Community lecture on obesity related complications
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Community lecture on obesity related complications
- 1. Complications of Obesity & Overweight A Bornstein, MD, FACCA Bornstein, MD, FACC Assistant Professor of Public HealthAssistant Professor of Public Health Weill Cornell Medical CollegeWeill Cornell Medical College
- 2. Obesity & Overweight as a Public Health ProblemObesity & Overweight as a Public Health Problem The rapidly growing epidemic of adult overweight & obesity isThe rapidly growing epidemic of adult overweight & obesity is shows no sign of abatingshows no sign of abating According to the American Public Health Association, in the US,According to the American Public Health Association, in the US, overweight & obesity is associated withoverweight & obesity is associated with 300,000 deaths/year300,000 deaths/year The APHA also reported that in 2000, economic cost of overweightThe APHA also reported that in 2000, economic cost of overweight & obesity in the US exceeded& obesity in the US exceeded $115,000,000,000$115,000,000,000 Tremendous health consequences and expenditures are a directTremendous health consequences and expenditures are a direct result of this epidemic; figures are likely to grow exponentially if theresult of this epidemic; figures are likely to grow exponentially if the problem is not adequately addressed and abatedproblem is not adequately addressed and abated
- 3. Global Projections for the DM Epidemic: 2000-Global Projections for the DM Epidemic: 2000- 20102010 14.214.2 17.517.5 23%23% 14.214.2 17.517.5 23%23% 15.615.6 22.522.5 44%44% 15.615.6 22.522.5 44%44% 26.526.5 32.932.9 24%24% 26.526.5 32.932.9 24%24% 1.01.0 1.31.3 33%33% 1.01.0 1.31.3 33%33% 9.49.4 14.114.1 50%50% 9.49.4 14.114.1 50%50% WorldWorld 2000 = 151 million2000 = 151 million 2010 = 221 million2010 = 221 million 46%46% 84.584.5 132.3132.3 57%57% 84.584.5 132.3132.3 57%57%
- 4. Trends in Child and Adolescent OverweightTrends in Child and Adolescent Overweight
- 5. Overweight & ObesityOverweight & Obesity
- 6. Overweight & ObesityOverweight & Obesity
- 7. Medical Complications of ObesityMedical Complications of Obesity Lancet. 2002; 360: 475 Doctors generally agree that the more obese a person is, the more likely he or she isDoctors generally agree that the more obese a person is, the more likely he or she is to have health problemsto have health problems People who are 20% or more overweight get large health benefits from losing weightPeople who are 20% or more overweight get large health benefits from losing weight
- 8. Complications of Childhood ObesityComplications of Childhood Obesity Lancet. 2002; 360: 475 Obesity is not just a cosmetic problem…it's a health hazard with a multitude ofObesity is not just a cosmetic problem…it's a health hazard with a multitude of associated health problemsassociated health problems Someone who is 40% overweight is 2X as likely to die prematurely as is anSomeone who is 40% overweight is 2X as likely to die prematurely as is an average-weight personaverage-weight person
- 9. What is Heart Disease?What is Heart Disease? Heart disease, also known as cardiovascular disorder, a term thatHeart disease, also known as cardiovascular disorder, a term that includes a number of different diseases which affect the heartincludes a number of different diseases which affect the heart Most common cause of heart disease in developed nations isMost common cause of heart disease in developed nations is coronary artery diseasecoronary artery disease, narrowing or blockage of the coronary, narrowing or blockage of the coronary arteries which supply blood to the heart muscle; usually caused byarteries which supply blood to the heart muscle; usually caused by atherosclerosisatherosclerosis, which occurs when fatty material and a substance, which occurs when fatty material and a substance called plaque builds up in the walls of your arteriescalled plaque builds up in the walls of your arteries Other causes of heart disease includeOther causes of heart disease include hypertensionhypertension, abnormal, abnormal heartheart valvevalve function, abnormalfunction, abnormal heart rhythmheart rhythm, weakening of the pumping, weakening of the pumping ability of the heart (ability of the heart (heart failureheart failure) which may be caused by either) which may be caused by either progressive atherosclerosis, infection, or toxinsprogressive atherosclerosis, infection, or toxins
- 10. What is a Heart Attack?What is a Heart Attack?
- 11. What is Coronary Artery Disease?What is Coronary Artery Disease? CAD happens when the arteries that supply blood to heart muscleCAD happens when the arteries that supply blood to heart muscle become hardened & narrowed due to the buildup of cholesterol &become hardened & narrowed due to the buildup of cholesterol & plaque, in the inner lining of the walls of the arteriesplaque, in the inner lining of the walls of the arteries As the buildup grows, less blood can flow through the arteriesAs the buildup grows, less blood can flow through the arteries resulting in the heart muscle not being able to get the blood orresulting in the heart muscle not being able to get the blood or oxygen it needsoxygen it needs This can lead to chest pain (This can lead to chest pain (anginaangina) or a heart attack () or a heart attack (MIMI); most heart); most heart attacks happen when a plaque ruptures causing a blood clot to formattacks happen when a plaque ruptures causing a blood clot to form which, along with plaque, suddenly totally cuts off the hearts' bloodwhich, along with plaque, suddenly totally cuts off the hearts' blood supply, causing permanent heart muscle damagesupply, causing permanent heart muscle damage
- 12. What is Coronary Artery Disease?What is Coronary Artery Disease? Normal ArteryNormal Artery
- 13. What is Coronary Artery Disease?What is Coronary Artery Disease?
- 14. What is Coronary Artery Disease?What is Coronary Artery Disease? Frequency of PlaqueFrequency of Plaque
- 15. What is Coronary Artery Disease?What is Coronary Artery Disease? Over time, CAD (repeated heart attacks or unstable angina) can alsoOver time, CAD (repeated heart attacks or unstable angina) can also weaken the heart muscle and contribute toweaken the heart muscle and contribute to heart failureheart failure andand arrhythmiasarrhythmias It is difficult to estimate exactly how common heart attacks areIt is difficult to estimate exactly how common heart attacks are because as many asbecause as many as 200,000-300,000200,000-300,000 people in the US die each yearpeople in the US die each year before medical help is sought, or before medical help arrivesbefore medical help is sought, or before medical help arrives It is estimated that approximatelyIt is estimated that approximately 1 million1 million patients visit thepatients visit the hospital each year with a heart attackhospital each year with a heart attack AboutAbout 1 death1 death out of everyout of every 5 deaths5 deaths are due to aare due to a heart attackheart attack
- 16. What is a Heart Attack? It is difficult to estimate exactly how common heart attacks are because as many as 200,000 to 300,000 people in the U.S. die each year before medical help is sought or medical help arrives Approximately 1 million patients visit the hospital each year with a heart attack About 1 death out of every 5 deaths are due to a heart attack
- 17. Heart Failure SymptomsHeart Failure Symptoms
- 18. What is a Stroke?What is a Stroke? A stroke is the rapidly developing loss ofA stroke is the rapidly developing loss of brain functions due to a disturbance in thebrain functions due to a disturbance in the blood vessels supplying blood to the brainblood vessels supplying blood to the brain
- 19. 1)1) Bad genes (hereditary factors, family history)Bad genes (hereditary factors, family history) 2)2) AgeAge 3)3) Being maleBeing male 4)4) Menopause in femalesMenopause in females 5)5) High blood pressureHigh blood pressure 6)6) SmokingSmoking 7)7) DiabetesDiabetes 8)8) ObesityObesity 9)9) Low levels of physical activityLow levels of physical activity 10)10) Poor diet; high stressPoor diet; high stress 111111 LDL (‘bad’) cholesterol &LDL (‘bad’) cholesterol & HDL (‘good’) cholesterolHDL (‘good’) cholesterol 111111 Homocysteine, CRP, &/or fibrinogenHomocysteine, CRP, &/or fibrinogen CAD & Heart Attack Risk FactorsCAD & Heart Attack Risk Factors
- 20. CAD & Heart Attack Risk Factors 1)1) Bad genes (hereditary factors, family history)Bad genes (hereditary factors, family history) 2)2) AgeAge 3)3) Being maleBeing male 4)4) Menopause in femalesMenopause in females 5)5) High blood pressureHigh blood pressure 6)6) SmokingSmoking 7)7) DiabetesDiabetes 8)8) ObesityObesity 9)9) Low levels of physical activityLow levels of physical activity 10)10) Too much fat in your dietToo much fat in your diet 111111 LDL (‘bad’) cholesterol &LDL (‘bad’) cholesterol & HDL (‘good’) cholesterolHDL (‘good’) cholesterol 111111 Homocysteine, CRP, &/or fibrinogenHomocysteine, CRP, &/or fibrinogen
- 21. How Is Obesity Linked to Heart Disease & Stroke?How Is Obesity Linked to Heart Disease & Stroke? Heart diseaseHeart disease && strokestroke are the leading causes of death and disabilityare the leading causes of death and disability in the USin the US Overweight people are 2X as likely to haveOverweight people are 2X as likely to have high BPhigh BP, a major risk, a major risk factor for heart disease & stroke, than people not overweightfactor for heart disease & stroke, than people not overweight High blood cholesterolHigh blood cholesterol levels can also lead to heart disease & oftenlevels can also lead to heart disease & often linked to being overweightlinked to being overweight Being overweight also contributes toBeing overweight also contributes to anginaangina (chest pain caused by(chest pain caused by decreased oxygen to the heart) &decreased oxygen to the heart) & sudden deathsudden death from heart diseasefrom heart disease without any signs or symptomswithout any signs or symptoms The good news is that losing a small amount of weight can reduceThe good news is that losing a small amount of weight can reduce your chances of developing heart disease or stroke (reducing weightyour chances of developing heart disease or stroke (reducing weight by justby just 10%10% can dramatically decrease your chance of developingcan dramatically decrease your chance of developing heart disease or stroke)heart disease or stroke)
- 22. Global CVD RiskGlobal CVD Risk Obesity: An Ill-Defined Modifiable CVD Risk FactorObesity: An Ill-Defined Modifiable CVD Risk Factor HypertensionHypertensionHypertensionHypertension CholesterolCholesterolCholesterolCholesterol DiabetesDiabetesDiabetesDiabetes SmokingSmokingSmokingSmoking LDLLDL HDLHDL ObesityObesity BMIBMI ?? OthersOthers BMI: body mass indexBMI: body mass index HDL: high-density lipoproteinHDL: high-density lipoprotein LDL: low-density lipoproteinLDL: low-density lipoprotein
- 23. How Is Obesity Linked to Diabetes?How Is Obesity Linked to Diabetes? Type 2 diabetesType 2 diabetes the body's ability to controlthe body's ability to control blood sugarblood sugar,, which is a major causewhich is a major cause of heart diseaseof heart disease,, strokestroke,, blindnessblindness,, kidney failurekidney failure, &, & early deathearly death Overweight people are more thanOverweight people are more than 2X2X as likely to developas likely to develop type 2 diabetestype 2 diabetes compared to normal weight peoplecompared to normal weight people You can reduce your risk of developing type 2 diabetes byYou can reduce your risk of developing type 2 diabetes by losing weightlosing weight && exercising moreexercising more; if you already have type 2; if you already have type 2 diabetes, losing weight & becoming more physically active candiabetes, losing weight & becoming more physically active can help control your blood sugar levels & may also allow you tohelp control your blood sugar levels & may also allow you to reduce the amount of diabetes medication you needreduce the amount of diabetes medication you need
- 24. Relative Risk of Mortality, CHD,Relative Risk of Mortality, CHD, and Type 2 Diabetes According to BMIand Type 2 Diabetes According to BMI Manson JE, et al. N Engl J Med. 1995;333:677–685. Willett WC, et al. JAMA. 1995;273:461–465. Colditz GA, et al. Ann Intern Med. 1995;122:481–486. 2.02.0 1.51.5 1.01.0 0.50.5 0.00.0 BMI (kg/mBMI (kg/m22 )) <19.0<19.0 >>32.032.0 4.04.0 3.03.0 2.02.0 1.01.0 0.00.0 BMI (kg/mBMI (kg/m22 )) <21.0<21.0 >>29.029.0 88 66 44 22 00 BMI (kg/mBMI (kg/m22 )) <22.0<22.0 >>35.035.0 MortalityMortality Relative Risk of:Relative Risk of: CHDCHD DiabetesDiabetes
- 25. Natural History of Type 2 DiabetesNatural History of Type 2 Diabetes 1)1) GeneticGenetic susceptibilitysusceptibility 2)2) EnvironmentalEnvironmental factorsfactors a) Nutritiona) Nutrition b) Obesityb) Obesity c) Physicalc) Physical inactivityinactivity HyperinsulinemiaHyperinsulinemia HDL-CHDL-C TriglyceridesTriglycerides AtherosclerosisAtherosclerosis HypertensionHypertension AtherosclerosisAtherosclerosis HyperglycemiaHyperglycemia HypertensionHypertension RetinopathyRetinopathy NephropathyNephropathy NeuropathyNeuropathy BlindnessBlindness Renal failureRenal failure CHDCHD AmputationAmputation Onset ofOnset of diabetesdiabetes ComplicationsComplications DisabilityDisability DeathDeathOngoing hyperglycemiaOngoing hyperglycemiaIGTIGTInsulin resistanceInsulin resistance
- 26. Burden of Diabetes in the U.S.Burden of Diabetes in the U.S. 17 million17 million Americans haveAmericans have diabetesdiabetes 16 million16 million Americans haveAmericans have prediabetesprediabetes 210,000210,000 diabetes-relateddiabetes-related deaths/yeardeaths/year Leading cause ofLeading cause of blindnessblindness,, kidney failurekidney failure,, amputationamputation 65%65% of patients sufferof patients suffer cardiovascular disease-related deathscardiovascular disease-related deaths Cost:Cost: $132 billion$132 billion in 2008in 2008 Mokdad, et al, JAMA . 2001 286,1195
- 27. 0 5 10 15 20 7.80% 10.20% 13% 15.10% Non-Hispanic WhitesNon-Hispanic Whites LatinosLatinos African AmericansAfrican Americans Native AmericansNative Americans & Alaska Natives& Alaska Natives Diabetes Prevalence AmongDiabetes Prevalence Among Minority Populations in the U.S.Minority Populations in the U.S. Centers for Disease Control and Prevention (CDC) 1999 www.cdc.gov/diabetes Percentage of each population with diabetesPercentage of each population with diabetes 7.8%7.8% (11.4 million)(11.4 million) 10.2%10.2% (2 million)(2 million) 13%13% (2.8 million)(2.8 million) 15.1%15.1% (105,000)(105,000) Asian Americans andAsian Americans and Pacific Islanders are 2-5Pacific Islanders are 2-5 times more likely to havetimes more likely to have diabetes than Non-diabetes than Non- Hispanic WhitesHispanic Whites
- 28. Obesity as a Risk Factor for Type 2 DiabetesObesity as a Risk Factor for Type 2 Diabetes Importance of Abdominal Fat AccumulationImportance of Abdominal Fat Accumulation Ohlson LO, et al. Diabetes. 1985;34:1055-1058. 13.5-year13.5-year incidence ofincidence of Type 2 DiabetesType 2 Diabetes (%)(%) (Overweight)(Overweight) IIIIII IIII II II IIII IIIIII (Lean)(Lean)BMIBMI (Tertiles)(Tertiles) Waist/Hip RatioWaist/Hip Ratio (Tertiles)(Tertiles) 2.92.9 2.92.9 0.50.5 9.19.1 9.19.1 0.50.5 15.215.2 12.512.5 0.50.5 (Overweight)(Overweight) (Lean)(Lean)
- 29. DyslipidemiaDyslipidemia HypertensionHypertension Type 2Type 2 DiabetesDiabetes Managing the High-Risk Patient withManaging the High-Risk Patient with Type 2 DM &/or ‘Hypertriglyceridemic Waist’Type 2 DM &/or ‘Hypertriglyceridemic Waist’ Després JP et al. BMJ. 2001;322:716-720. CoronaryCoronary Heart DiseaseHeart DiseaseRisk FactorsRisk Factors Type 2Type 2 Diabetic Patient:Diabetic Patient: HypertriglyceridemicHypertriglyceridemic WaistWaist TreatingTreating the Complicationsthe Complications Management of CoronaryManagement of Coronary Heart Disease RiskHeart Disease Risk Treating the CauseTreating the Cause
- 30. 0 1 2 3 4 0 10 20 30 40 Placebo (n=1082) Metformin (n=1073, p<0.001 vs. Plac) Lifestyle (n=1079, p<0.001 vs. Met , p<0.001 vs. Plac ) Percent developing diabetes All participantsAll participants Years from randomizationYears from randomization Cumulativeincidence(%)Cumulativeincidence(%) PlaceboPlacebo MetforminMetformin Lifestyle ChangesLifestyle Changes Type 2 Diabetes PreventionType 2 Diabetes Prevention Risk ReductionRisk Reduction 31% by Metformin31% by Metformin 58% by Lifestyle Changes58% by Lifestyle Changes The DPP Research Group, NEJM. 346:393-403, 2002
- 31. What is BMI?What is BMI? Body Mass Index (BMI) is a number calculated from a person’sBody Mass Index (BMI) is a number calculated from a person’s weightweight && heightheight that provides a reliable indicator ofthat provides a reliable indicator of body fatnessbody fatness & is an inexpensive & easy-to-perform method of& is an inexpensive & easy-to-perform method of screeningscreening forfor weight categories that may lead to health problemsweight categories that may lead to health problems BMI does not measure body fat directly, but research has shown thatBMI does not measure body fat directly, but research has shown that BMIBMI correlatescorrelates to direct measures of body fatto direct measures of body fat BMI is not a diagnostic tool; a person may have a high BMI, but, toBMI is not a diagnostic tool; a person may have a high BMI, but, to determine if excess weight is a health risk, a physician would need todetermine if excess weight is a health risk, a physician would need to perform further assessments includingperform further assessments including skin-fold thicknessskin-fold thickness measurement,measurement, evaluations ofevaluations of dietdiet,, physical activityphysical activity,, family historyfamily history, and other, and other appropriate health screeningsappropriate health screenings
- 32. What is BMI?What is BMI? Calculating BMI is one of the best methods forCalculating BMI is one of the best methods for population assessmentpopulation assessment of overweight and obesityof overweight and obesity Because calculation requires only height & weight, it isBecause calculation requires only height & weight, it is inexpensiveinexpensive andand easy to useeasy to use for clinicians and for the general public; BMI allowsfor clinicians and for the general public; BMI allows people topeople to comparecompare their own weight status to that of the generaltheir own weight status to that of the general populationpopulation Other methods to measure body fatness include skin fold thicknessOther methods to measure body fatness include skin fold thickness measurements (with calipers), underwater weighing, bioelectricalmeasurements (with calipers), underwater weighing, bioelectrical impedance, dual-energy x-ray absorptiometry (DXA), andimpedance, dual-energy x-ray absorptiometry (DXA), and computerized tomography, but, these methods are not always readilycomputerized tomography, but, these methods are not always readily available, expensive &/or need highly trained personnelavailable, expensive &/or need highly trained personnel
- 33. Obesity: Body Mass Index (BMI)Obesity: Body Mass Index (BMI) BMI (kg/mBMI (kg/m22 )) Risk of ComorbiditiesRisk of Comorbidities Healthy weightHealthy weight 18.5 – 24.918.5 – 24.9 NormalNormal OverweightOverweight 25.0 – 29.925.0 – 29.9 IncreasedIncreased Obese Class IObese Class I 30.0 – 34.930.0 – 34.9 HighHigh Obese Class IIObese Class II 35.0 – 39.935.0 – 39.9 Very HighVery High Obese Class IIIObese Class III >> 40.040.0 Extremely HighExtremely High Adapted from the World Health Organization. Obesity: Preventing and Managing the Global Epidemic. Geneva: WHO; 2000. Weight (kg)Weight (kg) Height (mHeight (m22 )) BMI =BMI =
- 34. Saving and Overconsuming EnergySaving and Overconsuming Energy
- 35. Android (Apple) vs. Gynoid (Pear) ObesityAndroid (Apple) vs. Gynoid (Pear) Obesity Jean Vague (1947)Jean Vague (1947) TributeTribute to a Pioneer:to a Pioneer: Vague J. Presse Med 1947;30:339–340.
- 36. Intra-abdominal (Visceral) Fat:Intra-abdominal (Visceral) Fat: The Dangerous Inner FatThe Dangerous Inner Fat SubcutaneousSubcutaneous adipose tissueadipose tissue FrontFront Visceral adiposeVisceral adipose tissuetissue Lemieux l, et al. Ann Endocrinol. 2001;62:255-261.
- 37. Inflammation and Cardiovascular Disease:Inflammation and Cardiovascular Disease: Is Abdominal Obesity the Missing Link?Is Abdominal Obesity the Missing Link? Després JP. Int J Obes Relat Metab Disord. 2003;27:S22-S24. Atherogenic,Atherogenic, insulin resistantinsulin resistant ‘dysmetabolic‘dysmetabolic milieu’milieu’ CRPCRP VisceralVisceral AdiposeAdipose TissueTissue IL-6IL-6 ?? TNF-TNF-αα ?? ?? Risk of ACSRisk of ACS (acute(acute coronarycoronary syndrome)syndrome)
- 38. What is The Metabolic Syndrome?What is The Metabolic Syndrome? The Metabolic syndrome is a group of health problems that includeThe Metabolic syndrome is a group of health problems that include visceral obesityvisceral obesity (too much fat around the waist),(too much fat around the waist), blood pressureblood pressure,, triglyceridestriglycerides,, HDL cholesterolHDL cholesterol,, && blood sugarblood sugar; together, this; together, this group of health problems increases your risk of heart attack, stroke,group of health problems increases your risk of heart attack, stroke, & diabetes& diabetes Metabolic syndrome is caused by an unhealthy lifestyle that includesMetabolic syndrome is caused by an unhealthy lifestyle that includes eating too many calories, being inactive, & gaining weight, particularlyeating too many calories, being inactive, & gaining weight, particularly around the waistaround the waist This lifestyle can lead to insulin resistance, a problem with the body'sThis lifestyle can lead to insulin resistance, a problem with the body's metabolism where your body cannot use insulin properly, &, as ametabolism where your body cannot use insulin properly, &, as a result, blood sugar will begin to rise; over time, this can lead to type 2result, blood sugar will begin to rise; over time, this can lead to type 2 diabetesdiabetes
- 39. • HypertriglyceridemiaHypertriglyceridemia • Insulin resistanceInsulin resistance • Low HDL cholesterolLow HDL cholesterol • HyperinsulinemiaHyperinsulinemia • Elevated apolipoprotein BElevated apolipoprotein B • Glucose intoleranceGlucose intolerance • Small, dense LDL particlesSmall, dense LDL particles • Impaired fibrinolysisImpaired fibrinolysis • Inflammatory profileInflammatory profile • Endothelial dysfunctionEndothelial dysfunction Features of the Metabolic Syndrome CommonlyFeatures of the Metabolic Syndrome Commonly Found in Viscerally Obese PatientsFound in Viscerally Obese Patients Genetic susceptibilityGenetic susceptibility to hypertension, type 2 diabetes, and coronary heartto hypertension, type 2 diabetes, and coronary heart disease ultimately affects the clinical features of the metabolic syndromedisease ultimately affects the clinical features of the metabolic syndrome Adapted from Lemieux l , Després JP. In: Management of Obesity and Related Disorders. 2001:45-63.
- 40. The Atherogenic Metabolic TriadThe Atherogenic Metabolic Triad Beyond LDL cholesterol, blood pressure, type 2 diabetes…Beyond LDL cholesterol, blood pressure, type 2 diabetes… Small, denseSmall, dense LDL particlesLDL particles TheThe AtherogenicAtherogenic TriadTriad HyperinsulinemiaHyperinsulinemia apo Bapo B concentrationsconcentrations LDL: low-density lipoproteinLDL: low-density lipoprotein
- 41. Potential Contribution of Ectopic Fat Deposition toPotential Contribution of Ectopic Fat Deposition to Cardiometabolic Risk of Viscerally Obese PatientsCardiometabolic Risk of Viscerally Obese Patients Després JP. Ann Med. 2006;38:52-63. InsulinInsulin GlucoseGlucose LiverLiver TriglycerideTriglyceride HDLHDL Apolipoprotein BApolipoprotein B VisceralVisceral adipose tissueadipose tissue Hepatic lipaseHepatic lipase Lipid depositionLipid deposition SkeletalSkeletal MuscleMuscle Insulin-resistantInsulin-resistant subcutaneoussubcutaneous adipose tissueadipose tissue LPLLPL Insulin resistanceInsulin resistance Coronary AtherosclerosisCoronary Atherosclerosis Unstable PlaqueUnstable Plaque SystemicSystemic FFAsFFAs Altered CardiometabolicAltered Cardiometabolic Risk ProfileRisk Profile PAI-1PAI-1 IL-6IL-6 TNF-TNF-αα AdiponectinAdiponectin PortalPortal FFAsFFAs ?? FFAs = Free Fatty AcidsFFAs = Free Fatty Acids
- 42. Prevalent Form of the Metabolic SyndromePrevalent Form of the Metabolic Syndrome as Defined by NCEP ATP III and IDFas Defined by NCEP ATP III and IDF AtherogenicAtherogenic DyslipidemiaDyslipidemia AtherogenicAtherogenic DyslipidemiaDyslipidemia InsulinInsulin ResistanceResistance InsulinInsulin ResistanceResistance ThromboticThrombotic StateState ThromboticThrombotic StateState InflammatoryInflammatory StateState InflammatoryInflammatory StateState Adapted from JAMA. 2001;285:2486-2497. Alberti KG, et al. Lancet. 2005;366:1059-1062. Grundy SM, et al. Circulation. 2005;112:2735-2752.
- 43. DeterioratedDeteriorated Lipid ProfileLipid Profile ImprovedImproved TriglyceridesTriglycerides HDL cholesterolHDL cholesterol Cholesterol/HDL cholesterolCholesterol/HDL cholesterol ?? LDL cholesterolLDL cholesterol ?? ?? LDL Particle ConcentrationLDL Particle Concentration and Sizeand Size ?? ObeseObeseViscerallyViscerally ObeseObese SubcutaneousSubcutaneous adipose tissueadipose tissue VisceralVisceral adiposeadipose tissuetissue PPAR-PPAR-γγ AgonistsAgonists DeterioratedDeteriorated Insulin SensitivityInsulin Sensitivity ImprovedImproved InsulinemiaInsulinemia GlycemiaGlycemia HbA1CHbA1C Coronary Heart Disease RiskCoronary Heart Disease RiskHIGHHIGH LOWLOW Weight Gain:Weight Gain: Subcutaneous Adipose TissueSubcutaneous Adipose Tissue HDL = high-density lipoprotein; LDL = low-density lipoproteinHDL = high-density lipoprotein; LDL = low-density lipoprotein
- 44. New Markers of CHD Risk:New Markers of CHD Risk: What to Look for; What to Target?What to Look for; What to Target? Does It Make a Difference?? We Should Not Treat a Black Box!Does It Make a Difference?? We Should Not Treat a Black Box!Does It Make a Difference?? We Should Not Treat a Black Box!Does It Make a Difference?? We Should Not Treat a Black Box! Atherogenic DyslipidemiaAtherogenic Dyslipidemia TriglyceridesTriglycerides HDL cholesterolHDL cholesterol Cholesterol/HDL cholesterol ratioCholesterol/HDL cholesterol ratio ‘‘Normal’ LDL cholesterol butNormal’ LDL cholesterol but apo Bapo B Small, dense LDL andSmall, dense LDL and HDLHDL Postprandial hyperlipidemiaPostprandial hyperlipidemia Atherogenic DyslipidemiaAtherogenic Dyslipidemia TriglyceridesTriglycerides HDL cholesterolHDL cholesterol Cholesterol/HDL cholesterol ratioCholesterol/HDL cholesterol ratio ‘‘Normal’ LDL cholesterol butNormal’ LDL cholesterol but apo Bapo B Small, dense LDL andSmall, dense LDL and HDLHDL Postprandial hyperlipidemiaPostprandial hyperlipidemia Insulin ResistanceInsulin Resistance Insulin resistanceInsulin resistance HyperinsulinemiaHyperinsulinemia HyperglycemiaHyperglycemia Type 2 diabetesType 2 diabetes Insulin ResistanceInsulin Resistance Insulin resistanceInsulin resistance HyperinsulinemiaHyperinsulinemia HyperglycemiaHyperglycemia Type 2 diabetesType 2 diabetes Thrombotic StateThrombotic State PAI-1PAI-1 FibrinogenFibrinogen Thrombotic StateThrombotic State PAI-1PAI-1 FibrinogenFibrinogen Inflammatory StateInflammatory State CRPCRP CytokinesCytokines Inflammatory StateInflammatory State CRPCRP CytokinesCytokines AbdominalAbdominal ObesityObesity Metabolic Risk FactorsMetabolic Risk Factors Risk of Acute CoronaryRisk of Acute Coronary SyndromeSyndrome InflammationInflammation Thin fibrousThin fibrous capcap LipidLipid corecore CoronaryCoronary atherosclerosisatherosclerosis Unstable plaqueUnstable plaque Adapted from Després JP, et al. Progress in Obesity Research: 9; 2003:29-35.
- 45. Managing CVD Risk in Patients WithManaging CVD Risk in Patients With Type 2 Diabetes or the Metabolic SyndromeType 2 Diabetes or the Metabolic Syndrome Beyond lowering LDL cholesterol, BP, glycemia....Beyond lowering LDL cholesterol, BP, glycemia.... Weight lossWeight loss Improves theImproves the TG -TG - HDL cholesterol,HDL cholesterol, and small dense LDL dyslipidemiaand small dense LDL dyslipidemia Fixes a dysmetabolic stateFixes a dysmetabolic state (including inflammation)(including inflammation) DietDiet Physical activityPhysical activity HDL = high-density lipoproteinHDL = high-density lipoprotein LDL = low-density lipoproteinLDL = low-density lipoprotein TG = triglyceridesTG = triglycerides
- 47. 00 11 22 33 44 Cumulative Incidence of DiabetesCumulative Incidence of Diabetes According to Study Group:According to Study Group: DPPDPP Diabetes Prevention Program Research Group. N Engl J Med. 2002;346:393-403. CumulativeIncidenceCumulativeIncidence ofDiabetes(%)ofDiabetes(%) Years from RandomizationYears from Randomization PlaceboPlacebo LifestyleLifestyle MetforminMetformin 28.828.8 21.721.7 14.414.4
- 48. ‘‘Normal’ Weight (BMI = 25 kg/mNormal’ Weight (BMI = 25 kg/m22 )) But Viscerally Obese Patient…But Viscerally Obese Patient… Després JP, et al. Int J Obes. 1995;19(suppl 1):S76-S86. After....After.... a weight loss of only 5 kgmsa weight loss of only 5 kgms BeforeBefore • Moderate weight loss (5-10%) by diet and/or exercise can induce aModerate weight loss (5-10%) by diet and/or exercise can induce a substantial (~30%) loss of atherogenic visceral fat and substantiallysubstantial (~30%) loss of atherogenic visceral fat and substantially improve the risk profile status of these patientsimprove the risk profile status of these patients • Thus, the importance ofThus, the importance of waistwaist rather thanrather than weightweight management ismanagement is emphasizedemphasized
- 49. Acute & Chronic Effects ofAcute & Chronic Effects of Regular Physical Activity/ExerciseRegular Physical Activity/Exercise Després JP, et al. In: Handbook of Exercise in Diabetes. 2nd ed. 2002:197-234. GlycogenGlycogen levellevel GlycogenGlycogen levellevel GlycogenGlycogen levellevel ImprovementsImprovements of lipoprotein –of lipoprotein – lipid profile &lipid profile & insulin/glucoseinsulin/glucose metabolismmetabolism Additional physicalAdditional physical and metabolicand metabolic improvementsimprovements MobilizationMobilization of visceral ATof visceral AT without significantwithout significant changes in adipositychanges in adiposity MobilizationMobilization of visceral ATof visceral AT and significantand significant weight lossweight loss SedentarySedentary ViscerallyViscerally ObeseObese Physically ActivePhysically Active Viscerally ObeseViscerally Obese Physically ActivePhysically Active Nonviscerally ObeseNonviscerally Obese
- 50. Elevated Waist Circumference:Elevated Waist Circumference: A Key FeatureA Key Feature in Patients with the Metabolic Syndromein Patients with the Metabolic Syndrome
Editor's Notes
- Body Mass Index (BMI) is a number calculated from a person’s weight and height. BMI provides a reliable indicator of body fatness for most people and is used to screen for weight categories that may lead to health problems. BMI does not measure body fat directly, but research has shown that BMI correlates to direct measures of body fat, such as underwater weighing and dual energy x-ray absorptionimetry (DXA). BMI can be considered an alternative for direct measures of body fat. Additionally, BMI is an inexpensive and easy-to-perform method of screening for weight categories that may lead to health problems. How is BMI used? BMI is used as a screening tool to identify possible weight problems for adults. However, BMI is not a diagnostic tool. For example, a person may have a high BMI. However, to determine if excess weight is a health risk, a healthcare provider would need to perform further assessments. These assessments might include skin-fold thickness measurements, evaluations of diet, physical activity, family history, and other appropriate health screenings. Why does CDC use BMI to measure overweight and obesity? Calculating BMI is one of the best methods for population assessment of overweight and obesity. Because calculation requires only height and weight, it is inexpensive and easy to use for clinicians and for the general public. The use of BMI allows people to compare their own weight status to that of the general population. What are some of the other ways to measure obesity? Why doesn&apos;t CDC use those to determine overweight and obesity among the general public? Other methods to measure body fatness include skin fold thickness measurements (with calipers), underwater weighing, bioelectrical impedance, dual-energy x-ray absorptiometry (DXA), and computerized tomography. However, these methods are not always readily available, and they are either expensive or need highly trained personnel. BMI = weight (kg) / [height (m)]2 BMI Weight Status &lt;18.5 = Underweight 18.5 – 24.9 = Normal 25.0 – 29.9 = Overweight &gt;30.0 = Obese
- A heart attack occurs when the supply of blood and oxygen to an area of heart muscle is blocked, usually by a clot in a coronary artery. If treatment is not started quickly, the affected area of heart muscle begins to die. This injury to the heart muscle can lead to serious complications, and can even be fatal. Sudden death from heart attack is most often due to an arrhythmia (irregular heartbeat or rhythm) called ventricular fibrillation. If a person survives a heart attack, the injured area of the heart muscle is replaced by scar tissue. This weakens the pumping action of the heart and can lead to heart failure and other complications. Effective treatments for heart attack are available that can decrease the chances of sudden death and long-term complications. To be most effective, these treatments must be given fast—within 1 hour of the start of heart attack symptoms. Acting fast can save your life and limit damage to your heart. Heart With Muscle Damage and Blocked Artery Figure A is an overview of the heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. Figure B shows a cross-section of the coronary artery with plaque buildup and a blood clot. A heart attack is a life-threatening event. Everyone should know the warning signs of a heart attack and how to get emergency help. Many people suffer permanent damage to their hearts or die because they do not get help immediately. Each year, more than a million persons in the United States have a heart attack, and about half (515,000) of them die. About one-half of those who die do so within 1 hour of the start of symptoms and before reaching the hospital. Emergency personnel can often stop arrhythmias with emergency cardiopulmonary resuscitation (CPR), defibrillation (electrical shock), and prompt advanced cardiac life support procedures. If care is sought soon enough, blood flow in the blocked artery can be restored in time to prevent permanent damage to the heart. Most people, however, do not seek medical care for 2 hours or more after symptoms begin. Many people wait 12 hours or longer. The warning signs and symptoms of a heart attack can include: Chest discomfort. Most heart attacks involve discomfort in the center of the chest that lasts for more than a few minutes or goes away and comes back. The discomfort can feel like uncomfortable pressure, squeezing, fullness, or pain. Heart attack pain can sometimes feel like indigestion or heartburn. Discomfort in other areas of the upper body. Pain, discomfort, or numbness can occur in one or both arms, the back, neck, jaw, or stomach. Shortness of breath. Difficulty in breathing often comes along with chest discomfort, but it may occur before chest discomfort. Other symptoms: Examples include breaking out in a cold sweat, having nausea and vomiting, or feeling light-headed or dizzy. Signs and symptoms vary from person to person. In fact, if you have a second heart attack, your symptoms may not be the same as for the first heart attack. Some people have no symptoms. This is called a &quot;silent&quot; heart attack. The symptoms of angina (chest pain) can be similar to the symptoms of a heart attack. If you have angina and notice a change or a worsening of your symptoms, talk with your doctor right away. Diagnosis of a heart attack may include the following tests: EKG (electrocardiogram). This test is used to measure the rate and regularity of your heartbeat. A 12-lead EKG is used in diagnosing a heart attack. Blood tests. When cells in the heart die, they release enzymes into the blood. These enzymes are called markers or biomarkers. Measuring the amount of these markers in the blood can show how much damage was done to your heart. These tests are often repeated at intervals to check for changes. The specific blood tests are: Troponin test. This test checks the troponin levels in the blood, considered the most accurate to see if a heart attack has occurred and how much damage it did to the heart. CK or CK-MB test. These tests check for the amount of the different forms of creatine kinase in the blood. Myoglobin test. This test checks for the presence of myoglobin in the blood. Myoglobin is released when the heart or other muscle is injured. Nuclear heart scan. This test uses radioactive tracers (technetium or thallium) to outline heart chambers and major blood vessels leading to and from the heart. A nuclear heart scan shows any damage to your heart muscle. Cardiac catheterization. A thin, flexible tube (catheter) is passed through an artery in the groin (upper thigh) or arm to reach the coronary arteries. Your doctor can use the catheter to determine pressure and blood flow in the heart&apos;s chambers, collect blood samples from the heart, and examine the arteries of the heart by x ray. Coronary angiography. This test is usually performed along with cardiac catheterization. A dye that can be seen by using x ray is injected through the catheter into the coronary arteries. Your doctor can see the flow of blood through the heart and see where there are blockages. Causes Most heart attacks are caused by a blood clot that blocks one of the coronary arteries (the blood vessels that bring blood and oxygen to the heart muscle). When blood cannot reach part of your heart, that area starves for oxygen. If the blockage continues long enough, cells in the affected area die. Coronary artery disease (CAD) is the most common underlying cause of a heart attack. CAD is the hardening and narrowing of the coronary arteries by the buildup of plaque in the inside walls (atherosclerosis). Over time, plaque buildup in the coronary arteries can: Narrow the arteries so that less blood flows to the heart muscle Block completely the arteries and the flow of blood Cause blood clots to form and block the arteries A less common cause of heart attacks is a severe spasm of the coronary artery that cuts off blood flow to the heart. These spasms can occur in persons with or without CAD. Artery spasm can sometimes be caused by: Taking certain drugs, such as cocaine Emotional stress Exposure to cold Cigarette smoking
- A stroke is the rapidly developing loss of brain functions due to a disturbance in the blood vessels supplying blood to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis or embolism or due to a hemorrhage. As a result, the affected area of the brain is unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate speech or inability to see one side of the visual field. In the past, stroke was referred to as cerebrovascular accident or CVA, but the term &quot;stroke&quot; is now preferred. A stroke is a medical emergency and can cause permanent neurological damage, complications and death. It is the leading cause of adult disability in the United States and Europe. In the UK, it is the second most common cause of death; the first being heart attacks and third being cancer. It is the number two cause of death worldwide and may soon become the leading cause of death worldwide. Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation. High blood pressure is the most important modifiable risk factor of stroke. The traditional definition of stroke, devised by the World Health Organization in the 1970s, is a &quot;neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours&quot;. This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely within 24 hours.[1] With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[5] A stroke is occasionally treated with thrombolysis (&quot;clot buster&quot;), but usually with supportive care (speech and language therapy, physiotherapy and occupational therapy) in a &quot;stroke unit&quot; and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins, and in selected patients with carotid endarterectomy and anticoagulation.
- Obesity: An Ill-Defined Modifiable CVD Risk Factor Although there has been a hectic investigation of potentially important modifiable cardiovascular disease (CVD) risk factors, obesity has failed to qualify as a well-recognized risk factor. BMI: body mass index HDL: high-density lipoprotein LDL: low-density lipoprotein
- Relative Risk of Mortality, CHD, and Type 2 Diabetes According to BMI Although it is well accepted that obesity is a health hazard and a risk factor for cardiovascular disease and type 2 diabetes, physicians have been perplexed by the remarkable heterogeneity that is seen among equally obese individuals. Some obese patients are not characterized by any cardiovascular disease risk factors, whereas others who have developed type 2 diabetes have clinical signs of coronary heart disease and are characterized by insulin resistance, an atherogenic dyslipidemia, and a constellation of risk factors. Thus, while we recognize that obesity causes prejudice to health, why is this condition so heterogeneous in terms of its clinical manifestations? One of the reasons why obesity needs to be redefined as a clinical entity is due to the fact that it appears in many faces. Evidence published over the last 25 years has established the notion that the subgroup of overweight or obese patients characterized by an excess of abdominal fat, especially by an elevated intra-abdominal or visceral adipose tissue deposition, have the highest risk of developing type 2 diabetes and cardiovascular disease. The relationship between body weight and mortality, coronary heart disease (CHD) or diabetes has been investigated in numerous epidemiological studies for decades. The Nurses’ Health Study showed the association between body mass index (BMI), as a crude marker of total adiposity, and mortality from all causes, CHD risk or type 2 diabetes. References: Manson JE, Willett WC, Stampfer MJ, Colditz GA, Hunter DJ, Hankinson SE, et al. Body weight and mortality among women. N Engl J Med. 1995;333:677-685. Willett WC, Manson JE, Stampfer MJ, Colditz GA, Rosner B, Speizer FE, et al. Weight, weight change, and coronary heart disease in women. Risk within the &apos;normal&apos; weight range. JAMA. 1995;273:461-465. Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med. 1995;122:481-486.
- Obesity as a Risk Factor for Type 2 Diabetes The group from the University of Gothenburg led by the late Professor Per Björntorp and Professor Lars Sjöström published results showing the overwhelming association between body fat distribution and the comorbidities of obesity. The Gothenburg Prospective Study presented the incidence of type 2 diabetes in a sample of middle-aged men over a 13.5-year follow-up period. When the men were stratified into tertiles of body mass index (BMI) and of waist-to-hip ratio (an index of the proportion of abdominal fat), even among lean individuals (men in the first BMI tertile), the highest waist-to-hip ratio tertile was associated with a 6-fold increase in the risk of developing diabetes (from 0.5% incidence to 2.9%). On the other hand, in the absence of an elevated waist-to-hip ratio, the highest BMI tertile was not associated with an increased risk of developing diabetes. Finally, among equally overweight/obese individuals (the three subgroups of men in the highest BMI tertile), the proportion of abdominal fat (waist-to-hip ratio) had a major impact on the risk of developing diabetes. The risk increased 30-fold among overweight individuals from the lowest to the highest waist-to-hip ratio tertiles. This study published one of the early key results that provided evidence for measuring beyond the BMI to better appreciate the risk (diabetes in the present case) associated with overweight and obesity. Reference: Ohlson LO, Larsson B, Svardsudd K, Welin L, Eriksson H, Wilhelmsen L, et al. The influence of body fat distribution on the incidence of diabetes mellitus. 13.5 years of follow-up of the participants in the study of men born in 1913. Diabetes. 1985;34:1055-1058.
- Managing the High-Risk Patient with Type 2 Diabetes and/or “Hypertriglyceridemic Waist” Remarkable progress has been made in clinical practice regarding the evaluation and management of traditional risk factors such as hypertension, dyslipidemia, and type 2 diabetes. For instance, in the 1950s, smoking, hypertension and hypercholesterolemia were major causes of coronary heart disease. The introduction of powerful drugs to reduce cholesterol levels and blood pressure has been associated with tremendous clinical benefits. However, the relative magnitude of abdominal obesity, type 2 diabetes, and features of the metabolic syndrome in the mosaic of modifiable cardiovascular disease risk factors has increased substantially. Therefore, many patients managed by internists, cardiologists, and primary care physicians have now developed cardiovascular complications because of the consequences of the metabolic complications associated with their visceral obesity and insulin resistance. In conclusion, physicians need to pay attention to the abdominally obese patient who has a large waistline and clinical features of the metabolic syndrome. Physicians need to target the root of the additional cardiometabolic risk: abdominal obesity. Unfortunately, until urban and living environments change to promote physical activity and healthy nutrition, improving the lifestyle of patients will be a challenge because the medical system is currently ill-equipped to handle this huge wave of patients with abdominal obesity, metabolic syndrome and type 2 diabetes. A multidisciplinary approach with all relevant stakeholders involved will be required to truly impact this epidemic of abdominal obesity and type 2 diabetes. Until then, it is hoped that the approach in clinical practice of aiming by the optimal assessment and management of high-risk abdominally obese patients will continue to improve. Reference: Després JP, Lemieux I, Prud&apos;homme D. Treatment of obesity: need to focus on high risk abdominally obese patients. BMJ. 2001;322:716-720.
- Obesity: Body Mass Index (BMI) When a relative index of weight over height is used, a linear or curvilinear relationship is observed between relative weight and the presence of comorbidities such as type 2 diabetes and cardiovascular disease. The most commonly used index is the body mass index (BMI), which is expressed as body weight in kg divided by height in m2. When populations are examined, higher BMI values are associated with a greater prevalence of comorbidities. However, in clinical practice, physicians have been perplexed by the fact that equally obese individuals may or may not be characterized by the expected comorbidities of obesity. 25 years ago, the reason for such heterogeneity was unclear. Body Mass Index (BMI) is a number calculated from a person’s weight and height. BMI provides a reliable indicator of body fatness for most people and is used to screen for weight categories that may lead to health problems. BMI does not measure body fat directly, but research has shown that BMI correlates to direct measures of body fat, such as underwater weighing and dual energy x-ray absorptiometry (DXA). BMI can be considered an alternative for direct measures of body fat. Additionally, BMI is an inexpensive and easy-to-perform method of screening for weight categories that may lead to health problems. How is BMI used? BMI is used as a screening tool to identify possible weight problems for adults. However, BMI is not a diagnostic tool. For example, a person may have a high BMI. However, to determine if excess weight is a health risk, a healthcare provider would need to perform further assessments. These assessments might include skin-fold thickness measurements, evaluations of diet, physical activity, family history, and other appropriate health screenings. Why does CDC use BMI to measure overweight and obesity? Calculating BMI is one of the best methods for population assessment of overweight and obesity. Because calculation requires only height and weight, it is inexpensive and easy to use for clinicians and for the general public. The use of BMI allows people to compare their own weight status to that of the general population. What are some of the other ways to measure obesity? Why doesn&apos;t CDC use those to determine overweight and obesity among the general public? Other methods to measure body fatness include skin fold thickness measurements (with calipers), underwater weighing, bioelectrical impedance, dual-energy x-ray absorptiometry (DXA), and computerized tomography. However, these methods are not always readily available, and they are either expensive or need highly trained personnel. BMI = weight (kg) / [height (m)]2 BMI Weight Status &lt;18.5 = Underweight 18.5 – 24.9 = Normal 25.0 – 29.9 = Overweight &gt;30.0 = Obese
- Obesity: Body Mass Index (BMI) When a relative index of weight over height is used, a linear or curvilinear relationship is observed between relative weight and the presence of comorbidities such as type 2 diabetes and cardiovascular disease. The most commonly used index is the body mass index (BMI), which is expressed as body weight in kg divided by height in m2. When populations are examined, higher BMI values are associated with a greater prevalence of comorbidities. However, in clinical practice, physicians have been perplexed by the fact that equally obese individuals may or may not be characterized by the expected comorbidities of obesity. 25 years ago, the reason for such heterogeneity was unclear. Body Mass Index (BMI) is a number calculated from a person’s weight and height. BMI provides a reliable indicator of body fatness for most people and is used to screen for weight categories that may lead to health problems. BMI does not measure body fat directly, but research has shown that BMI correlates to direct measures of body fat, such as underwater weighing and dual energy x-ray absorptiometry (DXA). BMI can be considered an alternative for direct measures of body fat. Additionally, BMI is an inexpensive and easy-to-perform method of screening for weight categories that may lead to health problems. How is BMI used? BMI is used as a screening tool to identify possible weight problems for adults. However, BMI is not a diagnostic tool. For example, a person may have a high BMI. However, to determine if excess weight is a health risk, a healthcare provider would need to perform further assessments. These assessments might include skin-fold thickness measurements, evaluations of diet, physical activity, family history, and other appropriate health screenings. Why does CDC use BMI to measure overweight and obesity? Calculating BMI is one of the best methods for population assessment of overweight and obesity. Because calculation requires only height and weight, it is inexpensive and easy to use for clinicians and for the general public. The use of BMI allows people to compare their own weight status to that of the general population. What are some of the other ways to measure obesity? Why doesn&apos;t CDC use those to determine overweight and obesity among the general public? Other methods to measure body fatness include skin fold thickness measurements (with calipers), underwater weighing, bioelectrical impedance, dual-energy x-ray absorptiometry (DXA), and computerized tomography. However, these methods are not always readily available, and they are either expensive or need highly trained personnel. BMI = weight (kg) / [height (m)]2 BMI Weight Status &lt;18.5 = Underweight 18.5 – 24.9 = Normal 25.0 – 29.9 = Overweight &gt;30.0 = Obese
- Saving and Overconsuming Energy Before addressing the question of which anthropometric index is most appropriate for use in clinical practice to assess the risks associated with obesity, the reason(s) for the current epidemic of obesity and type 2 diabetes should be pondered. “Mother Nature” has engineered humans to be quite efficient from an energy standpoint. Ancestors of humans had to survive very difficult environments, in which energy from food was sometimes limited yet the energy requirements of daily life were rather high. While the exponential development of equipment and devices have made life quite comfortable, the level of energy expenditure has been substantially reduced. Meanwhile, an increasing proportion of our population is exposed to energy dense food of poor nutritional value. Thus, for these simple and rather obvious reasons, there is currently a worldwide epidemic of obesity and no evidence that this phenomenon will plateau in the near future.
- Android (Apple) vs. Gynoid (Pear) Obesity A key factor responsible for the heterogeneity of obesity as a clinical entity is body fat distribution. Professor Jean Vague from the University of Marseille in France was the first to suggest, more than half a century ago, that the complications of obesity were not dependent upon excess body fat mass per se but were the consequence of the regional distribution of body fat. Vague coined the term “android” or male-type obesity to characterize the form of overweight and obesity observed among his patients with diabetes or clinical signs of cardiovascular disease, whereas he proposed that “gynoid” or the lower-body form of obesity, frequently found in premenopausal obese women, was mostly benign. These remarkable clinical observations did not receive immediate attention from the medical community, and more than 35 years passed before Vague’s hypothesis received further support from “modern” prospective epidemiological studies. Reference: Vague J. La différenciation sexuelle, facteur déterminant des formes de l&apos;obésité. Presse Med. 1947;30:339-340.
- Intra-abdominal (Visceral) Fat: The Dangerous Inner Fat A cross-sectional image of the abdomen is obtained by computed tomography and usually by scanning the abdomen at the level of L4–L5. Computed tomography was a specialized equipment found in academic centers 2 or 3 decades ago. It has now become available even in regional hospitals, which makes the measurement of visceral adiposity fairly easy for the patient and the physician. Because of differences in the attenuation values of adipose, muscle, and bone tissue, it is very easy to distinguish fat from muscle and bone on the image. The intra-abdominal, or visceral, adipose tissue is highlighted in white. Studies have indicated that among equally overweight or obese individuals, an excess of intra-abdominal, or visceral, adipose tissue is predictive of increased risk of the expected abnormalities of obesity. Reference: Lemieux l, Pascot A, Almeras N, Lamarche B, Bergeron J, Despres JP. Obesity in the 21(St) century: new approaches? Ann Endocrinol. (Paris) 2001;62:255-261.
- Inflammation and Cardiovascular Disease: Is Abdominal Obesity the Missing Link? The reason for this close relationship between the expanded waistline and the elevated C-reactive protein (CRP) levels could result from evidence of macrophage infiltration in adipose tissue of abdominally obese patients. These macrophages can become the source of production for inflammatory cytokines such as tumor necrosis factor-α (TNF- α) and interleukin-6 (IL-6), which could have a local impact on adipose tissue metabolism as well as systemic effects. This can exacerbate the dysmetabolic profile noted among patients with an excess of visceral adipose tissue. For instance, the TNF-α could make the adipose tissue insulin resistant, and it also has an inhibitory effect on the production of adiponectin (an important adipose tissue-derived cytokine that has been suggested to have anti-atherogenic and anti-diabetic properties). In addition, the release of IL-6 by fat cells is known to stimulate the production of CRP through the liver. Reference: Despres JP. Inflammation and cardiovascular disease: is abdominal obesity the missing link? Int J Obes Relat Metab Disord. 2003;27:S22-S24.
- Features of the Metabolic Syndrome Commonly Found among Viscerally Obese Patients Additional metabolic studies conducted in several laboratories around the world have shown that among equally obese patients, subjects with an excess of visceral adipose tissue have the most deteriorated metabolic risk profile. These subjects show insulin resistance and compensatory hyperinsulinemia as a sign of insulin resistance. Among genetically susceptible individuals, insulin resistance favors the development of glucose intolerance and eventually leads to type 2 diabetes when the insulin resistant state is accompanied by a relative deficit in insulin secretion. However, it is important to point out that even in the absence of glucose intolerance and marked hyperglycemia, the presence of visceral obesity and insulin resistance have been associated with a very typical dyslipidemic profile that includes hypertriglyceridemia, low HDL-C concentration, elevated apolipoprotein B as a marker of an increased concentration of atherogenic lipoproteins, and an increased concentration of small, dense LDL particles. In addition to the dyslipidemic insulin resistant profile of viscerally obese patients, these individuals are characterized by an impaired fibrinolysis, an increased susceptibility to thrombosis, an endothelial dysfunction (as an early sign of endothelial damage) and an inflammatory profile. HDL: high-density lipoprotein LDL: low-density lipoprotein Reference: Adapted from Lemieux I, Despres JP. Obesity and hyperlipidemia. In: Kopelman P, ed. Management of Obesity and Related Disorders. London: Martin Dunitz Ltd.; 2001:45-64.
- The Atherogenic Metabolic Triad The risk associated with some of the features of visceral obesity have not been examined in many prospective studies because markers of insulin resistance and related abnormalities have not been commonly measured. The Québec Cardiovascular Study, a prospective study conducted in a sample of initially asymptomatic middle-aged men, provided an opportunity to test the hypothesis that fasting hyperinsulinemia, as a basic marker of insulin resistance, could be a relevant marker of coronary heart disease risk. Furthermore, since hyperinsulinemic men are often characterized by elevated apolipoprotein B (apo B) and small LDL particles, the hypothesis that this atherogenic metabolic triad of abnormalities, which is commonly found in viscerally obese individuals, could increase the risk of coronary heart disease was tested. LDL: low-density lipoprotein
- Potential Contribution of Ectopic Fat Deposition to the Cardiometabolic Risk Profile of Viscerally Obese Patients Although the “portal free fatty acid (FFA) hypothesis” has been suggested to explain some of the metabolic abnormalities associated with excess adipose tissue accumulation, the hyperlipolytic state of the expanded visceral depot cannot, by itself, explain all of the metabolic abnormalities observed in viscerally obese patients. However, if the exciting new findings indicating that adipose tissue is an important endocrine organ and a site of production for inflammatory cytokines (such as interleukin-6 [IL-6] and tumor necrosis factor-α [TNF-α]) and a potentially protective cytokine (such as adiponectin, which is reduced in visceral obesity) are considered, the comprehensive alterations in the metabolic profile observed in viscerally obese patients can now be reconciled. Therefore, the hyperlipolytic state and pro-inflammatory profile of visceral obesity could explain the constellation of metabolic abnormalities found in viscerally obese patients. LPL: lipoprotein lipase PAI-1: plasminogen activator inhibitor-1 Reference: Despres JP. Is visceral obesity the cause of the metabolic syndrome? Ann Med. 2006;38:52-63.
- The Prevalent Form of the Metabolic Syndrome as Defined by NCEP ATP III and IDF The complications of visceral adiposity appear to increase the risk of coronary heart disease beyond what could be predicted from the presence of traditional risk factors. Since atherogenic dyslipidemia and insulin resistance are conditions frequently observed in clinical practice among patients with abdominal obesity and excess visceral adipose tissue accumulation, it has been suggested that the most prevalent form of the metabolic syndrome has been found among patients with an elevated waistline and an excess of visceral adipose tissue. In addition to these complications, inflammation in the context of abdominal obesity has also been examined, and studies have shown that it is associated with abdominal fat accumulation. Such a critical role played by the abdominal obesity associated with an excess of visceral fat justifies the recommendations of the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) and the recent guidelines of the International Diabetes Federation (IDF). Both organizations have recognized abdominal obesity as the most prevalent form of the metabolic syndrome. Therefore, both NCEP ATP III and IDF recommend the measurement of waist circumference over the body mass index to estimate the amount of abdominal fat. References: Adapted from Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001;285:2486-2497. Alberti KG, Zimmet P, Shaw J; IDF Epidemiology Task Force Consensus Group. The metabolic syndrome–a new worldwide definition. Lancet. 2005;366:1059-1062. Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al.; American Heart Association; National Heart, Lung, and Blood Institute. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005;112:2735-2752.
- Weight Gain: Subcutaneous Adipose Tissue In summary, there is a need to better understand the specific contribution of the proliferation of subcutaneous adipose tissue as one of the potentially key factors explaining the beneficial effects of peroxisome proliferator-activated receptor- (PPAR-) agonists on the cardiometabolic risk profile of patients with type 2 diabetes and the metabolic syndrome. However, data with PPAR- agonists provide additional evidence that subcutaneous fat accumulation is not as much of a health hazard as visceral fat accumulation.
- New Markers of CHD Risk: What to Look for, What to Target? The metabolic syndrome has been defined by the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) as a cluster of atherothrombotic, inflammatory abnormalities that increase the risk of type 2 diabetes and cardiovascular disease. It is most frequently found in patients with abdominal obesity and insulin resistance. However, this definition that describes a constellation of risk factors has been confused with the 5 clinical criteria proposed by NCEP ATP III that identify individuals who are likely to be characterized by these clustering atherothrombotic, inflammatory abnormalities. Reference: Adapted from Després JP, Pascot A, Lemieux I, et al. Obesity management: a priority in the primary and secondary prevention of cardiovascular disease. In: Medeiros-Neto G, Halpern A, Bouchard C, eds. Progress in Obesity Research: 9. France: John Libbey Eurotext; 2003:29-35.
- Managing CVD Risk in Patients with Type 2 Diabetes or the Metabolic Syndrome The importance of preventing abdominal obesity, or targeting abdominal obesity when it is present, is emphasized by results that show an increased risk of cardiovascular disease (CVD) and type 2 diabetes in the subgroup of abdominally obese patients and the general epidemic of abdominal obesity and type 2 diabetes. The importance of the benefits of moderate weight loss, by transforming sedentary patients into physically active individuals, and the reshaping of patients’ nutritional habits should be emphasized. In addition, further studies are needed to verify the extent of clinical benefits from the improvement of the high triglyceride (TG)/low HDL-C, small LDL phenotype seen in such patients. The literature regarding fibrate therapy has not consistently shown the clinical benefits of targeting the dyslipidemic profile, and further studies are needed. Finally, the further benefit of “fixing” the dysmetabolic, insulin-resistant state with compounds such as peroxisome proliferator-activated receptor- agonists is currently under investigation.
- Prevention… It could work!!!
- Cumulative Incidence of Diabetes according to Study Group: DPP The Finnish Diabetes Prevention Study and the American Diabetes Prevention Program (DPP) have shown remarkable effects on a group of patients with impaired glucose tolerance and abdominal obesity. Both studies used a lifestyle modification program that involved a multidisciplinary team who had regular contact with patients. The DPP reshaped the nutritional and physical activity habits of a group of high-risk patients with impaired glucose tolerance, inducing a weight loss of only a few kilograms that was associated with a spectacular reduction in the probability of developing type 2 diabetes over three years. Such reduction was greater than that achieved through the use of pharmacotherapy with the well-known agent metformin. Why was such a moderate weight loss associated with tremendous clinical benefits? Reference: Knowler WC, Barrett-Connor E, Fowler SE, et al., for the Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393-403.
- “Normal” Weight (BMI=25 kg/m2) but Viscerally Obese Patient There is now evidence that viscerally obese patients who lose a moderate amount of body weight show a selective mobilization of visceral fat. A computed tomography abdominal scan of a patient having lost only 5 kg illustrates that a moderate weight loss of 5-10% produced by diet and/or exercise can induce a substantial 30% and more loss of visceral adipose tissue. Such preferential mobilization of visceral fat could explain the substantial metabolic benefits of moderate weight loss in viscerally obese patients with atherogenic dyslipidemia or impaired glucose tolerance. Studies are currently in progress to further quantify the specific contribution of this selective loss of visceral fat on the cardiometabolic risk profile of viscerally obese patients. In a specific case, the 5 kg weight loss was associated with a 30% loss of subcutaneous abdominal fat but a 56% loss of visceral adipose tissue. This case provides evidence for a selective loss of visceral fat with moderate weight loss. BMI: body mass index Reference: Després JP, Lemieux S, Lamarche B, et al. The insulin resistance-dyslipidemic syndrome: contribution of visceral obesity and therapeutic implications. Int J Obes Relat Metab Disord. 1995;19 Suppl 1:S76-86.
- Acute and Chronic Effects of Regular Physical Activity/Exercise There is now substantial evidence that physical activity/exercise can induce a mobilization of glycogen stores, create a glucose storage space, and acutely improve insulin sensitivity. The sedentary, viscerally obese patient with insulin resistance and features of the metabolic syndrome should acutely benefit from simple forms of physical activity such as a daily 45-minute brisk walk. Additionally, if the patient is able to reshape his/her nutritional habits and lose a moderate amount of body weight, a moderate weight loss is likely to be associated with a selective loss of visceral adipose tissue (AT) accompanied by further improvements in his/her cardiometabolic risk profile. Therefore, both regular physical activity/exercise and reshaping of the nutritional habits to induce moderate weight loss could synergistically improve the cardiometabolic risk profile of the sedentary, viscerally obese, insulin-resistant patient. Reference: Després JP, Couillard C, Bergeron J, Lamarche B. Regional body fat distribution, the insulin resistance-dyslipidemic syndrome, and the risk of type 2 diabetes and coronary heart disease. In: Ruderman N, Devlin JT, Schneider SH, Kriska AM, eds. Handbook of Exercise in Diabetes. 2nd ed. Alexandria, VA: American Diabetes Association; 2002:197-234.
- Elevated Waist Circumference: A Key Feature in Patients with the Metabolic Syndrome Physicians must detect the presence of abdominal obesity in their practice, and waist circumference should be considered a “vital sign.” Waist circumference must be assessed as an initial step in identifying individuals who are characterized by the clustering abnormalities of the metabolic syndrome.