(obesity and chronic pain: similar physiology. same aetiology?)

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Obesity and Chronic Pai imilar physiology. Same aetiology?) Prof Garry Egger MPH PhD Southern Cross University hronic Pain & Lifestyle

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Chronic Pain & Lifestyle. (Obesity and Chronic Pain: Similar physiology. Same aetiology?). Prof Garry Egger MPH PhD Southern Cross University. …and if you get caught out - act sorry!. Main Points. • Obesity and chronic pain are linked biologically - PowerPoint PPT Presentation

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Page 1: (Obesity and Chronic Pain: Similar physiology. Same  aetiology?)

(Obesity and Chronic Pain:Similar physiology. Same aetiology?)

Prof Garry Egger MPH PhDSouthern Cross University

Chronic Pain & Lifestyle

Page 2: (Obesity and Chronic Pain: Similar physiology. Same  aetiology?)
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…and if you get caught out - act sorry!

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Main Points

• Obesity and chronic pain are linked biologically through a form of low-grade, systemic inflammation (‘metaflammation’), with glia playing a major role.

• Hence (much) chronic neuropathic (‘gliapathic’?) pain is lifestyle-related – leading to the conclusion that:

• Lifestyle change needs to be incorporated into any new ‘wholistic’ paradigm for chronic pain management.

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Lucky Boyd

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Obesity and Chronic Pain

Obesity Chronic Pain

• ~30 % of popn • ~20% of popn• Increasing (~2%pa) • Predicted increase (~4%pa)*• Lifestyle related • Lifestyle related (?)• Inflammatory link • Inflammatory base

Both a bigger problem in developed countriesBoth higher in lower SE groups

*Hohenberg KW, Lyons J, Daley TL. Chronic Pain. Decision Resources Report. March 2008.

Both have environmental aetiologies

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35.3%35.3%38.9%38.9%

5.3%5.3%

20.4%20.4%

Underweight Normal weight Overweight Obese

Risk Factors: • low income • age • frequency of snacks • amount of exercise

of owners50%

25%

o%

(UK) Prevalence of Overweight and ObesityPr

eval

ence

Ref: Courcier EA, Mellor DJ, Yam PS. J. Small Animal Practice 2010; 3rd Feb

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Ways of thinking about Obesity

The ‘linear’ approach:Weight = Energy in - Energy out X

A ‘systems’ approach:

BehaviourEnvironmentBiology

Influences

X Physiological adjustments

ModeratorsRef: Egger G, Swinburn B. Brit Med J. 1996; 20:227-231

Equilibrium fat stores

= Energy in-Energy out

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Obesity: Always offender or often just accomplice?

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Maximal adipocyte expandability (genetically determined)

Adipocyte (fat cell)

Lipid pool

Insulin sensitive

Pre-adipocyte

Blood Liver Muscle

Adipocyte expanded to maximal capacity

Macrophage accumulation

Inflammatory signaling

Expanded Lipid pool

Inflammation

Insulin resistant

Lipid‘spill-over’

The Fat ‘Spill-Over’ Hypothesis

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Our inflammatory internal environment – ‘metaflammation’

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Inflammation

ImmuneDefense

Resolution

Basal Homeostasis

Classical, Acute,Infectious Response

Im

mun

e Re

actio

n

Chronic Allostasis

Modern, Chronic.Non-infectious Response

Disease‘Dys-MetabOlism’

‘Meta-flammation’

Oxidative stress

InsulinResistance

Lifestyle/Environmental‘Inducer’

‘Agent’ (LDL)

MicrobialPathogen/‘Antigen’

Forms of Inflammation

Ref: Egger G, Dixon J. Obes Rev 2009 (in press)

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Ref: Lamon BD, Hajar DP. Am J Pathol 2008;173(5):1253-1264

Inflammation (“metaflammation”) in chronic disease

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Metaflammation

Chronic (Non-Communicable) Disease

Lifestyle Smoking Over-

Nutrition Starvation

Diet Stress/Depression

Inactivity Drug use

Over-exercise

Obesity

ExcessAlcohol

E N V I R O N M E N T

Pollution

+ Other Mechanisms(eg. oxidative stress, insulin resistance etc)

Ref: Egger G, Dixon J. Ob Rev 2009;10:237-249.

‘Inducers’ of Metaflammation

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ANTI-Inflammatory ‘Inducers’ PRO-Inflammatory ‘Inducers’

A. LIFESTYLEExercise/Physical activity/fitnessIntensive lifestyle changeNutrition - alcohol (moderate) - capsicum - cocoa - dairy calcium - eggs - energy intake (reduced) - fish/fish oils - fibre - garlic - grapes/raisons - herbs/spices - lean game meats - low GI foods/Low N6:N3 - Mediterranean diet - fruits and vegetables

A. LIFESTYLEExercise - too little / too muchNutrition - alcohol (excessive) - excessive energy intake - fast foods/’western’ diet - fat - saturated/trans - high fat/high N6:N3 - fibre (low intake) - fructose/ glucose - high GI foods/diet/ load - meat (domesticated) - sugar sweetened drinks - starvationObesitySmokingSleep deprivationStress/Anxiety/Depression

- mono-unsaturated fats/olive oil - nuts - soy protein - tea/green tea - vinegarSmoking cessationWeight loss

B. ENVIRONMENTAir pollution (indoor/outdoor)Atmospheric CO2Perceived organisational injustice (low)Second hand smokeSE Status

UNADAPTED – POST-INDUSTRIAL REVOLUTION

ADAPTED

– PR

E-IN

DUSTRI

AL REV

OLUTI

ON

~1800 today-100,000

Egger G, Dixon J. Ob Rev (in press)

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Affected Organs

• Endothelium(atherosclerosis)

•Lung(COPD)

• Brain(Alzheimer’s/Dementia)

• Joints(arthritis)

• Bowel (IBD)

• Neuron/Glia(neuropathic/‘gliapathic’? pain)

Range of ‘Metaflammatory’ Effects

Ref: Libby P. Nature, 2010

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Modulation of the Neurovascular Unit by Pain

Ref: Willis CL, Davis TP. Current Pharmaceutical Design, 2008, 14, 1625-1643

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Figure 1 | Glia–neuron interactions. Different types of glia interact with neurons and the surrounding blood vessels. Oligodendrocytes wrap myelin around axons to speed up neuronal transmission. Astrocytes extend processes that ensheath blood vessels and synapses. Microglia keep the brain under surveillance for damage or infection.

Ref: Allen NJ, Barres BA, Nature, 2009

Glia – More Than Just Brain Glue

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Neu

ron

Neu

ron

Neu

ron

The Potential Impact of Glia on Central Pain Signaling

Ref: Fields D. ‘The Other Brain’, 2009

GliaGliaGliaGlia

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The links between Chronic Pain and Lifestyle

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Ref: Saastamoinen P et al., Pain, 2008

Lifestyle Factors and Chronic Pain – SE Factors

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Ref: Kalameri et al., Eur J Pain, 2008

Number of Pain Sites by Lifestyle Behaviours –Norway

N=2926

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Lifestyle, ‘Metaflammation’ and Chronic Pain

Ref: Shiri R et al. Eur Spine J, 2007;16:2043-2054

Metaflam- Endothelial Chronic Chronic Prevalencemation Dysfunction Disease Pain

Lifestyle processesInactivity + + + ? 50%Smoking + + + + 20%Passive smoking + + + ? -Poor sleep + + + + 33%Overweight/Obesity + + + + 60%Stress + ? ? + ~20%Nutrition Sat/trans fat intake + + + + - High GI load + + + ? -

+ = positive effect? = not sufficient evidence

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obesity

diabetes

insulin resistance

CVD

cancer

aging

arthritis

gut healthimmune function

M E T A F L A M M A T I O N!!!

C H R O N I C P A I N???

Why nutrition & chronic pain?

”We literally eat ourselves into an inflamed and painful state and then seek out passive care from doctors to intervene on our behalf.”

Seaman DR. “The diet induced pro-inflammatory state: A cause of chronic pain and other degenerative diseases”. J Manip &Physio Ther 2002;25(3):168-179

Nutrition

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obesity

diabetes

insulin resistance

CVD

cancer

aging

arthritis

gut healthimmune function

M E T A F L A M M A T I O N!!!

C H R O N I C P A I N???

Why exercise & chronic pain?

” Recent evidence suggests that the protective effect of exercise may to some extent be ascribed to an anti-inflammatory effect of regular exercise.”

Inflammation PL et al.. “Persistent low grade inflammation and regular exercise.” Front Biosc 2010 Jan

Exercise

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Tissue inflammation

Neural sensitisation

Can we unknowingly contribute to the Can we unknowingly contribute to the persistence of pain ?persistence of pain ?

Inflammatory Inflammatory attitudesattitudes

Inflammatory Inflammatory actionsactions

Inflammatory Inflammatory relationshipsrelationships

Inflammatory Inflammatory eatingeating

Inflammatory Inflammatory environmentenvironment• toxinstoxins• smokingsmoking• medicationmedication

• stressstress• angeranger• bitternessbitterness

• excess starchy excess starchy carbohydrate carbohydrate

• over doingover doing• under doingunder doing• poor sleeppoor sleep

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Models in Pain Management

Traditional (dualistic) Model Emerging (Holistic) Model

• Medical or psychological focus • + Social and environmental focus• More clinician centred • More patient centred• Limited benefits for limited time • Significant, long term benefits• Individual treatment approach • individual + group treatment • Patient as recipient of treatment • Patient as partner in treatment• Potential dependency/ complications • Limited dependency/complications• Distracts recipient from active • Involves recipient in active self-

management management• “Siloed” health system approach • Integrated health system approach• Neural plasticity disregarded • Neural plasticity vital for treatment• Ongoing/discontinued biomedical • ‘Tapered’ biomedical treatment

treatment• Individual health perspective only • Population health perspective• Little or no attention to lifestyle • Significant attention given to lifestyle

change

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The Australian Lifestyle Medicine Association (ALMA)

www.ALMA.net.au

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Thank you

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Chronic Pain and Lifestyle MedicineGarry Egger Southern Cross University, Lismore and Centre for Health Promotion and Research, Sydney

Chronic pain is an increasingly common phenomenon in modern societies. It’s not coincidental that this corresponds to an increase in several other lifestyle-related chronic diseases or risk factors (type 2 diabetes, depression, cancers etc), which have recently been shown to have a common physiological aetiology in low grade, systemic, inflammation (‘metaflammation’). Coupled with findings of increased plasticity in the brain, it is not outrageous to speculate that metaflammation may extend to both central and peripheral glial connections associated with pain perception, thus linking lifestyle-related ‘inducers’ to non-specific and unresolvable chronic pain. Even without such a biological basis, there is evidence to suggest that lifestyle change may have a positive effect as part of a systems-theory approach to chronic pain management. The potential benefits of a ‘Lifestyle Medicine’ approach to chronic pain management are considered in this regard.