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GLOBESITY / DIABESITYTHE EPIDEMIC
DR. T. COOK FRCPC, MPH
LCOL (RET’D)
OVERVIEWDEFINITIONSEPIDEMIOLOGY / IMPORTANCESOME CONTROVERSIAL QUESTIONS
o How best to measure the problem?o Why do we have this epidemic?o What can HealthCare Providers do to
help change the course of this epidemic? o With individual patientso “Globally”
GLOBESITY
Worldwide increase in overweight and obesity
DIABESITY
METABOLIC SYNDROME
WHO / IDFMust 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
ALL INTERACT
OBESITYMET SYN
DIABETES
RIP
SCOPE OF PROBLEM HUGE! ESCALATING BUT... PREVENTABLE & MANAGEABLE
FIRST CONTROVERSY: HOW TO MEASURE OBESITY
BMI = 34BMI = 34
BMI = Wt (kg)/ Ht (m)2
BMI PROS & CONS Easy, consistent, reproducible Applicability questioned
Very muscular Young Old
Doesn’t distinguish visceral obesity
WAIST CIRCUMFERENCE WAIST:HIP RATIO
PROS & CONS Identifies visceral obesity May carry independent risk assoc Difficult to standardize, low “Kappa”
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)
BMI vs WC
MEASURING BODY FAT %
GOOD
BETTER
BEST
CalipersBioelectric Impedance Analyzer
“BodPod” (Air Displacement)
GLOBAL EPIDEMIC of OBESITY
OVERWEIGHT IN CANADA BY PROVINCE
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)
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
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
DIABETES IN CANADA OVER TIME
Doubled in 10 y, by 2050 1:3 adults AND 1:3 children PHAC 2009
WORLDWIDE DIABETES
WHO estCurrently 350 Million (6.5% world’s pop’n)Increase by 60% by 2030
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
WHY CARE? Obesity, Diabetes, Metabolic Syndrome
all assoc with Higher mortality Higher morbidity Lower longevity Increased health care cost Lower productivity
DIABETES
DM2 leading cause of blindness, CRF, Amputation, CVD
Heart34%
Cancer27%Res
pira-tory8%
Ac-ciden
ts4%
Dia-betes
3%
Psychi-atric4%
Neuro-
de-gen-era-tive2% Other
17%
Causes of Death, Canada
StatsCan
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)
ABDOMINAL OBESITY: MAJOR UNDERLYING CAUSE OF ACUTE M.I.
Yusuf S et al, 2004
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
Cardiometabolic risk factors in the INTERHEART Study
PAR
(%)a
Abdominal obesity predicts the risk of CVD beyond BMI
0
20
40
60
18
Hypertension
10
Diabetes
20
Abdominalobesity
49
Abnormallipids
Cardiometabolic Risk Adds to Traditional Risk
IFG / IGTAbdo obesity
TG
Cardio-Metabolic
RiskHyperT
G Waist
CONTROVERSY 2 WHY DO WE HAVE THESE EPIDEMICS?
GENETICS
SOCIAL
ENVIRONMENTAL
Income, Job, Education, Food security, Social support, Healthcare access
“Built” – urban vs rural plan, access to trails, ease of walking / activitiesHousingFood & Beverage marketing
Ethnicity +
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
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
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
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
HOW TO MANAGE DIABESITY
Population and individual based Multi-sectoral Multi-disciplinary Integrative Culturally relevant “one size can’t fit all”
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
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
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
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)
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
CMAJ April 2007: CPG on Prevention and Management of Obesity in Children and Adults
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, mult comorbidities
GLOBAL CV RISK MANAGEMENT IS CRUCIAL
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
QUESTIONS