1. 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 Cairns
Robyn McDermott
Centre for Chronic Disease Prevention
Australian Institute of Tropical Health & Medicine

2. 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

3. 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 that
Finally, what does all this mean for health services, the environment and the economy, and what can be done.

4. 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

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

7. Diabesity in the USA

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

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

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

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

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

16. 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

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

18. Aboriginal adults (Central Australia) 1930s

19. Torres Strait Islanders, 1930’s-40’s

20. Various theories 2: FOOD Global pandemic diabesity since 1980 and the hunt for culprit foods New foods: cheap calories and processing
Fats
Fructose
Portion size drift
Availability, affordability and the social gradient

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

22. Sugar consumption and obesity prevalence in the USA, 1700-2000
Source: Johnson et al, 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

23. Dietary fructose in non-alcoholic fatty liver disease
In NAFLD, ingested fructose may alter the microbiome, increasing movement of endotoxin into the portal system because of increased permeability of tight junctions. Endotoxin and fructose enter the liver where endotoxin increases inflammation and insulin resistance through activation of Toll‐like receptor 4 (TLR4). Fructose is rapidly metabolized, consuming adenosine triphosphate (ATP), which may result in increased adenosine monophosphate (AMP) and conversion to uric acid. Excess triglyceride produced through stimulation of de novo lipogenesis (DNL) is packaged onto large, TG‐rich very low density lipoproteins (VLDL) or in the setting of imbalance can result in increased steatosis in the liver. Steatosis may also be driven by increased return of nonesterified free fatty acids (NEFA) from adipose tissue.
© This slide is made available for non-commercial use only. Please note that permission may be required for re-use of images in which the copyright is owned by a third party.
Hepatology Volume 57, Issue 6, pages , 1 MAY 2013 DOI: /hep

24. Energy cost and food prices
When we applied this to the community food supply using the store data we found exactly the same picture as that of Drewnowski and team.
Sugar, flour, rice, margarine and oil all cost less than 20c/MJ.
On the other hand fruits and vegetables and fresh meat cost the most in terms of energy value.
You may ask well how does this apply to take away food – the cost, convenience and taste of buying a pie at $1.67/MJ may outweigh the cost of buying a prepared meat and salad pack at $7.30/MJ.
$2.72/MJ
$7.40/MJ
$54.60/MJ
$0.14/MJ
Source: Brimblecombe and O’Dea, MJA, May 18, 2009 24

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

26. Chronic short sleep has consequences for health
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)
Chronic short sleep has consequences for health
New York Times, 10 / 99 26

27. Sleep, Obesity and T2 Diabetes
43% increased risk of incident diabetes for every quartile of Obstructive Sleep Apnea severity (Botros, 2009)
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) 27

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

29. 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 genome
The micro-biome performs digestive and metabolic functions, and “evolves” over our life course
The micro-biome “talks” to the liver, the brain, organs controlling metabolism, inflammation and the immune system
The micro-biome is affected by what we put into our mouths

30. The gut micro biome has a regulatory function on host energy metabolism.
The gut microbiome has a regulatory function on host energy metabolism. By breaking down nondigestible polysaccharides, gut microorganisms produce monosaccharides and short-chain fatty acids (SCFAs). SCFAs bind to GPR 41/43 receptors and stimulate peptide YY (PYY) production, which inhibits gut motility and allows gut microbes to digest more polysaccharides. Gut microbes also regulate energy metabolism by reducing the expression of fasting-induced adipocyte factor (Fiaf) from gut epithelial cells. Suppressed Fiaf release results in the degradation of lipoproteins and deposition of free fatty acids in adipose tissues. The adiposity in liver and skeletal muscles is also regulated by microorganisms through the changes of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) levels. LPL, lipoprotein lipase; VLDL, very low-density lipoprotein.
Source: Krajmalnik-Brown R et al. Nutr Clin Pract 2012;27:

31. Effect of Intestinal Microbial Ecology on the Developing Brain
JAMA Pediatr. 2013;167(4): doi: /jamapediatrics
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.

32. Disruptions to the gut microbiome
Diet: eg High fat diet is associated with reduced microbiome diversity
Disease states: Mainly association studies (causal direction unclear) for diabetes, some cancers, obesity, “irritable bowel”, others
Antibiotics: 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.

33. What to do?
BAU – we go broke
One solution? Unlikely
Unhelpful sloganeering and ideological corners: “nanny state”, “personal responsibility” and the role of government
Technical individual-level solutions? Eg Bariatric surgery, various diets combined with sustainable exercise
Society-level solutions: town planning (active transport and healthy food supply), workplace re-design, taxation and regulation.

35. Michael Pollan, “What to eat”
…and finally,
Eat food,
mostly plants,
not too much
Michael Pollan, “What to eat”