
level is to organise specialised
clinics(diabetic clinic) and units
capable of providing diagnostic and
management skills of high order.

28. Vaccinations routinely provided for all
children and adults with diabetes
 Pneumococcal vaccine:
 Prevenar 13 is recommended for children below 2 years
 Children with diabetes aged between 2 to 5 years who
have not previously received PCV13 should receive 1 or 2
doses of PCV13
 Children with diabetes aged ≥ 2 years should also receive
pneumovax 23
 Pneumovax 23 is recommended for adults with diabetes
aged < 65 years
 Adults aged > 65 years should receive both PCV13 and
PPV23

29.  Hepatitis B vaccine:
 Recommended for adults with diabetes <60 years of age
 Also considered in unvaccinated adults aged >60years
 Influenza vaccine:
 Annually in all patients with diabetes aged >6 months

30. COMPLICATIONS

31. Acute complications:
 Diabetic Ketoacidosis
 Hyperglycemic hyperosmolar nonketotic coma
 Hypoglycemia

32. Chronic complications:
Microvascular
Nephropathy
Retinopathy
neuropathy
Macrovascular
Coronary artery
disease
Cerebrovascular
disease
Peripheral arterial
disease

35. RECENT ADVANCEMENTS
 Vaccination for type 1 Diabetes
 A prototype vaccine that could prevent type 1 diabetes in
children is ready to start clinical trials in 2018.
 It is expected to provide immunity against a virus(enterovirus)
that has been found to trigger the body’s defence into
attacking itself.
 The next phase will involve testing on healthy adult humans,
just to map out any complications.

36.  BCG vaccine for reversal of advanced type 1
Diabetes
 Interim results from a FDA-approved clinical trial
testing the generic vaccine BCG to reverse advanced type
1 diabetes demonstrate a potential new mechanism by
which the BCG vaccine may restore the proper immune
response to the insulin-secreting islet cells of the
pancreas.

37. BIBLIOGRAPHY
 www.who.int
 American Diabetes Association (www.diabetes.org)
 National Programme on Prevention and Control of
Diabetes in India
 Journal of Social Health and Diabetes
 Medscape
 Park’s Textbook of Preventive and Social Medicine
 www.google.co.in

38. Theme of 2017 : Women and diabetes- our right to a healthy
future