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

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

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)

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: 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

Aboriginal adults (Central Australia) 1930s

Torres Strait Islanders, 1930’s-40’s

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

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

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.

…and finally,

Eat food, mostly plants, not too much

Michael Pollan, “What to eat”