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OBESITY OBESITY IN FAMILY IN FAMILY PRACTICE PRACTICE

Management Of Obesity In Family Practice Cme 30 May08

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Page 1: Management Of Obesity In Family Practice Cme 30 May08

OBESITYOBESITYIN FAMILY IN FAMILY PRACTICEPRACTICE

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DR. G. C. DHAR.DR. G. C. DHAR.

MD., DTM&HMD., DTM&HFRSTM&H (UK), MCFP FRSTM&H (UK), MCFP

(CANADA)(CANADA)

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IN 1998, THE WORLD HEALTH IN 1998, THE WORLD HEALTH ORGANIZATION DESIGNATED ORGANIZATION DESIGNATED

OBESITY AS AOBESITY AS A

GLOBAL GLOBAL EPIDEMICEPIDEMIC

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TREATMENT OF OBESITY TREATMENT OF OBESITY CONSISTS OF 2 STEPSCONSISTS OF 2 STEPS

ASSESSMENT: determination of degree of ASSESSMENT: determination of degree of obesity and overall health status.obesity and overall health status.

MANAGEMENT: not only involves weight MANAGEMENT: not only involves weight loss and maintenance of body weight but loss and maintenance of body weight but also to control of other risk factors.also to control of other risk factors.

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WHAT IS OBESITY?WHAT IS OBESITY?

OBESITY IS THE OBESITY IS THE ABNORMAL ABNORMAL ACCUMULATION OF ACCUMULATION OF ADIPOSE TISSUE IN THE ADIPOSE TISSUE IN THE BODY, DEFINED AS BODY BODY, DEFINED AS BODY MASS INDEX (BMI) MASS INDEX (BMI) 30KG/M2 OR ABOVE.30KG/M2 OR ABOVE.

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OBESITY NOW IS NOT A OBESITY NOW IS NOT A PROBLEM OF HIGH INCOME PROBLEM OF HIGH INCOME

COUNTRIESCOUNTRIES

IT IS NOW DRAMATICALLY IT IS NOW DRAMATICALLY INCREASING IN MIDDLE AND INCREASING IN MIDDLE AND

LOW INCOME COUNTRIESLOW INCOME COUNTRIES

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CURRENT SITUATIONCURRENT SITUATION

IN USA 64.5% ADULT IN USA 64.5% ADULT POPULATION ARE EITHER POPULATION ARE EITHER OBESE OR OVERWEIGHT.OBESE OR OVERWEIGHT.

IN CHINA FROM 1991 TO IN CHINA FROM 1991 TO 2004, OBESITY INCREASED 2004, OBESITY INCREASED FROM 12.9% TO 27.3%.FROM 12.9% TO 27.3%.

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IN BANGLADESHIN BANGLADESH

Bangladesh Demographic and Health Bangladesh Demographic and Health Survey, 1999-2000 Survey, 1999-2000 Year: Year: 2000 shows:2000 shows:0.7% population aged 15-49 are of BMI 0.7% population aged 15-49 are of BMI equal or >30kg/m2equal or >30kg/m24.5% population aged 15-40 are of BMI 4.5% population aged 15-40 are of BMI equal or >25kg/m2equal or >25kg/m2As of 2004, prevalence of overweight has As of 2004, prevalence of overweight has been increased up to 9.1% in urban and been increased up to 9.1% in urban and 5.5% in rural population.5.5% in rural population.

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IMPORTANT FACTORS FOR IMPORTANT FACTORS FOR BANGLADESHBANGLADESH

ABUNDANCE OF FAST FOOD ABUNDANCE OF FAST FOOD OUTLETS.OUTLETS.ONLY 10% CHILDREN FROM BANGLA ONLY 10% CHILDREN FROM BANGLA MEDIUM AND 7% CHILDREN FROM MEDIUM AND 7% CHILDREN FROM ENGLISH MEDIUM SCHOOLS HAVE ENGLISH MEDIUM SCHOOLS HAVE ACCESS TO SPORTS.ACCESS TO SPORTS.ONLY 2-3 FROM MORE THAN 40 ONLY 2-3 FROM MORE THAN 40 PRIVATE UNIVERSITIES IN DHAKA PRIVATE UNIVERSITIES IN DHAKA HAVE PLAYING FIELDS.HAVE PLAYING FIELDS.

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CLASSIFICATION OF OBESITY CLASSIFICATION OF OBESITY

ACCORDING TOACCORDING TO BMI BMI+STARVATION: <15KG/M2+STARVATION: <15KG/M2

+UNDERWEIGHT: 15KG/M2 TO 18.4KG/M2+UNDERWEIGHT: 15KG/M2 TO 18.4KG/M2

+NORMAL: 18.5KG/M2 TO 24.9KG/M2+NORMAL: 18.5KG/M2 TO 24.9KG/M2

+OVERWEIGHT: 25KG/M2 TO 29.9KG/M2+OVERWEIGHT: 25KG/M2 TO 29.9KG/M2

+OBESITY CLASS I: 30KG/M2 TO 34.9KG/M2+OBESITY CLASS I: 30KG/M2 TO 34.9KG/M2

+OBESITY CLASS II: 35KG/M2 TO 39.9KG/M2+OBESITY CLASS II: 35KG/M2 TO 39.9KG/M2

+MORBIDLY OBESE: 40KG/M2 OR MORE+MORBIDLY OBESE: 40KG/M2 OR MORE..

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WHAT IS BMI?WHAT IS BMI?

BODY WEIGHT IN KG BODY WEIGHT IN KG DIVIDED BY HEIGHT IN DIVIDED BY HEIGHT IN

METER SQUAREMETER SQUARE

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ALTHOUGH WE DEFINE ALTHOUGH WE DEFINE OBESITY BY BMIOBESITY BY BMI

BMI EXACTLY DOES NOT BMI EXACTLY DOES NOT REFLECT THE ACTUAL REFLECT THE ACTUAL

ADIPOSITYADIPOSITY

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BECAUSEBECAUSE

BMI DOES NOT DIFFERENTIATE ADIPOSE BMI DOES NOT DIFFERENTIATE ADIPOSE TISSUE AND LEAN TISSUE. HIGH BMI CAN TISSUE AND LEAN TISSUE. HIGH BMI CAN BE FOUND IN MASCULAR ATHLETS WHO BE FOUND IN MASCULAR ATHLETS WHO ARE ABSOLUTELY NOT IN METABOLIC RISKARE ABSOLUTELY NOT IN METABOLIC RISK

BMI DOES NOT DIFFERENTIATE CENTRAL BMI DOES NOT DIFFERENTIATE CENTRAL OR VISCERAL OBESITY AND PERIPHERAL OR VISCERAL OBESITY AND PERIPHERAL OBESITY.OBESITY.

BMI DOES NOT DIFFERENTIATE GENDERBMI DOES NOT DIFFERENTIATE GENDER

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VISCERAL OR CENTRAL VISCERAL OR CENTRAL OBESITY IS RISKYOBESITY IS RISKY

MEASURED BY MEASURED BY

WAIST CIRCUMFERENCEWAIST CIRCUMFERENCE

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HOW TO MEASURE WAIST HOW TO MEASURE WAIST CIRCUMFERENCE?CIRCUMFERENCE?

USE A TAPE MEASUREUSE A TAPE MEASURE

START AT THE TOP OF THE RIGHT START AT THE TOP OF THE RIGHT ILIAC CREST, BRING IT ALL THE WAY ILIAC CREST, BRING IT ALL THE WAY AROUND AND LEVEL WITH THE NAVELAROUND AND LEVEL WITH THE NAVEL

TAPE SHOULD NOT BE TOO TIGHT TAPE SHOULD NOT BE TOO TIGHT AND MUST BE PARALLEL WITH THE AND MUST BE PARALLEL WITH THE FLOOR.FLOOR.

RELAX AND NOT TO HOLD BREATH.RELAX AND NOT TO HOLD BREATH.

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NORMAL WAIST NORMAL WAIST CIRCUMFERENCECIRCUMFERENCE

FOR NORTH AMERICANS:FOR NORTH AMERICANS: MEN: <102CM AND WOMEN: <88CMMEN: <102CM AND WOMEN: <88CM

FOR EUROPIANS:FOR EUROPIANS: MEM: <94CM AND WOMEN: <80CMMEM: <94CM AND WOMEN: <80CM

FOR SOUTH ASIANS:FOR SOUTH ASIANS: MEN: <90CM AND WOMEN: <80CMMEN: <90CM AND WOMEN: <80CM

FOR CHINESE:FOR CHINESE: MEN: <90CM AND WOMEN: <80CMMEN: <90CM AND WOMEN: <80CM

FOR AFRICANS:FOR AFRICANS: MEN: <84CM AND WOMEN: <80CMMEN: <84CM AND WOMEN: <80CM

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HIGHER WAIST HIGHER WAIST CIRCUMFERENCECIRCUMFERENCE

IS AN INDEPENDENT RISK IS AN INDEPENDENT RISK FACTORFACTOR

HIGH CONTENT OF HIGH CONTENT OF VISCERAL FAT =VISCERAL FAT =

HIGHER METABOLIC RISKHIGHER METABOLIC RISK

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NOT ALL PATEINTS WITH NOT ALL PATEINTS WITH ABDOMINAL OBESITY ARE ABDOMINAL OBESITY ARE

IN RISKIN RISK

STOP!!!STOP!!!

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ABDOMINAL FAT SHOULD BE ABDOMINAL FAT SHOULD BE DEFFERENTIATED INTODEFFERENTIATED INTO

VISCERAL FATVISCERAL FAT&&

SUBCUTANEOUS FATSUBCUTANEOUS FAT

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PRACTICAL TIP FOR PHYSICIANPRACTICAL TIP FOR PHYSICIAN

*If waist circumference exceeds limit, go for fasting *If waist circumference exceeds limit, go for fasting triglyceridetriglyceride

*If fasting triglyceride >177mg/dl (>2.0mmol/L)*If fasting triglyceride >177mg/dl (>2.0mmol/L)*Abdominal obesity is due to visceral fat which *Abdominal obesity is due to visceral fat which

leads to triad: hyperinsulinemia, high level of leads to triad: hyperinsulinemia, high level of small dense particles of LDL & high Apo-B and small dense particles of LDL & high Apo-B and ultimately CVD & T2DM ultimately CVD & T2DM

*If fasting TG <177mg/dl (<2.0mmol/L), high waist *If fasting TG <177mg/dl (<2.0mmol/L), high waist is due to suncuteneous fat & patients are not in is due to suncuteneous fat & patients are not in risk.risk.

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PERIPHERAL FAT e.g. PERIPHERAL FAT e.g. AROUND HIPAROUND HIP

CONTAINS MORE PUFA AND CONTAINS MORE PUFA AND MORE PHYSIOLOGICMORE PHYSIOLOGIC

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MODERN MARKER OF MODERN MARKER OF OBESITYOBESITY

WAIST HIP RATIOWAIST HIP RATIO

(WHR)(WHR)

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WHAT IS WAIST HIP RATIO?WHAT IS WAIST HIP RATIO?

MEASURE THE WAISTMEASURE THE WAIST

MEASURE THE WIDEST PART OF HIPSMEASURE THE WIDEST PART OF HIPS

MAKE RATIO WAIST/ HIPMAKE RATIO WAIST/ HIP

FOR MEN WHR <0.9FOR MEN WHR <0.9

FOR WOMEN WHR <0.7FOR WOMEN WHR <0.7

WHR DIFFERENTIATE THE CENTRAL FROM WHR DIFFERENTIATE THE CENTRAL FROM PERIPHERAL OBESITY, HENCE BETTER PERIPHERAL OBESITY, HENCE BETTER MARKER OF OBESITY RELATED RISK.MARKER OF OBESITY RELATED RISK.

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OTHER MEASUREMENTS FOR OTHER MEASUREMENTS FOR OBESITYOBESITY

BIOELECTRICAL IMPEDANCE BIOELECTRICAL IMPEDANCE ANALYSIS (BIA)ANALYSIS (BIA)

CT SCANCT SCAN

MRIMRI

DUAL ENERGY X-RAY DUAL ENERGY X-RAY ABSORPTIOMETRY (DXA)ABSORPTIOMETRY (DXA)

THESE ARE NOT ROUTINELY USEDTHESE ARE NOT ROUTINELY USED

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BODY MASS INDEX(BMI)BODY MASS INDEX(BMI)WAIST CIRCUMFERENCEWAIST CIRCUMFERENCE

The two important screening The two important screening methods of obesity accepted methods of obesity accepted

worldwideworldwide

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CAUSES OF OBESITYCAUSES OF OBESITY

1. LIFESTYLE AND DIET1. LIFESTYLE AND DIET

2. ENVIRONMENTAL FACTORS2. ENVIRONMENTAL FACTORS

3. GENETIC FACTORS3. GENETIC FACTORS

4. CERTAIN HORMONAL 4. CERTAIN HORMONAL DISEASESDISEASES

5. MEDICATIONS5. MEDICATIONS

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1. LIFESTYLE AND DIET1. LIFESTYLE AND DIET

MAIN REASONS FOR OBESITY MAIN REASONS FOR OBESITY IS “ENERGY IMBALANCE” e.g. IS “ENERGY IMBALANCE” e.g. CONSUMING MORE CALORIES CONSUMING MORE CALORIES THAN BODY NEEDSTHAN BODY NEEDS

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1. LIFESTYLE AND DIET cont’d1. LIFESTYLE AND DIET cont’d

SEDENTARYLIFESTYLE.SEDENTARYLIFESTYLE.

ENERGY DENSE FAST FOOD CONSUMING ENERGY DENSE FAST FOOD CONSUMING WORLDWIDE HAS INCREASED 4 TIMES WORLDWIDE HAS INCREASED 4 TIMES FROM 1977 TO 1995.FROM 1977 TO 1995.

EVEN DIET SODA AND ARTIFICIAL EVEN DIET SODA AND ARTIFICIAL SWEETENERS ALSO CAUSE OBESITY BY SWEETENERS ALSO CAUSE OBESITY BY “CEPHALIC PHASE INSULIN “CEPHALIC PHASE INSULIN RESPONSE”(CPIR)RESPONSE”(CPIR)

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1. LIFESTYLE AND DIET cont’d 1. LIFESTYLE AND DIET cont’d

OVERALL WORLD POPULATION INCLUDING IN OVERALL WORLD POPULATION INCLUDING IN BANGLADESH ARE NOW VERY MUCH PRONE TO BANGLADESH ARE NOW VERY MUCH PRONE TO SEDENTARY LIFESTYLE.SEDENTARY LIFESTYLE.SPENDING MUCH TIME IN FRONT OF COMPUTER, SPENDING MUCH TIME IN FRONT OF COMPUTER, TELEVISIONSTELEVISIONSDREADFUL EXAMPLE. SAMOA, A POLYNESIAN DREADFUL EXAMPLE. SAMOA, A POLYNESIAN ISLAND COUNTRY. AMERICAN GRANT AND FAST ISLAND COUNTRY. AMERICAN GRANT AND FAST FOOD OUTLETS (INTRODUCED IN 2000) HAVE FOOD OUTLETS (INTRODUCED IN 2000) HAVE LEAD TO OBESITY PREVALENCE 75%.LEAD TO OBESITY PREVALENCE 75%.FOR SAME REASON, HIGHEST PREVALENCE OF FOR SAME REASON, HIGHEST PREVALENCE OF OBESITY IN MICRONESIAN COUNTRY NAURU OBESITY IN MICRONESIAN COUNTRY NAURU WHERE OBESITY BEING 84.7% IN MALE AND 92% WHERE OBESITY BEING 84.7% IN MALE AND 92% IN FEMALE.IN FEMALE.

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2. ENVIRONMENTAL FACTORS2. ENVIRONMENTAL FACTORS

BIG PORTION SIZEBIG PORTION SIZEHIGH FAT/ENERGY DENSE FOODHIGH FAT/ENERGY DENSE FOODHIGH GLYCEMIC INDEX OF FOODHIGH GLYCEMIC INDEX OF FOODSOFT DRINKSSOFT DRINKSSUGAR SUGAR FAST FOODFAST FOODSNACK FOOD SNACK FOOD LOW CALCIUMLOW CALCIUM

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3. GENETIC FACTORS3. GENETIC FACTORS

RESEARCH SHOWS ABOUT 77% RESEARCH SHOWS ABOUT 77% CASES IN CHILDHOOD OBESITY ARE CASES IN CHILDHOOD OBESITY ARE INHERITED FROM OBESE PARENTS.INHERITED FROM OBESE PARENTS.CERTAIN GENETIC DISEASES: CERTAIN GENETIC DISEASES: Prader Willi Syndrome (7 genes in Prader Willi Syndrome (7 genes in chromosome 15 are missing or chromosome 15 are missing or unexpressed)unexpressed)Bardet-Biedle Syndrome (defect in Bardet-Biedle Syndrome (defect in chromosome 16)chromosome 16)

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4. HORMONAL DISEASES4. HORMONAL DISEASES

HYPOTHYROIDISMHYPOTHYROIDISM

CUSHING’S CUSHING’S SYNDROMESYNDROME

RECENT SMOKING RECENT SMOKING CESSATION (nicotine CESSATION (nicotine suppress appetite)suppress appetite)

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5. CERTAIN MEDICATIONS5. CERTAIN MEDICATIONS

ANTI-CONVULSANTS: Carbamazepine, ANTI-CONVULSANTS: Carbamazepine, ValporateValporate

CERTAIN ANTI-DIABETICS: CERTAIN ANTI-DIABETICS: sulfonylureas, TZDssulfonylureas, TZDs

CERTAIN ANTIDEPRESSANTSCERTAIN ANTIDEPRESSANTS

ORAL CONTRACEPTIVESORAL CONTRACEPTIVES

CORTICOSTEROIDSCORTICOSTEROIDS

ANTI-HISTAMINESANTI-HISTAMINES

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CHILDHOOD OBESITYCHILDHOOD OBESITYDO YOU KNOW?DO YOU KNOW?

More obese children proportional to more T2DM More obese children proportional to more T2DM in future adults.in future adults.Many obese children even at 5-6 years of age Many obese children even at 5-6 years of age found to be hypertensive and with high found to be hypertensive and with high cholesterol.cholesterol.Sleep apnea, in obese children can lead to Sleep apnea, in obese children can lead to problem with learning and memory.problem with learning and memory.Obese children have a high incidence of liver Obese children have a high incidence of liver disease and asthma.disease and asthma.Obese children have 70% chance of becoming Obese children have 70% chance of becoming obese in adults.obese in adults.

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CHILDHOOD OBESITYCHILDHOOD OBESITY

FOR CHILDREN FROM 2-20 FOR CHILDREN FROM 2-20 YEARS, BMI MEASUREMENT IS YEARS, BMI MEASUREMENT IS DIFFERENT FROM THOSE OF DIFFERENT FROM THOSE OF

ADULTSADULTS

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BMI FOR CHILDREN BMI FOR CHILDREN

AGE AND GENDER AGE AND GENDER SPECIFICSPECIFIC

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OBTAIN ACCURATE WEIGHT & OBTAIN ACCURATE WEIGHT & HEIGHT MEASUREMENTHEIGHT MEASUREMENT

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CALCULATE BMICALCULATE BMI

IN THE SAME WAY AS IN THE SAME WAY AS ADULTADULT

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BMI NUMBER IS PLOTTED ON BMI NUMBER IS PLOTTED ON THE BMI-FOR-AGE GROWTH THE BMI-FOR-AGE GROWTH

CHARTCHART

TO OBTAIN PERCENTILE RANKING.TO OBTAIN PERCENTILE RANKING.DIFFERENT CHART FOR BOYS AND DIFFERENT CHART FOR BOYS AND

GIRLSGIRLS

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CLASSIFICATION OF CLASSIFICATION OF CHILDHOOD OBESITYCHILDHOOD OBESITY

UNDERWEIGHT: BMI-for-age <5UNDERWEIGHT: BMI-for-age <5thth. . percentile.percentile.

HEALTHY: BMI-for-age 5HEALTHY: BMI-for-age 5thth. to 85. to 85thth. . percentile.percentile.

RISK FOR OVERWEIGHT: 85RISK FOR OVERWEIGHT: 85thth. to <95. to <95thth. . percentile.percentile.

OVERWEIGHT: Equal or >95OVERWEIGHT: Equal or >95thth. percentile.. percentile.

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WHY OBESITY IS RISKY?WHY OBESITY IS RISKY?

VISCERAL OBESITY LEADS TO THE VISCERAL OBESITY LEADS TO THE DEVELOPMENT OF:DEVELOPMENT OF:

CARDIOVASCULAR DISEASE AND CARDIOVASCULAR DISEASE AND STROKESTROKE

TYPE 2 DIABETESTYPE 2 DIABETES

HYPERCHOLESTEROLEMIAHYPERCHOLESTEROLEMIA

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OTHER COMPLICATIONS OF OTHER COMPLICATIONS OF OBESITYOBESITY

OSTEOARTHRITISOSTEOARTHRITIS

CANCERCANCER

NON ALCOHOLIC FATTY LIVER DISEASENON ALCOHOLIC FATTY LIVER DISEASE

POLYCYSTIC OVARY SYNDROME (PSOS)POLYCYSTIC OVARY SYNDROME (PSOS)

CHOLELITHIASISCHOLELITHIASIS

HYPERURICEMIAHYPERURICEMIA

INFERTILITYINFERTILITY

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KEY PATHOPHYSIOLOGICAL KEY PATHOPHYSIOLOGICAL MECHANISMSMECHANISMS

FOR THE DEVELOPEMENT FOR THE DEVELOPEMENT OF OBESITY RELATED OF OBESITY RELATED

DISEASESDISEASES

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ENDOTHELIALDYSFUNCTION

ATHEROSCLEROSIS

INFLAMMATION

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INCREASED ABDOMINAL INCREASED ABDOMINAL OBESITYOBESITY

INCREASES PLASMA FREE FATTY INCREASES PLASMA FREE FATTY ACID LEVELACID LEVEL

SECRETS ADIPOCYTOKINES (SPECIAL SECRETS ADIPOCYTOKINES (SPECIAL CYTOKINES) RELEASED BY CYTOKINES) RELEASED BY ADIPOCYTESADIPOCYTES

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INCREASED LEVEL OF FREE INCREASED LEVEL OF FREE FATTY ACIDSFATTY ACIDS

PREVENT INSULIN MEDIATED PREVENT INSULIN MEDIATED GLUCOSE ENTRY INTO CELL GLUCOSE ENTRY INTO CELL MITOCHONDIRA IN SKELETAL MUSCLE MITOCHONDIRA IN SKELETAL MUSCLE AND LIVER CAUSING INSULIN AND LIVER CAUSING INSULIN RESISTANCE.RESISTANCE.

INCREASE VLDL & TG AND REDUCE INCREASE VLDL & TG AND REDUCE HDLHDL

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FAT IS NO MORE AN INERT FAT IS NO MORE AN INERT ORGANORGAN

ADIPOSE TISSUE NOW PROVED ADIPOSE TISSUE NOW PROVED TO BE A VERY ACTIVE TO BE A VERY ACTIVE ENDOCRINE ORGAN.ENDOCRINE ORGAN.

AS ENDOCRINE ORGAN ADIPOSE AS ENDOCRINE ORGAN ADIPOSE TOSSUE SECRETS TOSSUE SECRETS ADIPOCYTOKINESADIPOCYTOKINES..

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ADIPOCYTOKINES OR ADIPOCYTOKINES OR ADIPOKINESADIPOKINES

MORE THAN 50 ADIPOKINES ARE MORE THAN 50 ADIPOKINES ARE

LISTEDLISTED

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IMPORTANT ADIPOKINESIMPORTANT ADIPOKINES

TNF-ALPHATNF-ALPHAINTERLUKIN-6 (IL-6)INTERLUKIN-6 (IL-6)LEPTINLEPTINC-REACTIVE PROTEIN (CRP)C-REACTIVE PROTEIN (CRP)ANGIOTENSINANGIOTENSINPLASMINOGEN ACTIVATOR INHIBITOR-1 PLASMINOGEN ACTIVATOR INHIBITOR-1 (PAI-1)(PAI-1)RESISTINRESISTINADIPONECTINADIPONECTIN

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TNF-ALPHATNF-ALPHA

Generally together with IL1 & Generally together with IL1 & IL6, increases the synthesis of IL6, increases the synthesis of

C Reactive ProteinC Reactive Protein

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INTERLUKIN-6 (IL-6)INTERLUKIN-6 (IL-6)

Increases C reactive ProteinIncreases C reactive Protein

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LEPTINLEPTIN

Leptin in normal person by acting on Leptin in normal person by acting on hypothalamus, reduces appetite.hypothalamus, reduces appetite.

In obese and patients with T2DM leptin level In obese and patients with T2DM leptin level is found much higher but these types of is found much higher but these types of patients become resistant to usual leptin patients become resistant to usual leptin function.function.

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C-Reactive Protein (CRP)C-Reactive Protein (CRP)

Number one inflammatory Number one inflammatory markermarker

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ANGIOTENSINANGIOTENSIN

Recent work suggests that angiotensin II Recent work suggests that angiotensin II has significant pro-inflammatory action on has significant pro-inflammatory action on endothelium.endothelium.

This is the reason why RAS blockers have This is the reason why RAS blockers have anti-atherosclerotic activity due to reduced anti-atherosclerotic activity due to reduced vascular inflammation.vascular inflammation.

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PLASMINOGEN ACTIVATOR PLASMINOGEN ACTIVATOR INHIBITOR 1 (PAI-1)INHIBITOR 1 (PAI-1)

Plasma level of PAI-1 strongly correlate with Plasma level of PAI-1 strongly correlate with BMI and has strong pro-inflammatory BMI and has strong pro-inflammatory function.function.

Ref: Ref: Circulation.Circulation. 2005;111:1938-1945.) 2005;111:1938-1945.)

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RESISTINRESISTIN

Plays both in inflammation Plays both in inflammation and insulin resistanceand insulin resistance

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ADIPONECTINADIPONECTIN

Adiponectin is found in large amount in Adiponectin is found in large amount in healthy individuals and markedly reduced healthy individuals and markedly reduced in obese and type 2 diabetics.in obese and type 2 diabetics.

All adipokines except adiponectin are pro-All adipokines except adiponectin are pro-inflammatoryinflammatory

Only adiponectin is anti-inflammatory and Only adiponectin is anti-inflammatory and inversely proportional to visceral obesityinversely proportional to visceral obesity

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ACUTE INFLAMMATIONACUTE INFLAMMATION

It is the first line defense of the body to any It is the first line defense of the body to any infection or healing any injuryinfection or healing any injury

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CHRONIC INFLAMMATIONCHRONIC INFLAMMATION

High blood pressure, hypercholesterolemia, High blood pressure, hypercholesterolemia, smoking and obesity causes release of smoking and obesity causes release of large amount of pro-inflammatory large amount of pro-inflammatory adipokines, which ultimately produce adipokines, which ultimately produce “Acute Phase Proteins”“Acute Phase Proteins”

These are C-reactive protein, serum amyloid These are C-reactive protein, serum amyloid A and fibrinogen.A and fibrinogen.

CRP, the most important inflammatory CRP, the most important inflammatory marker for clinical diagnosis.marker for clinical diagnosis.

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WHAT CRP DOES?WHAT CRP DOES?

CRP disturbs normal biology of the endothelium, the inner CRP disturbs normal biology of the endothelium, the inner most wall of blood vessels and cause injury in to most wall of blood vessels and cause injury in to endothelium.endothelium.

Endothelial injury stimulate production of more Endothelial injury stimulate production of more inflammatory markers which attract monocytes those go inflammatory markers which attract monocytes those go into the arterial wall and transform into macrophages.into the arterial wall and transform into macrophages.

Macrophage engulf cholesterol from blood and transform Macrophage engulf cholesterol from blood and transform into foam cells, the earliest stage for the formation of into foam cells, the earliest stage for the formation of plaques.plaques.

Plaques become larger, more inflammatory markers cause Plaques become larger, more inflammatory markers cause rupture of the plaques.rupture of the plaques.

Plaques come into contact with platelets and clotting Plaques come into contact with platelets and clotting factors causing heart attack and stroke.factors causing heart attack and stroke.

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INFLAMMATION AND T2DMINFLAMMATION AND T2DM

Research shows that women having high Research shows that women having high level of IL-6 are in 2 folds increased risk of level of IL-6 are in 2 folds increased risk of developing of T2DM.developing of T2DM.

If both IL-6 and CRP are increased, risk If both IL-6 and CRP are increased, risk goes to 6 folds.goes to 6 folds.

Ref: Brigham and Women's Hospital in Ref: Brigham and Women's Hospital in Boston Boston

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BEFORE GOING TO TREAT BEFORE GOING TO TREAT OBESITYOBESITY

1.1. LOOK FOR RISK FACTORSLOOK FOR RISK FACTORS

2.2. GET LABORATORY TESTSGET LABORATORY TESTS

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RISK FACTORSRISK FACTORS

Established coronary heart diseaseEstablished coronary heart diseaseH/O myocardial infarctionH/O myocardial infarctionAngina pectoris (stable or unstable)Angina pectoris (stable or unstable)H/O coronary artery surgery or angioplastyH/O coronary artery surgery or angioplastyFamily h/o CHD in first degree relativesFamily h/o CHD in first degree relativesPresence of atherosclerotic diseases e.g. PVD, abdominal aortic Presence of atherosclerotic diseases e.g. PVD, abdominal aortic aneurysm, symptomatic carotid artery diseaseaneurysm, symptomatic carotid artery diseasePre-diabetes or T2DMPre-diabetes or T2DMHypertensionHypertensionHypercholesterolemiaHypercholesterolemiaSleep apneaSleep apneaSmokingSmokingAge: Men >45 years, women >55 years (postmenopausal)Age: Men >45 years, women >55 years (postmenopausal)

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High absolute risk for obesity High absolute risk for obesity related diseaserelated disease

Who are overweightWho are overweight

and has three or and has three or

more risk factorsmore risk factors

EXCEPT EXCEPT

T2DMT2DM

T2DM alone is definedT2DM alone is defined

as high absolute risk.as high absolute risk.

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LABORATORY TESTS LABORATORY TESTS

Serum electrolytesSerum electrolytes

Liver Function tests (LFT)Liver Function tests (LFT)

Complete blood count (CBC)Complete blood count (CBC)

Lipid profileLipid profile

Thyroid function testsThyroid function tests

ECGECG

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TREATMENT OF OBESITYTREATMENT OF OBESITY

Non-pharmacologicalNon-pharmacological

PharmacologicalPharmacological

SurgicalSurgical

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GOAL FOR OBESITY GOAL FOR OBESITY TREATMENTTREATMENT

1.1. Achieve and maintain Achieve and maintain healthier weighthealthier weight

2.2. Risk factor managementRisk factor management

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WHAT IS THE AIM OF WHAT IS THE AIM OF HEALTHIER WEIGHT?HEALTHIER WEIGHT?

Aim to reduce 10% of the body weight during Aim to reduce 10% of the body weight during next 6 months.next 6 months.

1-2 pounds loss of body weight per week is the 1-2 pounds loss of body weight per week is the safest way.safest way.

Once achieved, patient enters in to the phase of Once achieved, patient enters in to the phase of weight maintenance and long term monitoring.weight maintenance and long term monitoring.

Monitoring is important because study shows, Monitoring is important because study shows, 80% may go back to their previous weight.80% may go back to their previous weight.

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NON-PHARMACOLOGICAL NON-PHARMACOLOGICAL TREATMENTTREATMENT

Dietary changeDietary change

Physical activityPhysical activity

Behavior modificationBehavior modification

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DIETARY CHANGEDIETARY CHANGE

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1. DIETARY CHANGE1. DIETARY CHANGE TARGET LOW CALORIE DIET TARGET LOW CALORIE DIET

Calorie intake must be reduced by 500-Calorie intake must be reduced by 500-1000kcal/day from the baseline.1000kcal/day from the baseline.For women calorie intake should be 1000 to For women calorie intake should be 1000 to 1200kcal/day1200kcal/dayFor men 1200-1600kcal/dayFor men 1200-1600kcal/dayThe above are called low calorie diet (LCD)The above are called low calorie diet (LCD)If patient feels hungry, 100-200kcal/day can be If patient feels hungry, 100-200kcal/day can be increased.increased.Very low calorie diet (VLCD) is <888kcal/dayVery low calorie diet (VLCD) is <888kcal/day

may be used for short period of time under the may be used for short period of time under the guidance of a specialist.guidance of a specialist.

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TARGET: LOW CALORIE TARGET: LOW CALORIE DIETDIET

CAUTION!CAUTION!Must not be less than Must not be less than

800kcal/day800kcal/day

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WHAT HAPPENS WHEN WHAT HAPPENS WHEN CALORIES REDUCED CALORIES REDUCED

BELOW MAINTENANCE?BELOW MAINTENANCE?

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RECENT INSTITUTE OF RECENT INSTITUTE OF MEDICINE (IOM) GUIDELINESMEDICINE (IOM) GUIDELINES

ACCEPTABLE MACRONUTRIENT ACCEPTABLE MACRONUTRIENT DISTRIBUTION RANGEDISTRIBUTION RANGE

(MDR)(MDR)

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WHAT ISWHAT IS

MDR?MDR?

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TIGHT RESTRICTIONTIGHT RESTRICTION

For ProteinFor Protein Tight control of protein can cause undue loss of Tight control of protein can cause undue loss of

lean tissue.lean tissue.For FatFor Fat

Intake of <20% of total calorie from fat can Intake of <20% of total calorie from fat can cause low level of HDL-C.cause low level of HDL-C.For CarbohydrateFor Carbohydrate

< 120gm of carbohydrate per day can cause < 120gm of carbohydrate per day can cause ketosis and associated hyperuricemia, ketosis and associated hyperuricemia, dehydration & electrolyte imbalance.dehydration & electrolyte imbalance.

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EATEAT

More fruits, vegetables, whole grainMore fruits, vegetables, whole grain

Limit sugar and other refined carbohydrateLimit sugar and other refined carbohydrate

Limit food containing large amount of saturated and trans Limit food containing large amount of saturated and trans fatfat

Consume backed, grilled, or roasted meat instead of fried.Consume backed, grilled, or roasted meat instead of fried.

Limit soft drinksLimit soft drinks

Total daily diet should be divided in to 4 to 5 meals per day.Total daily diet should be divided in to 4 to 5 meals per day.

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EXAMPLE OF LCDEXAMPLE OF LCD

Calorie: reduction 500-1000kcal/dayCalorie: reduction 500-1000kcal/dayTotal fat: <30% of total caloriesTotal fat: <30% of total caloriesSaturated fat: 8-10% of total caloriesSaturated fat: 8-10% of total caloriesMonounsaturated fatty acids: up to 15% of total caloriesMonounsaturated fatty acids: up to 15% of total caloriesPolyunsaturated fatty acids: up to 10% of total caloriesPolyunsaturated fatty acids: up to 10% of total caloriesCholesterol: <300mg/dayCholesterol: <300mg/dayProtein: 15% of total caloriesProtein: 15% of total caloriesCarbohydrate: 55% of total caloriesCarbohydrate: 55% of total caloriesTable salt: approx. 6gm/dayTable salt: approx. 6gm/dayCalcium: 1000-1500mg/dayCalcium: 1000-1500mg/dayFiber: 20-30gm/dayFiber: 20-30gm/day

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EGGEGG

One medium sized egg contains 78 Kcal, One medium sized egg contains 78 Kcal, contribute approx. 4% of the average daily contribute approx. 4% of the average daily energy requirement.energy requirement.Protein-12.5% Protein-12.5% Fat- 11.2% (17% PUFA, 32% saturated & 44% Fat- 11.2% (17% PUFA, 32% saturated & 44% MUFA)MUFA)Carbohydrate-traceCarbohydrate-traceMinerals: Iodine, Phosphorus, Zinc, Calcium, Minerals: Iodine, Phosphorus, Zinc, Calcium, SeleniumSeleniumVitamins: Most of the recognized vitamins Vitamins: Most of the recognized vitamins except Vit-C.except Vit-C.

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EGG cont’dEGG cont’d

Over 30 years of prospective epidemiological Over 30 years of prospective epidemiological surveys of CHD risk have consistently found no surveys of CHD risk have consistently found no independent relationship between dietary independent relationship between dietary cholesterol or egg consumption and CHD risk.cholesterol or egg consumption and CHD risk.

American studies found that by eating two eggs American studies found that by eating two eggs for breakfast, overweight and obese women ate for breakfast, overweight and obese women ate less at subsequent meals and lost more weight less at subsequent meals and lost more weight than those eating a bagel-based breakfast . It is than those eating a bagel-based breakfast . It is due to high “satiety index” (150%) of egg.due to high “satiety index” (150%) of egg.

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EGG cont’dEGG cont’dREFERENCESREFERENCES

McNamara DJ (2000) Dietary cholesterol and McNamara DJ (2000) Dietary cholesterol and atherosclerosis.atherosclerosis.Biochimica et Biophysica Acta 1529: 310-20.Biochimica et Biophysica Acta 1529: 310-20.

Lee A and Griffin B (2006) Dietary cholesterol, eggs Lee A and Griffin B (2006) Dietary cholesterol, eggs and coronary heart disease risk in perspective. and coronary heart disease risk in perspective. British Nutrition FoundationBritish Nutrition Foundation‘Nutrition Bulletin’ Volume 31 Number 1 pp21 – 27.‘Nutrition Bulletin’ Volume 31 Number 1 pp21 – 27.

Dhurandhar, NV (2007) Eggs for breakfast help Dhurandhar, NV (2007) Eggs for breakfast help promote weight loss.promote weight loss.Presented at Experimental Biology 2007. Astrup A, Presented at Experimental Biology 2007. Astrup A, Buemann B, Flint A, Raben A. Low fat diets and Buemann B, Flint A, Raben A. Low fat diets and energy balance: how does the evidenceenergy balance: how does the evidence

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2. PHYSICAL ACTIVITY2. PHYSICAL ACTIVITY

Walking, dancing, gardening, team or Walking, dancing, gardening, team or individual sports, cycling, rowing, rope individual sports, cycling, rowing, rope jumping, jogging.jumping, jogging.

Reducing sedentary activities e.g. Reducing sedentary activities e.g. watching TV, computer, games.watching TV, computer, games.

Most attractive: Walking. light walking-Most attractive: Walking. light walking-24min/mile, moderate-15min/mile & 24min/mile, moderate-15min/mile & high/jog-10min/mile.high/jog-10min/mile.

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PHYSICAL ACTIVITY SHOULD PHYSICAL ACTIVITY SHOULD BE STARTED GRADUALLY.BE STARTED GRADUALLY.

walking 10min/day-3days in a walking 10min/day-3days in a week, increase gradually up to week, increase gradually up to

45min/day-7days/week45min/day-7days/week

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ACSM's Guidelines for Exercise ACSM's Guidelines for Exercise Testing and Prescription -- Sixth Testing and Prescription -- Sixth

Edition, page 26Edition, page 26

Virtually all sedentary Virtually all sedentary individuals can begin a individuals can begin a

moderate exercise program moderate exercise program safely.safely.

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3. BEHAVIOR MODIFICATIONS3. BEHAVIOR MODIFICATIONS

Family Physician together with family Family Physician together with family members and friends and if possible with members and friends and if possible with psychologist should modify the behaviors psychologist should modify the behaviors responsible for obesity:responsible for obesity:These are:These are:practice self monitoring, stress practice self monitoring, stress management, stimulus control, management, stimulus control, contingency management, cognitive contingency management, cognitive restructuringrestructuring

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PHARMACOLOGICAL PHARMACOLOGICAL TREATMENT IS INDICATED IFTREATMENT IS INDICATED IF

BMI is equal or >30BMI is equal or >30

ANDAND

Non-pharmacological approach can not Non-pharmacological approach can not achieve goal maximum in six months e.g. achieve goal maximum in six months e.g. reduction of 10% body weight.reduction of 10% body weight.

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Non-pharmacological treatment Non-pharmacological treatment should be continuedshould be continued

together with pharmacological together with pharmacological agentsagents

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TWO DRUGS CURRENTLY TWO DRUGS CURRENTLY APPROVED BY FDAAPPROVED BY FDA

SIBUTRAMINESIBUTRAMINE

ORLISTATORLISTAT

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SIBUTRAMINESIBUTRAMINE

FDA approval in November 1997.FDA approval in November 1997.Centrally acting serotonine-norepinephrine-Centrally acting serotonine-norepinephrine-reuptake inhibitor (SNRI).reuptake inhibitor (SNRI).Centrally acting anorexiant or appetite Centrally acting anorexiant or appetite suppressant.suppressant.Doses: start with 5mg in the morning. Maximum Doses: start with 5mg in the morning. Maximum 15mg/day with or without food15mg/day with or without foodShould not be used in patients with HTN, CHD, Should not be used in patients with HTN, CHD, CHF, arrythmia or stroke.CHF, arrythmia or stroke.Should not be used in patients aged 16 or less.Should not be used in patients aged 16 or less.

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ORLISTATORLISTAT

FDA approval in April 1999.FDA approval in April 1999.Pancreatic lipase inhibitorPancreatic lipase inhibitorInhibit absorption of dietary fat up to 30%Inhibit absorption of dietary fat up to 30%Doses: 120mg three times a day with meal.Doses: 120mg three times a day with meal.As orlistst reduce absorption of fat soluble As orlistst reduce absorption of fat soluble vitamins and beta carotene , patient should get vitamins and beta carotene , patient should get the above vitamins, to be taken 2 hrs before or the above vitamins, to be taken 2 hrs before or after the dose of orlistat.after the dose of orlistat.Study does not support use of orlistat in patients Study does not support use of orlistat in patients less than 12 years of age.less than 12 years of age.

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THESE ARE FOR LONG THESE ARE FOR LONG TERM USETERM USE

If weight reduction is not If weight reduction is not achieved 2kg in 4 weeks, drug achieved 2kg in 4 weeks, drug

should be discontinuedshould be discontinued

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NEWER PHARMACOLOGICAL NEWER PHARMACOLOGICAL AGENTAGENT

Endocannabinoid (ECS) Endocannabinoid (ECS) receptor blockerreceptor blocker

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RIMONABANTRIMONABANT

Endocannabinoids, releasing from the cell Endocannabinoids, releasing from the cell membrane acting on ECS receptors CB1, induce membrane acting on ECS receptors CB1, induce appetite.appetite.In obese and T2DM patients, these are found in In obese and T2DM patients, these are found in large amount.large amount.Rimonabant, first ECS blocker are in use in 30 Rimonabant, first ECS blocker are in use in 30 countries of the world.countries of the world.Not yet approved by FDANot yet approved by FDAAlthough Rimonabant has some psychiatric side Although Rimonabant has some psychiatric side effects, research in on the way to find safer effects, research in on the way to find safer agents.agents.

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SURGICAL TREATMENT OF SURGICAL TREATMENT OF OBESITYOBESITY

If BMI is equal or more than 40If BMI is equal or more than 40

If BMI is equal or more than 35 plus any If BMI is equal or more than 35 plus any additional risk factor.additional risk factor.

no response to lifestyle and drug treatment.no response to lifestyle and drug treatment.

Liposuction is no more popular for its Liposuction is no more popular for its complications and long term side effects.complications and long term side effects.

Bariatric surgeryBariatric surgery

2 types of surgery are proven to be effective2 types of surgery are proven to be effective

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BARIATRIC SURGERY 1BARIATRIC SURGERY 1

Banded gastroplasty toBanded gastroplasty to

restrict gastric volumerestrict gastric volume

Vertical banded Vertical banded gastroplasygastroplasy

(VBG)(VBG)

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BARIATRIC SURGERY 2BARIATRIC SURGERY 2

Rous-en-Y gastric Rous-en-Y gastric

bypass. (RYGB)bypass. (RYGB)

In addition to limitingIn addition to limiting

food intake, it alter food intake, it alter

digestiondigestion

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Contraindications to Treatment Contraindications to Treatment of overweight & obesityof overweight & obesity

Active cancerActive cancer

Eating disorders e.g. anorexia Eating disorders e.g. anorexia nervosa and bulimia.nervosa and bulimia.

Pregnancy.Pregnancy.

Any severe illness or terminal Any severe illness or terminal illnessillness

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PRACTICAL TIPS FOR FAMILY PRACTICAL TIPS FOR FAMILY PHYSICIANSPHYSICIANS

PatientPatientMeasure height, weight, waist & find BMI.Measure height, weight, waist & find BMI.BMI equal or >25 OR Waist >102cm(M) OR BMI equal or >25 OR Waist >102cm(M) OR >88cm(F)>88cm(F)

For us: >90cm(M) or >80cm(F)For us: >90cm(M) or >80cm(F)Assess risk factors.Assess risk factors.Assess causes.Assess causes.Get laboratory tests.Get laboratory tests.Go for treatment options:Go for treatment options:Goal: 10% wt. loss in 6 months.Goal: 10% wt. loss in 6 months.

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MANAGEMENT OPTION IMANAGEMENT OPTION I

BMI 25-34.9 ORBMI 25-34.9 ORWAIST: >102cm (M) & >88cm(F) for North WAIST: >102cm (M) & >88cm(F) for North America.America.

For Bangladeshi, >90cm(M) & >80cm(F)For Bangladeshi, >90cm(M) & >80cm(F)START:START:

NON-PHARMACOLOGICAL TREATMENTNON-PHARMACOLOGICAL TREATMENT DIET CHANGEDIET CHANGE PHYSICAL ACTIVITYPHYSICAL ACTIVITY BEHAVIOR MODIFICATIONBEHAVIOR MODIFICATION

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MANAGEMENT OPTION IIMANAGEMENT OPTION II

10% weight lose not achieved in 6 months10% weight lose not achieved in 6 months

Along with non-pharmacological, startAlong with non-pharmacological, start

PHARMACOLOGICAL TREATMENTPHARMACOLOGICAL TREATMENT OrlistatOrlistat SibutramineSibutramineIf 2kg weight loss not achieved in 4 weeks, change If 2kg weight loss not achieved in 4 weeks, change

the drug.the drug.

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MANAGEMENT OPTION IIIMANAGEMENT OPTION III

BMI 35 or more plus 2 or more risk factors OR BMI BMI 35 or more plus 2 or more risk factors OR BMI 40 or more40 or moreStart both non-pharmacological & pharmacological Start both non-pharmacological & pharmacological approaches simultaneously.approaches simultaneously.If not reached goal e.g. 10% weight reduction in 6 If not reached goal e.g. 10% weight reduction in 6 months:months:

REFER TO SPECIALIZED CENTER FOR REFER TO SPECIALIZED CENTER FOR FURTHERFURTHERASSESSMENT OR POSSIBLE BARIATRIC ASSESSMENT OR POSSIBLE BARIATRIC SURGERYSURGERY Vertical banded gastroplasty or Gastric bypassVertical banded gastroplasty or Gastric bypass

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PRACTICAL TIPS FOR PRACTICAL TIPS FOR CHILDHOOD OBESITYCHILDHOOD OBESITY

Identify child’s risk by assessing family history, Identify child’s risk by assessing family history, birth weight, socioeconomic, cultural and birth weight, socioeconomic, cultural and environmental factors.environmental factors.Calculate & plot BMI once in a year for all Calculate & plot BMI once in a year for all children.children.Promote breastfeedingPromote breastfeedingEncourage parents for healthy food habits: Encourage parents for healthy food habits: whole grain, low fat dairy food, fruits and whole grain, low fat dairy food, fruits and vegetables.vegetables.Promote physical activity, playing both at home Promote physical activity, playing both at home and school.and school.

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PRACTICAL TIPS FOR PRACTICAL TIPS FOR CHILDHOOD OBESITY-con’dCHILDHOOD OBESITY-con’d

Recommend limitation of watching Recommend limitation of watching television and video games not more than television and video games not more than 2 hrs/day2 hrs/dayRecognize and monitor changes in Recognize and monitor changes in obesity-associated risk factors: obesity-associated risk factors: hypertension, dyslipidemia, hypertension, dyslipidemia, hyperinsulinemia, Impaired glucose hyperinsulinemia, Impaired glucose tolerance, and symptoms of obstructive tolerance, and symptoms of obstructive sleep apnea syndrome.sleep apnea syndrome.

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DOCTORS!DOCTORS!WHERE WE STAND?WHERE WE STAND?

WITH OBESITY?WITH OBESITY?

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References:References:

European Heart Journal 2003 24(16):1531-1537European Heart Journal 2003 24(16):1531-1537Tanaka K, Kodama H, Sasazuki S, et al. Obesity, body Tanaka K, Kodama H, Sasazuki S, et al. Obesity, body fat distribution and coronary atherosclerosis among fat distribution and coronary atherosclerosis among Japanese men & women Japanese men & women Int J Obes Relat Metab DisordInt J Obes Relat Metab Disord. . 2001;25:191–1972001;25:191–197((Circulation.Circulation. 2004;110:2246-2252.) 2004;110:2246-2252.)© 2004 American Heart Association, Inc© 2004 American Heart Association, IncBy Christine Gorman and Alice ParkBy Christine Gorman and Alice ParkTime Magazine, Feb. 23, 2004Time Magazine, Feb. 23, 2004NEJM Volume 352:1685-1695 April 21 2005 Number 16NEJM Volume 352:1685-1695 April 21 2005 Number 16Arteriosclerosis, Thrombosis, and Vascular Biology.Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1257.)2002;22:1257.)

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