MANAGEMENT OF OBESITY IN THE CLINIC

MANAGEMENT OF OBESITY IN THE CLINIC
MEMS Nor Azmi Kamaruddin Committee Member CPG for the Management of Obesity MOH, MASSO, MEMS, Academy of Medicine

THE OBESITY EPIDEMIC Malaysian scene

Father of Medicine (460 - 377 BC)
OBESITY “PERSONS WHO ARE NATURALLY FAT ARE APT TO DIE EARLIER THAN THOSE WHO ARE SLENDER” Hippocrates Father of Medicine ( BC) Hazardous waist

ISSUES Look at some factors that contribute to the increasing prevalence of obesity; where do we stand The new cut-off points for BMI & WC; significant of the WC Some practical approach A bit on diet & exercise Pharmacotherapy; guidelines & recommendations

OBESITY: A MEDICAL ILLNESS
Obesity is increasing in Malaysia, up to 5.6% of adults are obese & 20.4% overweight (NHMS II). Why is prevalence of obesity increasing? Mainly due to increase affluence, increase calorie intake and changes in life styles. Problem of cocacolonization and nintendonization of youth. As result, prevalence of obesity in children also increased esp urban areas.

Overweight and obesity (%) in women in some Commonwealth countries

Overweight in Malaysia by age and ethnic background
Ismail & James, 2001.

PREVALENCE OF OVERWEIGHT & OBESITY IN CHILDREN
KUALA LUMPUR & KOTA BHARU (N=12,521) Kuala Lumpur Kota Bharu O/weight 12.4% O/weight 18.1% Obese 8.5% At 9.6% Underweight 18.3% Obese 5.9% At % Underweight 23.4% Normal 63.6% Normal 64.2% At risk overweight=85th percentileBMI<95th percentile Obese=BMI95th percentile, WHO 1995

BASELINE CHARACTERISTICS OF METABOLIC SYNDROME AMONG 100 CHILDREN 9 – 11 YEARS OLD
Cases Control (Overweight & Obese) (Normal weight) P Mean BMI 26.4 17.6 0.00 % Body fat 33.5 21.3 0.0 Fat (kg) 8.9 7.33 0.016 Energy Intake 1907 1838 Triglyceride 1.2 0.8 Cholesterol 5.2 5.0 NS HDLC 1.27 1.47 LDLC 3.4 3.2 Systolic Blood Pressure 102.58 91.25 Diastolic 66.36 60.31 Fatimah Arshad

MAXIMUM METABOLIC EFFICIENCY
EVOLUTION & OBESITY HUNTER-GATHERER Thrifty gene MODERN SOCIETY FEAST & FAMINE FEAST STORAGE OF FOOD AS FAT TO SURVIVE FAMINE PERIODS MAXIMUM METABOLIC EFFICIENCY • DIET: HIGH IN ANIMAL FAT & REFINED SUGAR • SEDENTARY LIFE • VISCERAL OBESITY OBESITY & DIABETES SURVIVAL

OBESITY – AN IMBALANCE IN ENERGY INTAKE AND ENERGY EXPENDITURE
Proteins (20%) BMR (60-65%) Thermic effect Fats (25%) ENERGY INTAKE ENERGY EXPENDITURE of food (10%) Carbohydrates (55%) Physical activity (25-30%)

STANDARD SERVES 1955 & 2001 (COURTESY OF DEPT HUMAN NUTRITION, UNIVERSITY OF OTAGO)
Fries 205g Coke 950ml 1955 Fries 72g Coke 200ml

Predominantly rural areas
Relationship between dietary composition and Gross National Product per capita (1990) Predominantly rural areas Popkin B, 1998

“The major impact of television is not the behavior it produces, but the behavior it prevents [& prompts]” (Tucker, 1990) This quote from Tucker, now a dozen years old, is pertinent as Tucker argues that the reason why TV may be important is that it displaces physical activity. That is, whilst children are watching television, they are usually not being active! However, I have added to this quote the word “prompts”- it has also been argued by researchers that TV promotes and prompts people to eat and snack.

SECULAR TRENDS IN DIET AND ACTIVITY IN RELATION TO OBESITY IN BRITAIN
Prentice and Jobb (1995) 1950 1960 1970 1980 1990 40 60 80 100 120 140 160 180 Percentage of mean for all time Obesity Energy Intake Cars TV Viewing

BMI in relation to physical activity levels (PALs)
Schoeller, DA AJCN, 68: S

RELATIONSHIP OF BMI TO EXCESS MORTALITY
300 Age at Issue 20-29 250 30-39 200 Mortality Ratio 150 100 Low Moderate High 50 Risk Risk Risk 15 20 25 30 35 40 Body Mass Index Bray, 1987

DISEASES AND CONDITIONS FOR WHICH OBESITY IS A RISK FACTOR
Gallbladder disease*** Osteoarthritis** Infertility* Venous circulatory disease Increased anaesthetic risk* Low back pain* Polycystic ovary disease* Cancer* (ovarian, breast, endometrial, gallbladder, prostate, colon) Coronary artery disease** Type II Diabetes Mellitus*** Hypertension** Dyslipidemia*** Respiratory disease*** Gout** Reflux disease Psychological problems

HEALTH RISKS ASSOCIATED WITH OBESITY

CLASSIFICATION OF OBESITY AS PER FAT DISTRIBUTION
Android (or abdominal or central, males) Collection of fat mostly in the abdomen (above the waist) apple-shaped Associated with insulin resistance and heart disease Gynoid (below the waist, females) Collection of fat on hips and buttocks pear-shaped Associated with mechanical problems

ABDOMINAL OBESITY AND CARDIOVASCULAR RISK
Hypertension Left ventricular hypertrophy Congestive heart failure Prothrombosis Fibrinogen  PAI-1  Insulin resistance Glucose intolerance Hyperglycaemia Type 2 diabetes Endothelial dysfunction Dyslipidaemia Total-C  • LDL-C  Triglycerides  Apo-B  • HDL-C  Renal Hyperfiltration Albuminuria Inflammatory Response  Visceral Obesity The metabolic aspects of abdominal obesity represent only one of the contributors towards cardiovascular disease in visceral obesity. Other factors include: hypertension renal hyperfiltration and albuminuria increased inflammatory responses increased prothrombotic factors endothelial dysfunction and a whole array of lipid abnormalities Together, these contribute to the development of cardiovascular disease and end organ damage in obese patients.

WAIST CIRCUMFERENCE IS A SURROGATE MARKER OF VISCERAL FAT
Women >88 cm = Increased risk1 Asian = 80 cm Men >102 cm = Increased risk1 Asian = 90 cm 1Lean MEJ, et al. Lancet;1998:351:853–6 cm Slide 5: Waistline circumference is a surrogate marker of visceral fat Waistline circumference, perhaps the simplest of all measurements, provides an accurate assessment of visceral fat mass which has been shown to be a key indicator of risk factors for major cardiovascular disease. A waistline circumference >88 cm in women and >102 cm in men reflects a significantly increased risk of developing many of the comorbidities associated with obesity. Xenical Slide Kit August Section 1 5 5

WAIST CIRCUMFERENCE & WAIST-TO-HIP RATIO
Desired Ratio Women : <0.8 Men : < 1.0 Ratio = HIPS Waist Circumference diameter of the waist at the ASIS TO FIND RATIO Waist: Measure at narrowest point with stomach relaxed Risk increases if waist circumference is >90 cm in men and >80 cm in women Hips: Measure at fullest point

WHO CLASSIFICATION OF OBESITY BMI = weight(kg)/height(m)2
Risk of Comorbidity Underweight Below 18.5 Low Healthy weight Average Overweight (grade 1 obesity) Mild increase Obese (grade 2 obesity) Moderate/severe Morbid/severe obesity(grade 3) 40.0 and above Very severe World Health Organisation. Obesity: Preventing and Managing the Global Epidemic. Geneva: WHO, 1997 [3]

BMI Issues Are population specific BMI cut-off points for overweight and obesity necessary? Recent studies in Hong Kong, Singapore, Indonesia and Japan suggested that these populations have a relatively high body fat % at low BMI Meta-analysis in Asian populations revealed: - Caucasian prediction equation cannot be applied to all Asian populations. - In general, both male and female Asians have more body fat then their European counterparts of the same age and BMI. - Calculated BMI cut-off points vary considerably from (21.6 – 25.9) for overweight and from ( ) for obesity WHO Consultation, July 2002.

PROPORTION OF SINGAPOREAN ADULTS WITH AT LEAST ONE RISK FACTOR BY BODY MASS INDEX (BMI) CATEGORIES

PROPORTION OF SINGAPOREAN ADULTS WITH AT LEAST ONE RISK FACTOR BY WAIST CIRCUMFERENCE (WC) CATEGORIES

BARRIERS TO EFFECTIVE WEIGHT MANAGEMENT
Easier to treat effects of obesity Time Constraint Resources & Manpower Patients’ Attitude & Expectations Caregiver Frustration Patient’s Frustration Chronic problem

"Give it up Linda. You know he'll never change. He'll always eat nothing but meat until his first heart attack."

MANAGEMENT STRATEGY FOR OBESITY

MULTI-DISCIPLINE APPROACH TO WEIGHT MANAGEMENT
Behavioural & Motivational Therapist Endocrinologist Physical Therapist Patient/Peer Support Group Dietician Endocrine/Bariatric Surgeon Primary Physician Patient The metabolic aspects of abdominal obesity represent only one of the contributors towards cardiovascular disease in visceral obesity. Other factors include: hypertension renal hyperfiltration and albuminuria increased inflammatory responses increased prothrombotic factors endothelial dysfunction and a whole array of lipid abnormalities Together, these contribute to the development of cardiovascular disease and end organ damage in obese patients.

HOW MUCH WEIGHT LOSS IS SIGNIFICANT?
A 5-10% reduction in weight (within 6 months) and weight maintenance should be stressed in any weight loss program and contributes significantly to decreased morbidity

BENEFITS OF 10% WEIGHT LOSS
Mortality >20% fall in total mortality >30% fall in diabetes related deaths >40% fall in obesity related deaths Blood pressure fall of 10mmHg systolic and diastolic pressure Diabetes 50% fall in fasting glucose Lipids 10% dec. total cholesterol 15% dec. in LDL 30% dec. in triglycerides 8% inc. in HDL Jung 1997

ADVANTAGES OF WEIGHT LOSS
Weight loss of kg (n=43,457) associated with 53% reduction in cancer-deaths, 44% reduction in diabetes-associated mortality and 20% reduction in total mortality Survival increased 3-4 months for every kilogram of weight loss Reduced hyperlipidemia, hypertension and insulin resistance Improvement in severity of diseases Person feels ‘fit’ and mentally more active

TREATMENT GOALS Prevention of further weight gain
Weight loss to achieve a realistic, target BMI Long-term maintenance of a lower body-weight

APPROACHES TO OBESITY MANAGEMENT
Diet Activity Drugs VLCD Surgery BMI No risk factors DM/CHD/HT/HL  _ BMI 27.5–30  (consider) BMI > 30 BMI >35 (in  severe) BMI>40 (consider  in severe)

MANAGEMENT OF OBESITY IN THE CLINIC
1. History Aetiological factors Co-Morbidities Complications 2. Physical Examination 3. Laboratory Investigations 4. Treatment 5. Follow-up

HISTORY Aetiological factors Age of onset Duration of obesity
Psychological Depression, Stress Endocrine & Metabolic Metabolic Syndrome Cushing’s, Hypothyroid Genetic Lawrence Moon Biedl, Prader Willi Neurological Hypothalamic Steroid-Containing Traditional Treatment

SECONDARY CAUSES OF OBESITY
Endocrine 1. Hypothyroidism 2. Polycystic Ovarian Syndrome 3. Cushing’s Syndrome 4. Acromegaly 5. Hypothalamic disorders 6. Hypogonadism e.g. Klinefelter’s syndrome and Kallman’s syndrome Genetic 1. Intracranial tumours, infections and trauma such as Craniopharyngioma 2. Prader-Willi Syndrome 3. Ainstrom Syndrome 4. Laurence-Moon Biedl Syndrome 5. Carpenter Syndrome 6. Cohen Syndrome 7. Blount disease and others.

THE GENETIC DISEASES ASSOCIATED WITH OBESITY
The Prader-Willi syndrome consists of short stature, mental retardation, cryptorchidism, small hands and feet, neonatal hypotonia, and obesity. The face is also characteristic, with almond-shaped eyes and fish-like mouth. The disorder is associated with a deletion in the 15th chromosome. The Aistrom syndrome is manifested by childhood blindness related to retinal degeneration, infantile obesity, nerve deafhess, type 2 diabetes mellitus, acanthosis nigricans, chronic nephropathy, and hypogonadism in males. The Laurence-Moon-Biedl syndrome exhibit retinitis pigmentosa, mental retardation, obesity, polydactyly, and hypogonadism. The Carpenter syndrome is characterised by obesity, mental retardation, male hypogonadism, polydactyly, and syndactyly. Cohen syndrome patients have microcephaly, mental retardation, short stature, facial abnormalities, and obesity. Blount disease consists of bowed legs, tibial torsion, and obesity.

EATING HABITS & BEHAVIOUR
Frequency of Meals Amount Which meal is heaviest ? Types of Foods Way food is prepared In between meals snacks Eating Behaviour Watching TV Eating Out Fast Food Outlets Food Diary Eating the wrong food vs just eating a lot at a time.

EXERCISE Do you do any exercise ? Do you do any physical activities ?
Level, Duration & Frequency ?

PSYCHOLOGICAL ASSESSMENT
Are you going through a period of life where you are stressful ? Anxious ? Tensed ? Do you feel down ( depressed ) ? Do you feel they are contributing to your weight or eating problem? Boils down to either Stress Or Depression.

MOTIVATION Do you want to do something about this problem?
Do you see yourself as having a problem? Do you want to do something about this problem? Relationship of obesity to physical & emotional health. If patient is not motivated no amount of dieting or pills will alleviate the weight problem. Once patient is willing to do something about their weight then only will your management be helpful.

NOCTURNAL EATING DISORDER
Features Breakfast Satiety More than 50 % total calories after dinner Wake at least once Higher rate of depression May need SSRI anti-depressant

PHYSICAL EXAMINATION BMI Waist Circumference BP
Signs of Genetic, Endocrine or Metabolic Diseases - Metabolic Syndrome - Cushing’s Syndrome - Hypopthyroidism Co-morbidities & Complications - BP, DM - Hyperlipidemia - Cardiac Failure - Sleep Apnoea Syndrome - Arthritis

BASELINE INVESTIGATIONS
Fasting Serum Lipids Fasting Blood Glucose OGTT if FBG is bet 6.1 – 6.9 mmol/l If indicated; 24 hour urinary cortisol TFT esp in the above 60 yrs old Investigations for PCOS

BASIC PRICINPLES OF THERAPY THAT CAN BE IMPLEMENTED IN THE CLINIC
Basic Dietary Principles Do not skip meals Heavy Breakfast, Light Dinner Drink lots of water Increase Fruits & Vegetables Reduce oily foods Eat Slowly Choose favourite food with low calories Physical Activities Avoid lifts for few floors Walk to the grocery shops etc Cycle with families

BASIC PRICINPLES OF THERAPY THAT CAN BE IMPLEMENTED IN THE CLINIC 2
Exercises Choose favourite sport with friends Behavioral Changes Reduce eating out Do not eat in front of TV Snacking while watching sports Conscious of what goes in the mouth Pharmacotherapy Lipase Inhibitor Appetite Suppressant Duration Surgery Assess Success

ASSESSMENT IN THE CLINIC (7)
Measure Weight, BMI & WC Assess Comorbidities Assess understanding & perception Do you feel you have a weight problem? Assess Motivation Most important of all Quick Dietary History Binge vs Fat (Quantity vs Quality) Quick Daily Activity History Assess underlying psychological issues Relieve stress, Nocturnal Binge Disorder

MANAGEMENT PLAN IN THE CLINIC
Five dietary advice Regular meals – Do not skip meals Frequent small meals Heavy breakfast, light dinner Cut Carbos & Fat (Diet drinks, sweeteners etc) Lots of Vegetables & Fruits Simple physical activity recommendations Return appointment & assess compliance On Return; Prescribe short term pharmacotherapy Assess every 1-2 months Revise management plans

FOOD PYRAMID Use fats, alcohol, sugar and salt sparingly Have small serves of protein foods with preference for low fat variety Choose wide variety of fruits and vegetables Use these foods as basis of every meal

Does Coke make you fat ? Sugar versus sweetener
Astrup et al., NAASO 2001, Quebec.

European Multi-center RCT: complex versus sugar carbohydrates
As produced by Astrup, A

Long-term weight maintenance on different diets.
VLCD Average Hypocaloric balanced Anderson et al. Am J Clin Nutr, 2001; 74:

Time needed for activity to achieve energy balance
MET 3.0 MET 3.3 MET 5.0 MET 12.5 Erlichman, Kerbey & James, Whistler Conference, Vancouver.

PHYSICAL ACTIVITY ISSUES
How much physical activity is enough to prevent unhealthy weight gain? Current guidelines of 30 minutes of moderate activity daily is important for limiting health risks to chronic diseases For preventing weight gain or regain, compelling evidence suggest a minutes of moderate activity To prevent a transition to overweight and obesity, a PAL of 1.7 or approximately minutes per day of moderate activity is needed. For children even more activity time is recommended Stock Conference, March 2002

DRUG THERAPY Appetite suppressants
Adrenergic agents (e.g. amphetamine, methamphetamine, phenylpropanol amine, phentermine) Serotonergic agents (e.g. fenfluramine, dexfenfluramine, SSRIs like sertraline, fluoxetine) Thermogenic agents ephedrine, caffeine New ones Sibutramine ; Orlistat

ORLISTAT – MECHANISM OF ACTION
Intestinal lumen Mucosal cell Lymphatics TG GI lipase + Xenical® FA FFA MG Slide 6: Inhibition of fat absorption by Xenical® Xenical exerts its anti-obesity action by inhibiting the action of gastrointestinal lipase in the small intestine. By blocking the activity of lipase, Xenical decreases the digestion and subsequent absorption of triglycerides by preventing their hydrolysis. Intact triglycerides therefore pass through the gastrointestinal tract and are subsequently excreted in the faeces. MG Bile acids Micelle 30% not absorbed 6 10 2 6

ORLISTAT-INDUCED WEIGHT LOSS
Change in body weight (%) Placebo (n=340) –2 Orlistat 120 mg (n=343) *p<0.001 –4 –6 –6.1% –8 Clinical efficacy: weight loss Slide 13: Xenical®-induced weight loss Weight loss over 12 months was consistently significantly greater with Xenical compared with placebo in all clinical studies. Weight change was comparable during the 4-week run-in period on diet alone. A noticeable difference in weight loss between the two groups began to emerge as early as 4 weeks after randomisation. At 1 year, weight loss was significantly greater in the Xenical group, with a 10.2% decrease from initial body weight compared with a 6.1% decrease in the placebo group (p<0.001 for between-group treatment effect). * –10 –10.2% –12 –4 10 20 30 40 52 Week (Sjöström L, et al. Lancet 1998, 352; 167172) ITT population: BM14119C Xenical Slide Kit August Section 2 13 13

WEIGHT LOSS IN THE PRIMARY CARE SETTING
Change in body weight (%) Placebo (n=212) Orlistat 120 mg (n=210) –2 *p<0.001 –4 –4.2% –6 * Slide 15: Weight loss in the primary care setting The management of obesity now increasingly lies within the remit of the primary care physician. However, due to a lack of awareness of the comorbidities and cardiovascular risk factors associated with obesity, treatment is often not optimal. A randomised, double-blind, placebo- controlled study was undertaken in 796 obese patients in the primary care setting to determine the long-term efficacy of Xenical (US Primary Care Study) in which patients were given little dietary or behavioural counselling. Weight loss was identical in Xenical and placebo groups during the 4-week run-in period, in which patients received a mildly hypocaloric diet. Weight reduction stabilised after 8 weeks in the placebo group, but there was a continuing decrease in weight throughout 12 months of Xenical therapy. After 1 year, weight loss was 7.9% in the Xenical group compared with 4.2% for placebo. During the second year (in which patients received a eucaloric, weight maintenance diet) the tendency for weight regain was much more marked in the placebo group and at the end of the study, the weight lost in the Xenical group was significantly greater compared with placebo (p<0.001). –8 –7.9% –10 –10 –4 4 8 12 16 20 24 28 32 36 40 44 48 52 Week ITT population: BM14161 Xenical Slide Kit August Section 2 15 15

CHANGE IN BODY WEIGHT OVER 2 YEARS
(%) Placebo Orlistat 60 mg –2 Orlistat 120 mg *p<0.01 –4 –6 * Slide 19: Change in body weight over 2 years A similar pattern of weight loss was observed in a 2-year, US, multicentre, randomised, double-blind trial (US Multicenter Study), involving obese patients randomised to placebo (n=244) or Xenical 120 mg tid (n=668) for 12 months, in conjunction with a mildly hypocaloric diet. At the end of year 1, patients in the Xenical group were randomly reallocated to treatment with placebo, Xenical 60 mg tid, or Xenical 120 mg tid. Patients treated with placebo lost 5.8% of their initial body weight by the end of year 1, compared with 8.8% in the Xenical-treated patients. After conversion to the eucaloric diet at the start of year 2, there was a predictable regain of lost weight in all of the treatment groups. However, weight regain was significantly lower in those patients on Xenical 60 or 120 mg tid (p<0.01 vs placebo). Xenical-treated patients who switched to placebo during year 2 regained approximately 66% of their lost weight, and by the end of the study overall weight regain in this group was indistinguishable from that of placebo-treated patients. * –8 –10 –4 10 20 30 40 52 60 70 80 90 100 104 Week ITT population: NM14185 Xenical Slide Kit August Section 2 19 18

SIBUTRAMINE INHIBITS SEROTONIN AND NORADRENALINE REUPTAKE

STORM STUDY : EFFECT OF SIBUTRAMINE ON WEIGHT LOSS
104 Placebo 102 100 98 Bodyweight (kg) 96 94 92 90 Sibutramine 2 4 6 8 10 12 14 16 18 20 22 24 Month Weight loss Weight maintenance Lancet 2000; 356:

STORM STUDY: MEAN WEIGHT LOSS AT TWO YEARS
Mean Weight Loss (Kg)

STORM STUDY : PROPORTION OF PATIENTS MAINTAINING AT LEAST 5% AND 10% WEIGHT LOSS
5% responders 10% responders Sibutramine 100 Placebo 80 60 Proportion of patients (%) 40 20 6 12 18 24 6 12 18 24 Lancet 2000; 356:

STORM STUDY: EFFECT ON WAIST CIRCUMFERENCE AND WAIST/HIP RATIO
(a) Waist Circumference (b) Waist/Hip Ratio Decrease in waist circumference (cm) Change

STORM STUDY : EFFECTS ON LIPIDS
Triglycerides VLDL cholesterol 5 5 Placebo Placebo e e g g -5 n -5 n a a h -10 -10 h c c % -15 -15 % -20 -20 -25 Sibutramine -25 Sibutramine 6 12 18 24 6 12 18 24 Lancet 2000; 356:

STORM STUDY : EFFECTS ON LIPIDS (CONTD.)
HDL cholesterol 30 25 e Sibutramine g 20 n a h 15 c Placebo 10 % 5 6 12 18 24 Month of assessment Weight loss Weight maintenance Lancet 2000; 356:

STORM STUDY : EFFECT ON INSULIN AND HBA1C
Placebo Placebo % Change . % Change Sibutramine Sibutramine Month of Assessment Month of Assessment Lancet 2000; 356:

STORM STUDY: OTHER METABOLIC EFFECTS
Variable Baseline Month Month 24 SIB PLAC SIB PLAC SIB PLAC Uric acid Glucose Insulin C-peptide HbA1c

STORM STUDY: CONCLUSIONS
Almost all patients who persist with a weight management program consisting of sibutramine, diet and exercse can achieve at least a 5% weight loss with sibutramine Over half can lose more than 10% weight within 6 months Weight loss was sustained in most patients continuing therapy for two years

SIBUTRAMINE VS. DEXFENFLURAMINE
Sibutramine 10 mg Dexfenfluramine 30 mg -0.5 -1 -1.5 -2 Weight loss (kg) -2.5 -3 -3.5 -3.2 -4 -4.5 -4.5 -5 n=226; 12 wks Int J Obes 1995; 19. Suppl 2: 144

ADVERSE EFFECTS OCCURRING IN >5% OF PATIENTS TREATED WITH SIBUTRAMINE COMPARED WITH PLACEBO
Sibutramine % Placebo % Adverse Effects Incidence (n=2068) Incidence (n=884) Headache Dry Mouth Anorexia Constipation Insomnia Dizziness Nausea Nervousness Dyspepsia Ann Pharmacother 1999;33:

SIBUTRAMINE: SAFETY Discontinuation rates: 9% with placebo and 7% with sibutramine Has been associated with a mean increase in BP and heart rate of approximately 1-3mmHg and 4-5 beats/min Cardiac side effects viz. hypertension, tachycardia and palpitations < 2.6% vs % in placebo group Caution to be exercised in patients with history of hypertension and should not be given to patients with uncontrolled or poorly controlled hypertension Not associated with cardiac valve abnormalities or primary pulmonary hypertension

STORM STUDY : WITHDRAWALS DUE TO BP INCREASE
Dose of Sibutramine % patients who withdrew due to increase in BP 10 mg % 15 mg % 20 mg % Lancet 2000; 356:

INDICATIONS & DOSAGE Recommended for obese patients with a BMI > 30 kg/m2 or > 27 kg/m2 in the presence of other risk factors (e.g. hypertension, diabetes, dyslipidemia) In Asian patients, sibutramine could be considered in patients with BMI > 27.5 kg/m2 or those with BMI of 23 kg/m2 with 2 comorbid conditions Recommended starting dose is 10 mg once daily. If there is inadequate weight loss, the dose may be titrated after four weeks to a total of 15 mg once daily. The 5 mg dose should be reserved for patients who do not tolerate the 10 mg dose.

MALAYSIAN RECOMMENDATIONS
Indications for anti-obesity drugs BMI > 27.5 kg/m2 BMI > 25 plus 2 CVS Risk Factors Drugs should never be used alone. Drugs should be used in combination with diet, exercise, and behavior modification. Drugs may have role in weight maintenance. “Malaysian CPG for The Management of Obesity 2004” The major role of medications should be to help patients stay on a diet and physical activity plan while losing weight. Medication cannot be expected to continue to be effective in weight loss or weight maintenance once it has been stopped. The use of the drug may be continued as long as it is effective and the adverse effects are manageable and not serious. There are no indications for specifying how long a weight loss drug should be continued.

M’SIAN CPG ON MANAGEMENT OF OBESITY SUMMARY OF RECOMMENDATIONS
The BMI should be used to classify overweight and obesity and to estimate relative risk for disease compared to normal weight (Evidence Level B) The waist circumference should be used to assess abdominal fat content (Evidence Level B). Based on current evidence in adults, overweight is defined as BMI > 23 kg/m2 and obesity as BMI > 27.5 kg/m2 (Evidence Level C) Current evidence suggests that waist circumference of > 90 cm in men and > 80 cm in women is associated with increased risk of comorbidities (Evidence Level C). In overweight & obese individuals, weight loss is recommended to(Evidence Level B):- Lower elevated blood pressure Lower elevated levels of total cholesterol, low-density lipoprotein cholesterol and triglycerides Raise low levels of high-density lipoprotein cholesterol Lower elevated blood glucose levels

WHO APRIL 2001 “Obesity cannot be prevented or managed solely by governments (or health professionals). The food industry, international agencies, the media, communities and individuals need to work together so that the environment is less conducive to weight gain”

MANAGEMENT OF OBESITY IN THE CLINIC

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