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Epidemic obesity: where did it come from, what does it mean and where do we go from here Epidemic obesity: where did it come from, what does it mean and where do we go from here

Epidemic obesity: where did it come from, what does it mean and where do we go from here - PowerPoint Presentation

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Epidemic obesity: where did it come from, what does it mean and where do we go from here - PPT Presentation

Epidemic obesity where did it come from what does it mean and where do we go from here Science and Society in the Tropics Public Lecture May 21 2014 Cairns Robyn McDermott Centre for Chronic Disease ID: 772983

diabetes obesity source sleep obesity diabetes sleep source system 2013 risk gut biome theories food central micro nervous time

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Epidemic obesity: where did it come from, what does it mean and where do we go from here? Science and Society in the TropicsPublic Lecture May 21 2014 CairnsRobyn McDermottCentre for Chronic Disease PreventionAustralian Institute of Tropical Health & Medicine

Epidemics appear, and often disappear without traces, when a new culture period has started; thus with leprosy, and the English sweat. The history of epidemics is therefore the history of disturbances in human culture Virchow, 1870

Tonight…. The health transitions which have taken place in humans in the past million or so years,The various theories behind the global obesity and diabetes pandemic seen in the last 30 years, Ethnic variation in susceptibility to “diabesity”, and what we can infer from thatFinally, what does all this mean for health services, the environment and the economy, and what can be done.

Reasons to be optimistic Perhaps the single greatest achievement of the modern world has been a reduction in death rates nearly everywhere and probably a very substantial increase in the proportion of the world’s inhabitants who feel really well most of the time.John Caldwell, 1989

25 50 % Communicable diseases, maternal and perinatal conditions and nutritional deficiencies Injuries DALYs, by broad cause group 1990 - 2020 in Developing Countries (baseline scenario) DALY = Disability adjusted life-year 1990 2020 Source: WHO, Evidence, Information and Policy, 2000 Noncommunicable conditions

Diabesity in the USA

Obesity spread via social networks: The Framingham offspring study Source: Christakis, NEJM 2007

Prevalence of diabetes, Indigenous NQ (WPHC) and Australia ( AusDiab), 1999-2000 Source: McDermott et al, AHR 2003

Generational transmission of diabesity Low birth weight, combined with weight gain in adulthood, increases risk of CVD, diabetes, some cancersMaternal obesity amplifies the risk of diabetes in pregnancy, birth defects, childhood obesity and type 2 diabetesMaternal obesity increases early death (before age 60) by 35% in the offspring (BMJ 2013)

Mean women’ s waist change over 5 years (cm), 1999-2005 FNQ Source: McDermott et al, PHN 2009

Dementia = “type 3 diabetes”Risk of incident dementia by baseline glucose (no diabetes) Source: Crane et al NEJM 2013 369:6 (pp540-8)

Various theories 1: GENES Observations on ethnic differences in susceptibility and genetic adaptation in populations in a changing environment“Thrifty gene”“Drifty gene”“Out of Africa”: Migration and metabolic adaptation to climate stressors

Source: Sellayah D, et al “On the evolutionary origins of obesity: a new hypothesis. Endocrinology 2014:doi: 10.1210en.2013-2113Human migrations and metabolic adaptation to different environmental stressors: a new theory for ethnic obesity variation

Aboriginal adults (Central Australia) 1930s

Torres Strait Islanders, 1930’s-40’s

Various theories 2: FOOD Global pandemic diabesity since 1980 and the hunt for culprit foodsNew foods: cheap calories and processingFatsFructosePortion size driftAvailability, affordability and the social gradient

Coronary mortality (deaths per 100,000) as a function of saturated fat intake Source: Kromhout et al Seven Countries Study, 1995 Prev Med

Sugar consumption and obesity prevalence in the USA, 1700-2000 Source: Johnson et al, 2007. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease and cardiovascular disease. Am J Clin Nutrition

Dietary fructose in non-alcoholic fatty liver disease Hepatology Volume 57, Issue 6, pages 2525-2531, 1 MAY 2013 DOI: 10.1002/hep.26299 http://onlinelibrary.wiley.com/doi/10.1002/hep.26299/full#fig1

Energy cost and food prices $0.14/MJ $2.72/MJ $7.40/MJ $54.60/MJ Source: Brimblecombe and O’Dea, MJA, May 18, 2009

Various theories 3: SITTING and not sleeping Immobility (screen and car time) and sleep deprivation

Creeping Sleep Loss Under sleep: Australians sleep 7.25 ± 1.48 h/night during the week and 7.53 ± 2.01 h/night on weekends 18.4% working age group sleep <6.5 h/night Chronic sleepiness in 11.7% (Bartlett 2007) Longer workday: Since 1969, Americans have added 158 hours/year to the workday (USA census data) Longer commute: Work time and travel time the primary activities reciprocally related to sleep time among Americans (ATUS, Basner 2007 ) New York Times, 10 / 99 Chronic short sleep has consequences for health

Sleep, Obesity and T2 Diabetes 125-193% Risk of future obesity in short sleepers (Gangwisch 2005) 50-150% Greater risk of short sleepers for developing type 2 diabetes ( Gangwisch 2007 & Gottlieb 2005) 43% increased risk of incident diabetes for every quartile of Obstructive Sleep Apnea severity ( Botros , 2009)

Pathways linking sleep loss to insulin resistance and diabetes Sleep apnoea Sleep loss “Lifestyle choices” Elevated sympathetic activity Insulin resistance Diabetes Hypoxia Inflammation Obesity Diabetic autonomic neuropathy Mechanical airway obstruction Disordered appetite regulation Source: McDermott R. Diabetes Management, 2012

Various theories 4:The gut micro-biome Our gut hosts billions of microorganisms which contain more than 150 times the genetic diversity of the human genomeThe micro-biome performs digestive and metabolic functions, and “evolves” over our life courseThe micro-biome “talks” to the liver, the brain, organs controlling metabolism, inflammation and the immune systemThe micro-biome is affected by what we put into our mouths

The gut micro biome has a regulatory function on host energy metabolism . Source: Krajmalnik -Brown R et al. Nutr Clin Pract 2012;27:201-214

Effect of Intestinal Microbial Ecology on the Developing Brain JAMA Pediatr . 2013;167(4):374-379. doi:10.1001/jamapediatrics.2013.497 Enteric nervous system, providing bidirectional communication between gastrointestinal cells and the central nervous system. Intestinal epithelial cells mediate interactions between gut bacteria and the central nervous system or the immune system. As bacteria (shown in green) in the intestine come into contact with receptors (shown in black) on the intestinal wall cell surface, the receptors transmit signals to the central nervous system via the vagus nerve pathways (curved arrow to central nervous system) and to the immune system (curved arrow) via Toll-like receptor pathways.

Disruptions to the gut microbiome Diet: eg High fat diet is associated with reduced microbiome diversityDisease states: Mainly association studies (causal direction unclear) for diabetes, some cancers, obesity, “irritable bowel”, othersAntibiotics: Effects are immediate and potentially long lasting, especially important for children Bariatric Surgery : Rapid changes in food intake, metabolism (including reversal of T2diabetes), fat mass, inflammation, microbiome composition .

What to do? BAU – we go brokeOne solution? UnlikelyUnhelpful sloganeering and ideological corners: “nanny state”, “personal responsibility” and the role of governmentTechnical individual-level solutions? Eg Bariatric surgery, various diets combined with sustainable exerciseSociety-level solutions: town planning (active transport and healthy food supply), workplace re-design, taxation and regulation.

…and finally, Eat food, mostly plants, not too muchMichael Pollan, “What to eat”