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The Roots of the Obesity Epidemic

The Roots of the Obesity Epidemic . Katherine L Tucker, Phd Chair, Department of health sciences Northeastern university. “Obesity is the loss of the coordinated control of caloric intake and energy expenditure” ( Velloso , 2012).

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The Roots of the Obesity Epidemic

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  1. The Roots of the Obesity Epidemic Katherine L Tucker, Phd Chair, Department of health sciences Northeastern university

  2. “Obesity is the loss of the coordinated control of caloric intake and energy expenditure” (Velloso, 2012) “Today, 66 percent of adults in the United States are considered overweight or obese. Obesity puts people at increased risk for chronic diseases such as heart disease, type 2 diabetes, high blood pressure, stroke, and some forms of cancer.” http://win.niddk.nih.gov/publications/understanding.htm By 2015 the numbers of overweight and obese individuals globally are expected to reach 2.3 billion and 700 million, respectively Malik, V.S., et al. Sugar Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk. 2010. Contemporary Reviews In Cardiovascular Medicine. Vol. 121. pp. 1356-1364 Velloso, L.A. Maternal consumption of high fat diet disturbs hypothalamic neuronal function in the offspring: implications for the genesis of obesity. 2012. Endocrinology. Vol. 153, No. 2, pp. 543-545 http://www.cdc.gov/obesity/causes/index.html

  3. Obesity Trends* Among U.S. AdultsBRFSS, 1985 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14%

  4. Obesity Trends* Among U.S. AdultsBRFSS, 1986 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14%

  5. Obesity Trends* Among U.S. AdultsBRFSS, 1987 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14%

  6. Obesity Trends* Among U.S. AdultsBRFSS, 1988 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14%

  7. Obesity Trends* Among U.S. AdultsBRFSS, 1989 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14%

  8. Obesity Trends* Among U.S. AdultsBRFSS, 1990 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14%

  9. Obesity Trends* Among U.S. AdultsBRFSS, 1991 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19%

  10. Obesity Trends* Among U.S. AdultsBRFSS, 1992 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19%

  11. Obesity Trends* Among U.S. AdultsBRFSS, 1993 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19%

  12. Obesity Trends* Among U.S. AdultsBRFSS, 1994 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19%

  13. Obesity Trends* Among U.S. AdultsBRFSS, 1995 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19%

  14. Obesity Trends* Among U.S. AdultsBRFSS, 1996 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19%

  15. Obesity Trends* Among U.S. AdultsBRFSS, 1997 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% ≥20%

  16. Obesity Trends* Among U.S. AdultsBRFSS, 1998 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% ≥20%

  17. Obesity Trends* Among U.S. AdultsBRFSS, 1999 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% ≥20%

  18. Obesity Trends* Among U.S. AdultsBRFSS, 2000 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% ≥20%

  19. Obesity Trends* Among U.S. AdultsBRFSS, 2001 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% ≥25%

  20. Obesity Trends* Among U.S. AdultsBRFSS, 2002 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% ≥25%

  21. Obesity Trends* Among U.S. AdultsBRFSS, 2003 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% ≥25%

  22. Obesity Trends* Among U.S. AdultsBRFSS, 2004 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% ≥25%

  23. Obesity Trends* Among U.S. AdultsBRFSS, 2005 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

  24. Obesity Trends* Among U.S. AdultsBRFSS, 2006 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

  25. Obesity Trends* Among U.S. AdultsBRFSS, 2007 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

  26. Obesity Trends* Among U.S. AdultsBRFSS, 2008 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

  27. Obesity Trends* Among U.S. AdultsBRFSS, 2009 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

  28. Obesity Trends* Among U.S. AdultsBRFSS, 2010 (*BMI ≥30, or ~ 30 lbs. overweight for 5’ 4” person) No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

  29. Obesity Trends* Among U.S. AdultsBRFSS,1990, 2000, 2010 (*BMI 30, or about 30 lbs. overweight for 5’4” person) 2000 1990 2010 No Data <10% 10%–14% 15%–19% 20%–24% 25%–29% ≥30%

  30. So What Happened?

  31. The Environment an environment that promotes excessive food intake and discourages physical activity. Although humans have evolved excellent physiological mechanisms to defend against body weight loss, they have only weak physiological mechanisms to defend against weight gain when food is abundant. Control of portion size, consumption of a diet low in fat and energy density, and regular physical activity are behaviors that protect against obesity, but it is difficult to maintain these behaviors in the current environment. • James O. Hill and John C. Peters Environmental Contributions to the Obesity Epidemic • DOI: 10.1126/science.280.5368.1371

  32. Popkin B, The World is Fat “…from 30 years ago to today, we've had an exponential explosion in what we can think of as the "obesogenic environment." You see food available everywhere. ..In most of the world, it used to be that people mostly drank water… The average American has … added 22 ounces of caloric beverages to his diet, …300 extra calories per day. We naturally prefer sweet and fatty foods because of what those foods used to mean for survival when we were hunter-gatherers. They had the nutrients we needed, and they let us store more energy for the hungry season. Popkin, B., The world is fat. Scientific American. 2007 . Vol. 297, pp. 88 – 95  doi:10.1038/scientificamerican0907-88

  33. Sweetness Preference was Essential to Survive: Huge Shift in Amounts, Energy Density Popkin, B., The world is fat. Scientific American. 2007 . Vol. 297, pp. 88 – 95  doi:10.1038/scientificamerican0907-88

  34. P=0.005 P=0.235 Gene*Diet Interaction • Mattei, J., et al. Apolipoprotein A5 Polymorphisms Interact with Total Dietary Fat Intake in Association with Markers of Metabolic Syndrome in Puerto Rican Older Adults. 2009. The Journal Of Nutrition Genomics, Proteomics, and Metabolomics. Vol. 139, pp. 2301-2308 Ghr.nlm.nih.gov

  35. Technological clashes with human Biology Popkin, B.M., et al. Global Nutrition transition and the pandemic of obesity in developing countries. 2011. Nutrition Reviews. Vol. 70, No. 1, pp. 3-21. doi:10.1111/j.1753-4887.2011.00456.x

  36. Sources of Major Global Dietary Shifts Popkin, B., The world is fat. Scientific American. 2007 . Vol. 297, pp. 88 – 95  doi:10.1038/scientificamerican0907-88 Globally: large increases in consumption of caloric beverages and increasing snacking increased intake of ultra processed foods, refined carbohydrate reduced intake of fruits and vegetables and legumes reduced preparation time, increased use of precooked foods Lower income countries: increased edible oil

  37. Sugar Sweetened Beverages & Artificial Sugar • In the U.S., calories from caloric beverages reached 21.0% by 2002 • Several metabolic outcomes relate to regular diet beverage consumption, particularly when coupled with certain dietary patterns such as a Western diet • “fructose acutely increases thermogenesis, triglycerides, lipogenesis and blood pressure…In controlled feeding studies, changes in body weight, fat storage and triglycerides are observed as well as an increase in inflammatory markers.“ Bray 2010 • Diet soda has been associated with a greater risk of incident metabolic syndrome, type 2 diabetes, and doubled the risk of overweight and obesity • Tate, D.F., et al. 2012. Am J ClinNutr. Vol. 95, pp. 555-63. • Duffey, K.J., et al. 2012. Am J ClinNutr. Doi: 10.3945/ajcn.111.026682 • Bray, G.A. Current Opinion in Lipiology. 2010. Vol 21 , No. 1 , p p.51–57 • fatshapeofitshape.blogspot.com

  38. Behavior People who consume >= 1 sugar sweetened beverage per day have a 26% greater risk of developing type 2 diabetes and 20% greater risk of developing the Metabolic Syndrome. Malik et al Metabolic Syndrome was highest in women with an Empty Calorie dietary pattern in the Framingham Heart Study. Sonnenberg et al Malik, V.S., et al.. 2010. Diabetes Care. Vol. 33, No. 11, pp. 2477-2483. Sonnenberg, L., et al. 2005. Obesity Research. Vol. 13, No. 1, pp. 153-162. Dietsinreview.com

  39. Baltimore Longitudinal Study of Aging 459 men and women, 30-80 y Newby et al Am J ClinNutr2003;77:1417–25.

  40. Change in BMI(Kg/m2/y) *

  41. Change in Waist Circumference(cm/y) *

  42. Glycemic Index • Foods high on the GI chart can increase appetite, cause weight gain and increase risk for obesity (Monsivais, 2011) • Replacing saturated fatty acids with carbohydrates low on the GI was protective against MI • Replacing them with carbohydrates high on the GI yielded a higher risk of MI (Jakobsen 2010) • Lower risks of CHD from a low GI diet may be through lower insulin and blood glucose (Rahelic, 2011) • Monsivais, P., et al. s. 2011. Appetite. Vol. 56, pp. 9-14 • Jakobsen, M.U., et al.. 2010. Am J ClinNutr. Vol. 91, pp. 1764-8 Prostate-cancer.org, peaknutrition.wordpress.com • Rahelic, D, et al.2011. CollAntropol. Vol. 35, No. 4, pp. 1363-1368

  43. Culture Many food companies are ignoring the caloric value requirements and recommendations for the public to view in their establishments (Mooney, 2012) • Evidence that a diet high in fat yields a significant percentage of new cells in a part of the brain related to the hypothalamus where hunger, thirst, and eating controls are executed. • The heightened level of brain cells in this area may interrupt normal hunger and eating regulations in that area • Fox News Report • http://www.foxnews.com/health/2012/03/26/fatty-diet-may-casue-new-brain-cells-to-sprout/ Theblaze.com, yogiwellnesshourney.blogspot.com , healthdoctrine.com Mooney, H. BMJ2012;344:e2131

  44. Marketing & Advertisement • Huang et al state: • Human imaging studies suggest that the brain has automatic approach responses to food that these can be influenced by product advertisingand pricing. • The reward and executive control patterns in the brain can be induced and modulated by palatable, energy-dense foods in a way similar to addictive substances. • These neural systems are powerful in defending the body from undernutrition but have little capacity to defend against overnutrition. (Huang, 2009) Huang, T.T., et al. A systems oriented multilevel framework for addressing obesity in the 21st century. 2009. Preventing Chronic Disease. Vol. 6, No. 3, pp. 1-10 Writingfordesigners.com, esquire.com, goncava.com

  45. Childhood Obesity

  46. Factors in childhood obesity • Maternal diet and health can affect the risk of a child developing obesity via fetal programming. • A child is “biologically programmed” to more readily gain weight from signals in the womb and when they are later exposed to an obesigenic environment they then become overweight. • Bottle fed infants may have more childhood obesity than breastfed infants, due to overfeeding leading to loss of satiety signals. • More meals eaten outside the home (including fast-food), larger portion sizes, unhealthy school food and vending machines • Children no longer regularly walk or bike to school, reduced time in schools for PE, and lack of a safe environment for children to be active in. • Watching television, playing video games, and spending time on the computer are all sedentary activities Petersen C, http://eruditiononline.co.uk/experimentation/article.php?id=1306

  47. Metabolism & BehaviorChildhood Obesity • Overweight and obese children are at risk for: • 1. Respiratory disorders • 2. Decreased ventilatory function • 3. Hyperlipidemia • 4. Hyperinsulinemia • 5. Glucose intolerance • 6. Hypertension • 7. Joint problems • 8. Fatty liver disease • 9. Gall stones • 10. Acid reflux • 11. Social and psychological problems • Modifiable risk factors is KEY for • targeting and preventing childhood • obesity • Newby, P.K. et al. Beverage Consumption is not associated with changes in weight and body mass index among low-income preschool children in North Dakota. JADA. , 2004, doi:10.1016/j/jada.2004.04.020 • CDC.gov/childhoodoverweightobesity) Healthontherun.net, Epianalysis.wordpress.com,

  48. Environment Urbanization plays a significant role in the global obesity pandemic • Malik, V.S., et al. Sugar Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk. 2010. Contemporary Reviews In Cardiovascular Medicine. Vol. 121. pp. 1356-1364

  49. Environmental Estrogens and Endocrine Disrupting Compounds • Association of environmental estrogens – such as the synthetic estrogen diethylstilbestrol (DES), bisphenolA (BPA) used in the production of plastics, and phytoestrogens in foods such as soy isolates – has been shown with the development of obesity. • Links to other EDCs, such as organotins, phthalates, pesticides, and persistent organic pollutants in animal studies … are supported by both experiments with cells in culture and epidemiology studies. Newbold, R.R. Contribution of Endocrine Disrupting Chemicals to the Obesity Epidemic: Consequences of Developmental Exposure. Research and Perspectives in Endocrine Interactions, 2011, 101-112

  50. Medications Sympathetic activation is an important metabolic adaptation limiting weight gain. Weight-matched β-blocker users, compared to controls, showed diet-induced thermogenesis, fat oxidation rate and weekly habitual activity were lower by 50%, 32% and 30% (all P<0.04), respectively. Adjusted mean body weight of β-blocker users was 9.2 kg higher at baseline among those attending a diabetes clinic, 17.2 kg higher in a hypertension clinic compared with patients not treated with β-blockers. (all P<0.01) Conclusions: EE is reduced and body weight increased in chronic β-blocker users. Chronic β-blockade may cause obesity by blunting estradiol. Lee P, Kengne AP, Greenfield JR, Day RO, Chalmers J, Ho KKY. MetabolicSequelae of Β-blockerTherapy: Weighing in on The ObesityEpidemic? Int J Obesity 2011;35:1395-1403

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