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GLOBESITY / DIABESITY THE EPIDEMIC

GLOBESITY / DIABESITY THE EPIDEMIC. DR. T. COOK FRCPC, MPH LCOL (RET’D). OVERVIEW. DEFINITIONS EPIDEMIOLOGY / IMPORTANCE SOME CONTROVERSIAL QUESTIONS How best to measure the problem? Why do we have this epidemic?

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GLOBESITY / DIABESITY THE EPIDEMIC

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  1. GLOBESITY / DIABESITYTHEEPIDEMIC DR. T. COOK FRCPC, MPH LCOL (RET’D)

  2. OVERVIEW DEFINITIONS EPIDEMIOLOGY / IMPORTANCE SOME CONTROVERSIAL QUESTIONS • How best to measure the problem? • Why do we have this epidemic? • What can HealthCare Providers do to help change the course of this epidemic? • With individual patients • “Globally”

  3. GLOBESITY Worldwide increase in overweight and obesity

  4. DIABESITY

  5. METABOLIC SYNDROME • WHO / IDF Must have Insulin Resistance (DM2, IFG, IGT) Includes additional risk factor - Urinary albumin • ATP III (Adult Treatment Panel US NCEP - 2001) Any 3 of : • Abdominal Obesity (WC) • HyperTG • Low HDL • Hypertension • Impaired FBG

  6. ALL INTERACT OBESITY MET SYN DIABETES RIP

  7. SCOPE OF PROBLEM • HUGE! • ESCALATING • BUT... PREVENTABLE & MANAGEABLE

  8. FIRST CONTROVERSY: HOW TO MEASURE OBESITY BMI = Wt (kg)/ Ht (m)2 BMI = 34 BMI = 34

  9. BMI PROS & CONS • Easy, consistent, reproducible • Applicability questioned • Very muscular • Young • Old • Doesn’t distinguish visceral obesity

  10. WAIST CIRCUMFERENCE WAIST:HIP RATIO • PROS & CONS • Identifies visceral obesity • May carry independent risk assoc • Difficult to standardize, low “Kappa”

  11. WC THRESHOLDS • Caucasian • Male 102 cm (40 in) • Female 88 cm (35 in) • S. Asian / Asian • Male 90 cm (36 in) • Female 80 cm (32 in)

  12. BMI vs WC

  13. MEASURING BODY FAT % Bioelectric Impedance Analyzer Calipers “BodPod” (Air Displacement) BEST GOOD BETTER

  14. GLOBAL EPIDEMIC of OBESITY

  15. OVERWEIGHT IN CANADA BY PROVINCE

  16. FRIGHTENING STATS on OBESITY • 1995 • 200 million adults obese worldwide • 18 million children • 2008 • 300 million adult females obese worldwide • 200 million adult males • 42 million children • 35 million of these children live in LDC (less developed countries) • 2030 • 1.5 billion obese worldwide! (WHO data)

  17. OBESITY Associated Conditions • Hypertension • Diabetes Mellitus • Dyslipidemia • Coronary Artery Disease • Malignancies • Breast • Uterus • Pancreas • Prostate • Colorectal • Psychological Disorders • depression • anorexia nervosa • bulimia • Obstructive Sleep Apnea • Susceptibility: AMS, Heat Illness, Gout, Urolithiasis, Hypogonadism

  18. DIABETES IN CANADA PHAC - 2009 • 2.4 million Cdn • 6.8% pop’n • 8.7% (1:11) of 20 yo + • 3.7 million by 2019 • Increasingly affects children / productive age grps

  19. DIABETES IN CANADA OVER TIME Doubled in 10 y, by 2050 1:3 adults AND 1:3 children PHAC 2009

  20. WORLDWIDE DIABETES WHO est Currently 350 Million (6.5% world’s pop’n) Increase by 60% by 2030

  21. PRE-DIABETES / MET SYN • Pre-Diabetes is IFG +/- IGT • Addt’l 5 million Cdn (over 20 yo) have • Progression to diabetes ~ 30% in 10 yrs if IFG or IGT • Progression to diabetes ~ 60% in 10 yrs if IFG AND IGT • 15% Cdn meet criteria for Metabolic Syndrome

  22. WHY CARE? • Obesity, Diabetes, Metabolic Syndrome all assoc with • Higher mortality • Higher morbidity • Lower longevity • Increased health care cost • Lower productivity

  23. DIABETES DM2 leading cause of blindness, CRF, Amputation, CVD

  24. StatsCan

  25. INTERHEART STUDY Landmark Case-Control Study Lancet Vol 364, 11 Sept 2004 Dr. S. Yusuf – McMaster U. one of PI 15152 cases of Acute Myocardial Infarction 14820 controls - matched Worldwide (52 countries incl. 450 Canadians)

  26. ABDOMINAL OBESITY: MAJOR UNDERLYING CAUSE OF ACUTE M.I. Cardiometabolic risk factors in the INTERHEART Study 60 49 Abdominal obesity predicts the risk of CVD beyond BMI 40 PAR (%)a 20 18 20 10 0 Abnormallipids Abdominal obesity Hypertension Diabetes aProportion of MI in the total population attributable to a specific risk factor; CVD: cardiovascular disease; BMI: body mass index; PAR: population attributable risk; MI: myocardial infarction Yusuf S et al, 2004

  27. Cardio- Metabolic Risk HyperTG Waist • IFG / IGT • Abdo obesity • TG Cardiometabolic Risk Adds to Traditional Risk

  28. CONTROVERSY 2 WHY DO WE HAVE THESE EPIDEMICS? Ethnicity + Income, Job, Education, Food security, Social support, Healthcare access SOCIAL GENETICS “Built” – urban vs rural plan, access to trails, ease of walking / activities Housing Food & Beverage marketing ENVIRONMENTAL

  29. OBVIOUS BUT... NOT SOLE EXPLANATIONS • Excessive consumption of calorie-dense but nutrient poor, highly processed food • $110 billion USD spent on fast food worldwide /y • Sedentary lifestyles • Aging populations

  30. GENETICS OF OBESITY / DM2 • Rapid development s since human genome project • Single-gene , “causal” • Diabetes • Familial MODY = Glucokinase mutations • Mitochondrial diabetes with deafness • Obesity • Leptin or leptin receptor gene mutations • Orexin hormone abnormalities • Prader-Willi syndrome • These are RARE

  31. GENE ASSOCIATIONS • Obesity – 30 + gene changes • FTO “Fat Mass” gene  Satiety • “Appetite” gene • Nutrigenomics – SNPs predict best diet and exercise regimen • Diabetes – 40 + gene changes • TCF7L2 – modulates pancreatic islet cell function • IRS1 – insulin receptor substrate • TBC1D3 CNV (Copy Number Variation) may be primary player in insulin resistance

  32. NEW GENOMIC RISK FACTORS • Telomere length / Telomerase levels • High correlation with biological age, metabolic disease (obesity / DM2), stress effects and CVD! • Use is controversial! • Test annually • If telomeres are shorter than avg or shortening over time  BAD NEWS • Lifestyle modification will lengthen

  33. HOW TO MANAGE DIABESITY • Population and individual based • Multi-sectoral • Multi-disciplinary • Integrative • Culturally relevant • “one size can’t fit all”

  34. RECOMMENDATIONS • Lifestyle Modification  Sustained Behaviour changes for better health is goal • Must address all factors • Nutrition • Fitness (physical) • Fitness (mental) • Barriers to change • Education • Experiential, guidance, practice

  35. CONTROVERSY: WHAT IS BEST DIET? • Many studies, many conclusions • Must be individualized, ?guided by genomics • Long-term adherence • Micro and macro nutrients must be sufficient • “Balance and Moderation” • Avoid excessive liquid • Avoid processed foods • Vegetables, nuts, legumes, fruit predominate

  36. CONTROVERSY: HOW MUCH EXERCISE? • WHO Guidelines • 5 – 17 yo • 60 min mod to vigorous intensity daily • mostly aerobic • vigorous intensity activity that strengthens muscles and bones 3 / wk • >17 yo • 150 min mod intensity / wk OR • 75 min vigorous intensity / wk OR • equivalent combination • strengthen major muscle groups at least 2 / wk

  37. WHAT ABOUT N.E.A.T.? • Non-Exercise Activity Thermogenesis • Orexin “fidget” hormone • Small muscle groups used subconsciously eg. Posture • Mimic Orexin • Stand as much as possible • Sit on a Yoga ball • Avoid conveyances (elevators, escalators, cars)

  38. ROLE OF STRESS MANAGEMENT • Critically important for all diabesity patients • Stress hormones contribute to weight gain and raise glucose • Regular induction of the “relaxation response” improves BP and lengthens telomeres (Dr. D. Ornish) • Contemplative practice > 15 min daily assoc with improved health, well-being • MB-EAT (Mindfulness Based Eating Awareness Training) • Learn to pay attention to body signals for hunger, satiety, control emotional eating • Effective weight management program

  39. CMAJ April 2007: CPG on Prevention and Management of Obesity in Children and Adults

  40. CONTROVERSY: WHAT ARE GLYCEMIA CONTROL TARGETS? • Intensive glycemic control reduces microvascular complications • BUT... No RCT has demonstrated improved macrovasc outcomes in DM2 with intensive Rx • ACCORD and ADVANCE trials showed incr risk • Other risk factors (esp lipids, HTN, smoking, stress) more important • Glycemic targets need to be individualized • HbA1 6.5 - 7% if no AE in avg DM2 • HbA1 7 - 8% in elderly, multcomorbidities • GLOBAL CV RISK MANAGEMENT IS CRUCIAL

  41. SUMMARY • Obesity, Metabolic Syndrome and DM2 all reflect a prevalent genetic, social and environmental interaction • Their prevalence is increasing dramatically throughout the world. • All are associated with adverse CV and other health outcomes • All can be prevented and managed at an individual and global level, though there remain many challenges and controversies

  42. QUESTIONS

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