Managing obesity the rea lities striking a balance


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This presentation provides a better understanding of the biologic REALities and impact of weight bias on pediatric obesity management. The paradigm shift in pediatric obesity management is also explored, with a review of Health At Every Size (HAES) and the use of the Edmonton Obesity Staging System to help guide management.

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  • Here we have Shaq at his peak as a Laker (before he played for the HEAT, SUNS, Cavs and finally as an anathema to all Laker fans the Celtics). and while Keith is exceptionally resilient most would agree that Shaq is living a more traditionally healthy lifestyle and has better overall global health.
  • While weight gain occurs when energy consumption exceeds energy expenditure there are a myriad of influencers in this seemingly simple well known equation. A significant # of these influencers are non-modifiable on an individual level. WE know that our genetic programming plays a large role in our risk for weight gain. Children of obese parents are 6-8 times more likely to be obese and when looking at biologic offspring parent pairs and adoptive offspring parent pairs, BMI is more highly correlated with biologic parent BMI. WE continue to learn more and more about the role of intrauterine exposures in risk for obesity. Our very own Dr. Kristi Adamo is doing work in this area. Exposure to diabetes in utero, maternal smoking, maternal weight and gestational weight gain have all been associated with increased risk for weight gain and obesity.
  • Biology plays a very big role in how our bodies will respond to obesigenic stimuli in our environment. This figure also demonstrates the broader determinants of health at play- our mental health has plays a significant role in obesity and is influenced by our social surroundings. Our ability to be active is affected by our built environment, Our food consumption/choices are heavily influenced by food production and the food insustry
  • We all live in an obesogenic environment and engage to some degree in obesogenic behaviours. The impact of these obesogenic stimuli our modified through our genetics and pre-natal programming- leading to continued weight stabilization in some, weight gain and weight gain + complications in others,
  • Lets dig deeper and ask our selves how we got here. Dr. Whitaker did just that in a recent commentary published in Archives of Pediatr Adol Medicine. He asked how our societal values and way of life might give way to obesigenic environments and behaviours. A deeper look at The why behind our physical activity levels and the food choices we make Connectedness is critical to well being. While we are more connected on a global level than ever before, we are less connected on a more local level- to our cities, our communities and our neighbourhoods. Communication/contact occurs more and more through electronic media. Time pressures are increasing we are working more than ever (even southern Europeans), Increased work hours means less time for sleep, play, cooking etc. Income inequality has reached levels not seen since the Great Depression- This leads to increasing food insecurity, social unrest and possible decreased neighbourhood safety. Economic Policy has affected the way we design our cities- urban sprawl, Agricultural subsidies and food industry lobbyists, Media and advertising and the billion $ diet industry affect our food choices
  • These changes to our social fabric, way of life, our values can affect health on multiple levels- rising raies of obesity but also mental health disorders, eating disorders, bullying, stigma and negatively impact our environment
  • Zooming in now- looking at the biology REALities behind the energy balance equation. The drive to eat/burn or store energy is to a large extent hardwired. Our bodies were designed to protect against starvation NOT obesity. Our body will therefore defend the highest weight attained through a complex neuroendocrine system. There are peripheral signals of short term and long term nutritional status that our integrated within the ventromedial hypothalamus where neuropeptides that stimulate or decrease appetite are secreted and where there is a drive towared energy expenditure or energy storage. We will focus on just a few of these today. Ghrelin is secreted by the stomach and increases at meal times and acts at the VMH to promote secretion of appetitie stimulating hormones to make us feel hungry- in response to a meal Ghrelin levels will decrease. PYY3-36 is secreted by the intestine to let you know when you have had enough to eat. It acts at the level of the VMH to stimulate production of neuropeptides that signal satiety. Leptin is secreted by your adiposites and is a long term signal of nutritional status. In the presence of lots of leptin your body should feel like it is ok to spend energy and not feel hungry. A drop in leptin with increase secretion of appetite signaling neuropeptides- making you feel hungry and will cause your body to want to store energy.
  • Leptin is your body’s long term signal of nutritional status – Obese individuals are Leptin RESISTANT- so there Leptin set point is higher than non-obese individuals= this results in defense of a higher weight.Obese individuals have lower levels of PYY3-36- now remember- PYY3-36 is the peripheral signal that tells your body you’ve had enough to eat at a meal time- perhaps this signal is muted in obese individuals as they have lower levels- leading to increased intake?
  • Hormonal adaptations to weight loss promote weight REGAIN. These adaptations are present up to a year post weight loss. Ghrelin your hunger hormone- the peripheral signal to the VMH to increase secretion of appetitie stimulating neuropeptides increases after weight loss. A stronger stimulus of hunger- leading us to eat more and regain weight
  • In the face of weight loss Leptin levels decrease- this drop in leptin increases secretion of appetite stimulating neuropeptides and decreases secretion of anorexic neuropeptides making us feel more hungry – A drop in Leptin also results in promotion of energy storage and a decrease in energy expenditure.
  • Any decrease in body weight results in decreased day to day energy expenditure- it takes less energy for yoru body to function since it is now smaller and weighs less. At the same time hormonal adaptations to weight loss lead to increased energy conservation. This means for your body to continue to lose weight you will need to decrease your intake further and ramp up your physicial activity more- this becomes untenable. Remember if you have a patient whose lost weight and now has plateaud or re-gained the weight- it may not be because they are no longer engaging in the health behaviiours you discussed with them- but rather secondary to the biologic realities of weight loss.
  • Many feel that a contributing factor to weight gain in obese kids is the fact that they are less active. Well through the work of HALO’s Rachel Colley, looking at CHMS data at Health Canada we can see that there is no marked difference in physical activity levels between overweight and lean kids.
  • We all recognize obesity as a risk factor for some chronic diseases- but increasingly we are seeing evidence of the obesity chronic disease paradox in the literature. = In fact OWT and moderate obesity is NOT associated with a decrease in life expectancy and may provide a survival advantage in a # of chronic diseases including Renal Failure, Heart Failure, T2DM
  • In this study by Dohner- they looked at all cause mortality (A) and all cause mortality and hospitalization in 5000 patients with T2DM and pre-existing CVD and found that the lowest mortality was in those patients with BMI of 30-35. Weight loss was associated with increased total mortality and cardiovascular mortality.
  • Stage 0 patients have no obesity related risk factor, physical, psychological symptoms and no functional limitationsStage 1 have sibclinical obesity related risk factors, mild physical symptoms- not requiring medical treatment for comorbidities. Mild obesity related psychological disturbance. Or mild impairment in well being- Stage 4 have severe end stage form of obesity related chronic disease, severe disabling psych symptoms or severe functional impairment.
  • EOSS is compared to the more classic classification of obesity based on BMI developed by the WHO – Class I- 30-35, ClassII 35-40, ClassIII>40
  • Managing obesity the rea lities striking a balance

    1. 1. Managing Obesity: The REALities Striking a Balance... Weigh in with Knowledge, Research, Practice SYMPOSIUM September 30th 2013
    2. 2. The REALities: Objectives • Biologic REALities • Psychosocial REALities • Impact of Weight Bias • Debunking Common Myths • Paradigm Shift • Health At Every Size (HAES) • Edmonton Obesity Staging System • The Pediatric 5A’s
    3. 3. Obesity is Defined as BMI > 95th%
    4. 4. Limitations of BMI • Not sensitive/ specific for: • Presence of obesity related risk factors • Health behaviours • Co-morbid conditions • Psychopathology • Global functioning • Global health • Quality of Life
    5. 5. Limitations of BMI BMI= 32 kg/m2 BMI= 21 kg/m2
    6. 6. Obesity is…. • A sign or symptom • A disorder of energy balance • Adaptive/ Maladaptive? • A risk factor for disease • Modifiable through health behaviours
    7. 7. Obesity is not…. • A sensitive indicator of health • A sensitive indicator of health behaviours • A character flaw • A lack of will power
    8. 8. WEIGHT = ENERGY CONSUMPTION – ENERGY EXPENDITURE Genetics SES Culture Stress Sleep Media Parental influence Peer influence School environment Neighbourhoods Gender Policy Medications Microbes Environmental Toxins Built Environment Safety Screen Invasion Food Insecurity Automobile Reliance Societal Influences Education Access Perinatal programming Mental health Eating disorders Body Image
    9. 9. Obesogenic Environment Obesogenic behaviours Weight Gain Weight Stable Weight Gain & Co-morbidities Sensitivity to obesogenic environments and behaviours modified through genetic and pre-natal programming Beyerlein et al, PLoS one (2011)
    10. 10. Digging Deeper Connectedness electronic virtual Time pressures more work hours sleep less cook less increased stress Income Inequality food insecurity neighbourhood safety Economic Policy urban sprawl agricultural subsidies food industry media/advertising Our Way of Life Societal Values Whitaker R, Arch Pediatr Adol Med (2011)
    11. 11. Impact of Social Values • Obesity • Mental Health • Eating Disorders • Bullying, Stigma • Health of our environment Common Ground/Partnerships Whitaker R, Arch Pediatr Adol Med (2011)
    12. 12. A Lot on My Plate JackLightfootaka Heavyhand
    13. 13. Neuroendocrine Control of Energy Balance Science, Feb 7, 2003
    14. 14. Neuroendocrine Differences: Lean vs. Obese PYY3-36 Batterham, R. L. et. al. N Engl J Med 2003;349:941-948 Leptin
    15. 15. Hormonal Adaptations to Weight Loss: Ghrelin Cummings, D. E. et. al. N Engl J Med 2002;346:1623-1630
    16. 16. Hormonal Adaptations to Weight Loss: Leptin
    17. 17. Decrease in Body Weight Decreased Energy Expenditure Increased Energy Conservation Additional weight loss can only be achieved by a more severe diet and further increases in physical activity Katan B et al JAMA (2010)
    18. 18. Debunking Some Myths
    19. 19. Are Obese Kids less Active? • No marked difference in physical activity between overweight and lean kids • Overweight and obese girls had the same minutes of moderate to vigorous physical activity as lean girls • Overweight boys had 14 min and obese boys had 22 min less of daily activity than lean boys Colley R et al, Health Reports (2011)
    20. 20. Obesity-Chronic Disease Paradox • Overweight and moderate obesity (BMI < 35), is not associated with a decrease in life expectancy • Overweight is associated with increased longevity • Survival advantage: • Renal Failure • Heart Failure • Type 2 Diabetes McGee DL et al, Ann Epidemiol (2005) Curtis JP et al, Arch Int Med (2005) Beddhu S, Seminars in Dyalisis (2004) Doehner et al, Int J Cardiology (2011)
    21. 21. Obesity Chronic Disease Paradox 5202 patients with T2DM and pre-existing CVD: • Lowest mortality: BMI 30-35 kg/m2 • Weight loss associated with increased total mortality, cardiovascular mortality Doehner et al, Int J Cardiol (2011)
    22. 22. Abdulla J et al. Eur Heart J (2008) Myocardial Infarction (MI) Heart Failure (HF) 21,570 patients admitted for MI or HF All cause mortality after 10 year follow up • BMI > 35 associated with increased risk in MI but not HF • BMI 30-35 not associated with increased risk
    23. 23. Edmonton Obesity Staging System(Kuketal,2011) • New risk-stratification system that classifies adult obese individuals into 5 graded categories based on morbidity and health-risk profiles • EOSS independently predicted increased mortality even after adjustment for common methods of classifying obesity (Padwal et al., 2011)
    24. 24. Sharma AM & Kushner RF. Int J Obes 2009
    25. 25. Sharma AM & Kushner RF. Int J Obes 2009
    26. 26. Kuk et al, App. Physiol. Nutr. Metab. (2011) 29, 533 obese individuals Morbidity and Mortality Risk based on EOSS at 16 year follow up compared to normal weight controls
    27. 27. Padwal R S et al. CMAJ (2011) EOSS BMI Class Survival Curves diverge when stratified by EOSS score but not by BMI Class
    28. 28. Padwal R S et al. CMAJ (2011) EOSS-prediction of all cause mortality across BMI classes
    29. 29. Expected Change in BMI (6-12 months) Lifestyle Medication (orlistat) Surgery Δ BMI (kg/m2) -1.9-3.3 -0.85 -8.5 USPSTF Task Force, Pediatrics (2010) Journal of Pediatric Surgery (2010)
    30. 30. The Psychosocial REALities What is it like for children and youth who have a higher BMI?
    31. 31. Psychosocial REALities Overweight youth: • Are stigmatized • Are often bullied by peers • Tend to have poor body image • Tend to have lower self-confidence, self- esteem and higher incidence of mental health problems Puhl et al. Obesity (2009) Storch et al. J. Pediatr. Psychol. (2007)
    32. 32. Bullying • 30% of overweight girls and 25% of overweight boys experience weight focused peer victimization • 60% of the most severely overweight kids report harassment • 40% of youth report that obesity is the primary reason why peers are teased or bullied • 37% reported being gay or lesbian as the primary reason • 10% reported race, ethnicity, disability, religion Eisenberg M et al Arch Pediatr Adolesc Med (2003) Puhl RM et al, J Sch Health (2011)
    33. 33. Weight Bias at home • 47% of overweight girls and 34% of overweight boys report being teased about their weight by their parents • 72% of overweight adults reported they had experienced weight bias from family members as children Puhl RM et al, J Sch Health (2011) Puhl RM et al, Psych Bull (2007)
    34. 34. Societal Pressures • In Western Society the media is a powerful influence and pressure on youth today • Body image messages are ever present and typically state: • Thin women are beautiful, successful and happy • Muscular, lean men are handsome and successful Grabe et al. Psychological Bulletin (2003)
    35. 35. THIN, THIN, THIN
    37. 37. Body Image in Youth Today • 40-50% of girls aged 11-15 say they need to lose weight • 61% of grade 7/8 students trying to lose weight Canadian study: Jones et al. 2001
    38. 38. Weight Based Teasing and Discrimination
    39. 39. Youth Often Feel • Angry • Frustrated • Sad • Helplessness • Hopelessness • Anxious • Worried
    40. 40. Families Often Feel • Guilty • Helpless • Frustrated • Tired • A desire to try and fix or “control” things • A loss of trust with the youth
    41. 41. The Diet Industry Culture Familiar Claims:  “Lose weight quickly”  “Reset your genetic code”  “Eat all you want – Lose up to 30 pounds in 3 weeks”  “Scientifically sound”, “Based on proven studies” Private weight loss industry in the US estimated at $58.6 billion annually (Marketdata Enterprises, 2009) Pawlak, 2009
    42. 42. Mixed Messages in the Media around Food
    43. 43. Set Point Theory Our bodies have a Set Point (range) it wants to stay at and would if we eat “normally” • Our bodies are self-regulating • Think of shoe size, height and body temperature • Set point is a range & genetically determined • Our body works hard to keep us in the range • Altering metabolic rate Wilmore et al. (1999)
    44. 44. Restraint Theory • Research has examined eating behaviour of Dieters vs. Non-Dieters • Laboratory studies demonstrated that Dieters are more likely to ‘overeat’ or disinhibit when exposed to: • Stress • Emotional Cues • Food Cues Herman & Polivy, 1985
    45. 45. Restraint Theory Results in “What the Hell Effect” BATTLE Dieters cognitive or mental efforts to resist that drive Dieters physiological drive to eat (e.g., hormones & peptides)
    46. 46. Culture of Valuing Thinness • High body self-consciousness • Healthy body esteem • High weight preoccupation • Increased overeating • Emotional eating • Binge eating • Dieting practices • Weight loss strategies Feelings of shame, guilt, anger, sadness Increased weight over time Negative Spiral
    47. 47. The Impact of Living with Weight Management Issues in Today’s World Puhl RM et al, J Sch Health (2011) Puhl RM et al, Psych Bull (2007 Low body satisfaction High depressive symptoms Isoloation/withdrawal Poor-self-perception of physical appearance Disordered eating Poor academic outcomes Poor peer relationships Increase risk & unhealthy behaviours School absences
    48. 48. Medical Versus Self Esteem Concerns Most Kids: • Want to lose weight to make the teasing and harassment stop • They would prefer to have diabetes and be thin than to be “fat” and “healthy” But by suggesting that children focus on weight as an outcome we are setting them up for weight preoccupation, dieting and likely weight gain
    49. 49. A paradigm shift… A growing trans-disciplinary movement called: Health at Every Size HAES challenges the value of promoting weight loss and argues for a shift in focus to weight- neutral outcomes
    50. 50. Bacon & Aphramor (2011)
    51. 51. The HAES Approach The HAES approach is associated with statistically and clinically relevant improvements in:  Physiological measures (e.g. blood lipids)  Health behaviours (e.g. eating & activity habits)  Psychosocial outcomes (e.g. self esteem and body image) Bacon L et al, 2011
    52. 52. Key Principles
    53. 53. Key Principles Obesity Management is About Improving Health and Well- being, and not Simply Reducing Numbers on the Scale
    54. 54. Weight bias can be a barrier to weight management Key Principles
    55. 55. Interventions should include addressing ‘root causes’ of obesity and removing roadblocks for families to make healthy changes Key Principles
    56. 56. A Child’s ‘Best’ BMI May Never Be His or Her ‘Ideal’ BMI Key Principles
    57. 57. Success is different for every child and family Key Principles
    58. 58. The 4Ms of Pediatric Obesity Mental Anxiety Depression Body image ADHD Learning disorder Sleep disorder Eating disorder Trauma Mechanical Sleep apnea MSK pain Reflux disease Enuresis Encopresis Intertrigo Metabolic IGT/T2DM Dyslipidemia Hypertension Fatty liver Gallstones PCOS Medication Genetics Milieu Parent health/disability Family stressors Family income Bullying/Stigma School attendance School support Neighbourhood safety Medical insurance Accessible facilities Food Environment Opportunities for physical activity ASSESS
    59. 59. Questions?
    60. 60. CHAL Team Dr. Stasia Hadjiyannakis – Pediatric Endocrinologist Dr. Katie Baldwin– Pediatrician Dr. Annick Buchholz – Psychologist Dr. Laurie Clark – Psychologist Jane Rutherford – Exercise Specialist Nicole Charette – Registered Dietitian Shaun Reid – Child & Youth Counsellor Maura Manuel– Social Worker Michèle Levasseur – Registered Nurse, Case Manager Corrie Raymond – Administrative Assistant Charmaine Mohipp – Research Associate
    61. 61. Mission To improve the health and quality of life of children with weight related health complications and support them and their families in achieving a healthy active lifestyle.
    62. 62. Severe Complex Obesity • BMI > 99th% AND/OR • Complications of obesity requiring subspecialty care • Hyperlipidemia requiring pharmacotherapy • Hypertension requiring pharmacotherapy • OSA/Sleep Disordered Breathing • PCOS • NAFLD • T2DM/Persistent IGT • Hypothalamic Obesity • Obesity Syndromes
    63. 63. Referral Invitation to Information Session Full Day Assessment/Care Plan
    64. 64. Treatment Options Care Plan REAL Program Care Coordination Clinic visits to assess readiness Community Resources
    65. 65. PHASE I Family Education Group (for teens 14-18 yrs + parents)  Education on Family approach to healthy living and lifestyle change  6 weeks Parent Group (for parents of children ≤ 13 yrs)  Education on parenting approaches to healthy living and lifestyle change  8 weeks What is the REAL Program?
    66. 66. What is the REAL Program PHASE II Family Group (for teens 14-18 yrs + parents)  Skill building for families to make lifestyle changes together  Topics include:  Healthy Eating & Active Living  Problem Solving and Practical Solutions to meet goals  12 weeks (parents attend 5 weeks)
    67. 67. What is the REAL Program? PHASE III Teen & Parents Alumni Groups  Peer support for maintaining lifestyle changes  Skill building for “slips” and “getting back on track”  Theme based modules  Offered in 4 week modules
    68. 68. REAL Program Goals • Improve quality of life • Decrease medical and psychological co-morbidities • Improve eating behaviours • Improve fitness, increase activity levels • Decrease sedentary behaviour • Empower/strengthen families • Stabilize BMI trajectory
    69. 69. Baseline Mental Health Concerns Diagnosis Frequency ADHD and/or LD 25.7% Anxiety Disorder 24.2% Developmental Delay/Autism 11.4% Depression 11.4% TOTAL 60%
    70. 70. Conclusions • Understand your patients’ REALities • Focus on health behaviours and well being • Health is possible across a range of BMI • Help without harming • Weight bias increases risk for co-morbidities • Take your time- no quick fixes