GLOBESITY / DIABESITYTHE EPIDEMIC

DR. T. COOK FRCPC, MPH

LCOL (RET’D)

OVERVIEW

DEFINITIONSEPIDEMIOLOGY / 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%

Respira-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

PA

R (

%)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

Risk

HyperTG

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