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Diabetes Epidemic in India:
Is it subsiding?
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TOP TEN COUNTRIES FOR THEIR
ESTIMATED NUMBER OF ADULTS
WITH DIABETES(IN MILLIONS).
Country Year 1995 Year 2025
India
China
U.S.A.
Russian
Federation
Japan
Brazil
Indonesia
Pakistan
19.4
16.013.9
8.9
6.3
4.9
4.5
4.3
57.2
37.621.9
12.2
8.5
11.6
12.4
14.52
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STUDIES OF PREVALENCE OF DM IN INDIA
FROM 19792001YEAR AUTHOR PLACE PREVALANCE RATE
19861988
1989
1989
19911992
1997
1999
20002001
Patel J. C.Ramchandran et al
Kodali et al
Rao et al
Ahuja et alRamchandran et al
Ramchandran et al
Ashabai et al
Ramchandran et al(DESI)
Misra et al
BhadranKudremkh
Gangarathi
Eluru
New DelhiMadras
Madras
Chennai
National
Northern India
3.8 ( R )5.0 ( U )
2.2 ( R )
1.6 ( R )
6.7 ( R )8.2 ( U )/2.4 ( R )
11.6 ( U )
17.4% ( U )
12.1 ( U )
10.3 DM
15.2 IFG
U = Urban IFG = Impaired Fasting GlucoseR = Rural DESI = Diabetes E idemic Studies in India
3
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ESTIMATED PREVALENCE IN
URBAN AND RURAL INDIA
0
10
20
30
40
50
60
1990
1995
2000
2005
2010
2015
2020
2025
UrbanRural
Number (millions)
4
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Chennai Urban Rural Epidemiological Study (CURES- 17)(Diabetologia 2006)
Prevalence of Diabetes in Chennai rose by:
39.8% in years 1989 1995
16.3% in years 1995 2000
6% in years 2000 2004
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Factors likely to influence prevalence oftype 2 diabetes
Factors Factor likely toincrease prevalence
Factor likely todecrease prevalence
1 Demography ofthe
population
Increasing life span Increase in younger agegroups
2 Obesity Increasing obesity Decreasing obesity
3 Education Continuing lower educationalstatus
Rapidly increasing generaland health education
4 Income Increasing income
(specially when accompanied
by poor educational inputs)
Increasing income(specially whenaccompanied byenhancededucational inputs)
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Factors likely to influence prevalence of type2 diabetes
5 Genetic factors Increased prevalencetill adverseenvironment has actedon most geneticallysusceptible population
Stabilizing influence ofgenetically non-susceptiblegroup
6 Physical activity Decreased activity dueto urbanization and
poor built environment
Increased physical activity byintroducing healthylifestylethrough education and bettertown planning
7 Diet Increased calories,
saturated fat, sugarand
refined food intake
Decreased calories, saturated
fat, sugar and refinedfood intake
8 Mental stress High stress with poorquality of life
Peaceful and good quality of life
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Percentage distribution of 2001 censuspopulation for India
Age Group Persons(%)0-4 11.8
5-9 12.0
10-14 11.7
15-19 10.1
20-24 8.925-29 8.1
30-34 7.4
35-39 6.6
40-44 5.6
45-49 4.6
50-54 3.6
55-59 2.9
60-64 2.5
65-69 2.0
70-74 1.6
75-79 0.5
80+ 0.3 Source: Population Projection report - 2006
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Demographic Structure (India, 2001)
Ages 0-19 45.6%
Ages 50-80 13.4%
9
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Is there possibility of second
epidemic of DM in India?
Yes: when the population structure changes in favourof elderly subjects
No: Education
Behavior changes
Town planning
may counter the epidemic
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Diabetes MellitusFactors influencing Incidence & Prevalence
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Increased life span Increased elderly population
Decreased life spanIncreased young population
Prevalence
Birth & Death rate
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ECONOMIC DEVELOPMENT
AND OBESITYObese Percent of Population
Worldwide 8.2
Least developed countries 1.8
Developing Countries 4.8
Emerging Economies 17.1Developed Economies 20.4
( The Economist, Dec 2003)
HBC- DENMARC12
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BMI TRENDS IN FINLAND & INFLUENCE OFEDUCATION
(Pekkanen, J Epidemiol Commun Health, 1995) HBC- DENMARC13
With increasing education, BMI goes down
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SHORT TERM WEIGHT LOSS
IMPROVES INSULIN SENSITIVITY
0
5
10
15
20
2530
35
40
45
Before Weight Loss After Weight Loss
*
*P
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LIFESTYLE CHANGES PREVENT
TYPE 2 DIABETES
(Finnish study) (Toumilehto, NEJM, 2001)
N= 522, IGTInterventions :
F.U. 3.7 yrs
Control group
Lifestyle intervention : Weight reduction,
Fat and SFA, fibre
Results : Wt loss: Intervention group 3.5 kg, placebo 0.3 kg
Cumulative incidence of diabetes
Control group 23%
Intervention group 11% (58% reduction) 15
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DIABETES PREVENTION PROGRAM
(DPP) (NEJM, 2002)
n= 3234, IGT, mean age 51 yrs, BMI 34Interventions :
F.U. for 2.8 yrs
Placebo Metformin : 850 mg/day : 150 min/wk Exercise
Life style modifications : 7% wt. reduction
Results :
Incidence of Diabetes (Cases per 100 person/year)
Placebo : 11
Metformin 7.8 % (31% reduction)
Lifestyle Intervention 4.8 (58 % reduction) 16
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Built Environment(Pasala, Rao, Sridhar: Built Environment and Diabetes, International Journal of
Diabetes in Developing countries, 2010)
Environment modified by humans: Home,
School, Workplace, Highways, Urbansprawls
Accessibility to amenities, leisure
Pollution
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Genetics of Type 2 DM
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Susceptibility Genes
Present : PrevalenceAbsent : Stabilising effect
Protective Geneseg: Nephropathy
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Outcome Measures in Diabetes
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Outcome measures
1. Hard and Soft end points define: outcome
2. Non-diabetic or diabetic controls
3. Adjudicated outcome
4. Primary and Secondary outcome
5. Number needed to save one life
6. Mechanism of favorable or adverse outcome
may be difficult to unravel
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Medical Records
1. Quality of records
2. Manual or Computerization: designed to yieldto detailed analysis
3. Casual and regular patients
4. Follow up reminders
5. Cohort follow up
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Significance of outcome measures
1. All treatments modalities should undergooutcome studies
eg: CV outcome with newer agents
Malignancy
2. Efficacy versus outcome
eg: Torcetrapiband HDL-C
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DCCT : Benefits of good glycemic control
Mean HbA1c in intensive group was 7.2 % vs 9.2
% in conventional control group
Intensive glycemic control reduced the risks of
Neuropathy by 57-69 %
Retinopathy by 54-76 %
Nephropathy by 34-56 %N Engl J Med 1991
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UKPDS : Benefits of good glycemic control
Intensive glucose control maintained a lower HbA1cover a period of 10 years with reduction in risk of :
33 % for albuminuria
25 % for microvascular end-points
24 % for cataract extraction
21 % for retinopathy
16 % for myocardial infarction
12 % for any diabetes-related end-point
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Kumamoto Study :Benefits of Good
Glycemic ControlIntensive glycemic control reduced the risks of
progression of :
Nephropathy by 70 % Retinopathy by 69 %
Macrovascular events by 54 %
Preserved nerve conduction velocity better
Hypoglycemia was rareOkhubo et al, Diab Res Clin Pract 1995;28:103-117
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O A Q A A CO O G
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HOW ADEQUATELY ARE WE CONTROLLING
DIABETES MELLITUS?
Targets:
ADA 7%
ACCE 6.5%
The targets can only be achieved, if prandial
blood glucose is targeted
Gl i G l EASD
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Glycemic Goals: EASDTYPE 2 DMLow risk Arterial
riskMicrovascular
risk
HbA1c (DCCT
Standardized)
%Hb
6.5 >7.5
Venous plasma glucose
Fasting / pre-prandial
mg/dl=110 >125
Self-monitored blood glucose
Fasting / pre-prandial
mg/dl=100 >=110
Post-prandial (peak)
mg/dl=135 >160
27
Gl cemic Go ls EASD
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Glycemic Goals-EASDTYPE 1 DM
Non-diabetic Adequate Inadequate
HbA1c (DCCT
standardized %Hb7.5
Self monitored blood glucose
Fasting/preprandial
mg/dl70-90 91-120 >120
Post-prandial (peak)
mg./dl70-135 136-160 >160
Pre-bed mg/dl 70-90 110-135 >135
It can be dangerous to strive for non-diabetic glucose levels.28
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HBA1C GOALS
Targets:
In general: HbA1c
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Only 26% of all type 2 diabetics inGermany achieve HbA1c < 6.5%
(Leibl A et al. CODE
2 Study, 2001)
Average HbA1c in US, 8.5-9.0%
(ADA, Diabetes Care 2000)
Global Scenario
DENMARC
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Global status of Glycemic control
1. Canada: Prim care; Mean HbA1c: 7.3 %
49 % not at target (A1c 7%)
(Harris, Diab Res Clin Pract, 2005)
2. Finland: 76 clinics; Mean HbA1c 8.6 1.9 %
(Type 1: 8.8, Type 2: 8.5) Lowest HbA1cvalues associated with short duration of DM
3. USA: NHANES III Preliminary report
HbA1c < 7 %: 44.5 % in 1988-94
35.5 % in 1999-2000
USA: 30 US academic centers: HbA1c
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PATIENTS AND METHODS
Type 2 DM on regular follow up (minimum
2 years)
2 study groups: group 1 DM 10 yrs (n =167), group 2 DM 10 yrs (n = 301)
Glycated hemoglobin done by total GHb or
HbA1c
;
results expressed as percent above
good control (good control GHb8%,HbA1c 7%).
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PATIENTS AND METHODS - 2
Initial GHb/HbA1c was compared with
average follow up values
average follow up 5.39 years (minimum 2
years)
average no. of GHb/HbA1c performed were
6.25/patient.
A total of 3400 values .
Paired t test used for data analysis.
33
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Patient CharacteristicsDENMARC DATA
Glycemic control
GHb/HbA1c (Above upper limit of good control)
Number of Patients: 330
Initial HbA1c ( n= 330 )(Mean SD) : 8.07 1.82
Number of Patients: 330
Average of subsequent HbA1c ( n= 465 )(Mean SD) : 8.01 0.59
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Change in Glycemic Control
GHb/HbA1c(MeanSD) n=468
p
Baseline Follow Up
Diabetes< 10 years
n=167
1.9
1.4 1.5
1.2 10 years
n=301
2.4
1.5 1.9
1.2
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Change in Glycemic ControlDENMARC DATA
(2007-2009)
GHb/HbA1c*
(Mean SD) n = 330
Baseline Follow Up2.22 0.67 1.33 0.22
*% above good glycemic control (HbA1c < 7.0%; GHb < 8.0%)
DENMARC
Diabetes Endocrine Nutrition Management and
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Diabetes Endocrine Nutrition Management andResearch Centre (DENMARC)
HbA1C achieved currently
27.30%
23.70%
49%8
9.7 1.34
6.2 0.5
7.5 0.31
Average of all values (n =1000):8.2 1.80 %
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HYPOGLYCEMIC AGENTS vs
ANTIHYPERGLYCEMIC AGENTS
Hypoglycemic agents Antihyperglycemic agents
Sulfonylureas
Non-SU insulin secretagogues Repaglinide
Nateglinide
Insulin
Metformin
Glitazone Nutrient blockers: acarbose,
voglibose, miglitol
GLP-1 analogues
DPP IV Inhibitors
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GLYCEMIC INDEX OF FOODS
Classification GI range Examples
Low GI 55 or less most fruit and vegetables (except
potatoes), whole grains, pulses,
soyabean, multi-grain bread,bran bread
Medium GI 56 - 69 sucrose, pasta, Icecream,
sheera, whole-wheat bread,
durham wheat
High GI 70 or more corn flakes, baked potato, white
rice, whitebread, watermelon,
coconut water
PULSES AND PULSE INCORPORATED
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PULSES AND PULSE-INCORPORATED
CEREAL FOODS(Chandalia et al, IJDDC, 1992)
White Bread 100 100
Wheat Gram meal 66.4 118.6
Gram Meal 48.3 202.1
Glycemic index Insulinemic index
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TREATMENT RELATED WEIGHT GAIN
IN DIABETES
Outline of talk:
1. Concept of set-point weight and settling pointweight
2. Obesity and Diabetes
3. Treatment- related weight gain
a. Conventional drugs
b. Newer drugs
4. Countering weight gain in DM and its benefits
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SET POINT vs. SETTLING POINT
Set-point Model: Individual defends preferred
level of body weight : Pre-determined and
constant environment
Settling Point Model: Individual defends a specific
body weight level within a changing environment
with constant genetic factors : environment
changes over time
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DEMOGRAPHIC DATA AND TREATMENT MODALITIES
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n Male;Female
Age (Years)
(Mean SD)
BMI(Kg/m2)
StableBody
Weight (Kg)
(Mean SD)
Duration ofDiabetes(Years)
(Mean SD)SU 108 67; 41 51.5 8.3 24.9
3.167.5 6.7 9.3 5
SU+MF 171 99; 72 51.5 7.7 27.24.3
73.5 10.1
11.6 5.5
INSULIN
89 55; 34 55.110.4
25.24.6
68.7 9.4 13.4 6.6
SU+I 85 50; 35 55.6 9.5 24.93.8
66.9 9.7 14.7 5.1
SU+MF+I
16 8; 8 57.6 6.8 27.14.9
77 12 17.8 5.6
SU : Sulfonylurea
SU + MF : Sulfonylurea + Metformin
SU + I : Sulfonylurea + Insulin
SU+MF+I : Sulfonylurea + Metformin + InsulinChandalia HB, Metabolic Syndrome & Related Disorders,2005.
WEIGHT CHANGE WITH DIFFERENT THERAPEUTIC MODALITIES
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WEIGHT CHANGE WITH DIFFERENT THERAPEUTIC MODALITIES
n InitialWeight (Kg)
(MeanSD)
Weight atStudy Point(Kg)(Mean SD)
Weight Gain(Kg)
(Mean SD)
P
SU 108 66.0 8.8 67.2 8.8 1.2 2.9 NS
SU+MF 171 72.2 13.2 72.8 13.5 0.6 2.9 NS
INSULIN 89 66.0 12.6 6 7.8 12.1 1.8 4.9 NS
SU+I 85 65.0 11.7 67.9 12 2.9 3.8
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58
60
626466
6870
72
7476
Group with Pre-
Treatment Weight
Loss (n=253)
Group without Pre-
Treatment Weight
Loss (n=216)
Stable weight
Intial weight
Post treatment
Weight
( )
PRE-TREATMENT WEIGHT LOSS AND THOSE
WITHOUT PRE-TREATMENT WEIGHT LOSS
Group with Pre-treatment