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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 Cairns
Robyn McDermottCentre for Chronic Disease Prevention
Australian 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 that
• Finally, 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 - 2020in Developing Countries (baseline scenario)
DALY = Disability adjusted life-year
1990
2020
Source: WHO, Evidence, Information and Policy, 2000
Noncommunicableconditions
Prevalence of diabetes, Indigenous NQ (WPHC) and Australia (AusDiab), 1999-2000
0
10
20
30
40
50
60
15-24 25-34 35-44 45-54 55-64 65+
Non-IndigenousAboriginalTorres Strait Islander
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 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)
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: GENESObservations 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.2013-2113
Human migrations and metabolic adaptation to different environmental stressors: a new theory for ethnic obesity variation
Various theories 2: FOODGlobal pandemic diabesity since 1980 and the hunt
for culprit foodsNew foods: cheap calories and processing
• Fats• Fructose• Portion size drift• Availability, 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
0200400600800
100012001400
0 5 10 15 20 25
Sugar consumption and obesity prevalence in the USA, 1700-2000
1700 1750 1800 1850 1900 1950 20000
10
20
30
40
50
60
70
80
Sugar consumption (kg/p)Obesity prevalence (%)
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
HepatologyVolume 57, Issue 6, pages 2525-2531, 1 MAY 2013 DOI: 10.1002/hep.26299http://onlinelibrary.wiley.com/doi/10.1002/hep.26299/full#fig1
Energy cost and food prices
soft drink
biscuit
bread
cake
flourgrain/starch
pies
margarine
oil
dried Fruit
fruits
beef
chicken
egg
processed meat
milk confectionarysugar
hot chips
dried Veg
vegetablesFrozen Veg
crisps
01
02
03
04
0E
nerg
y de
nsi
ty (
MJ/
kg)
-2 0 2 4Energy cost ($/MJ)
Beverages
Cereals
Fats & oils
Fruit
Meat & meat products
Milk & milk products
Sugar & confectionary
Vegetables
$0.14/MJ $2.72/MJ $7.40/MJ $54.60/MJ
Source: Brimblecombe and O’Dea, MJA, May 18, 2009
Creeping Sleep LossUnder 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
Insulinresistance
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 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
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 BrainJAMA 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 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.
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.
High Risk & PopulationApproaches to Prevention
Truncate high risk end ofexposure distribution (e.g.organise an obesity clinic).
Clinical approach to diseaseprevention.
Reduce a small amount of risk in alarge number of people (e.g. reducefat a little in fast-food outlets).Lifestyle change plus environmentalapproach.