Transcript Chronic Pain

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
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.
Lucky Boyd
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 countries
Both higher in lower SE groups
Both have environmental aetiologies
*Hohenberg KW, Lyons J, Daley TL. Chronic Pain. Decision Resources Report. March 2008.
(UK) Prevalence of Overweight and Obesity
Prevalence
50%
Risk Factors:
• low income
of owners
• age
• frequency of snacks
• amount of exercise
25%
38.9%
35.3%
20.4%
o%
5.3%
Underweight
Normal weight
Overweight
Ref: Courcier EA, Mellor DJ, Yam PS. J. Small Animal Practice 2010; 3rd Feb
Obese
Ways of thinking about Obesity
X
The ‘linear’ approach:
Weight = Energy in -
Energy out
A ‘systems’ approach:
Influences
Environment
Equilibrium fat
stores
Biology
Behaviour
=
Energy in-Energy out
X
Physiological
adjustments
Moderators
Ref: Egger G, Swinburn B. Brit Med J. 1996; 20:227-231
Obesity: Always offender or often just accomplice?
The Fat ‘Spill-Over’ Hypothesis
Inflammatory signaling
Maximal adipocyte expandability
(genetically determined)
Inflammation
Adipocyte (fat cell)
Pre-adipocyte
Macrophage accumulation
Lipid pool
Expanded Lipid pool
Insulin sensitive
Insulin resistant
Adipocyte expanded to
maximal capacity
Lipid
‘spill-over’
Blood
Liver
Muscle
Our inflammatory internal environment
– ‘metaflammation’
Forms of Inflammation
Basal Homeostasis
Immune Reaction
Resolution
Microbial
Pathogen/
‘Antigen’
Lifestyle/
Environmental
‘Inducer’
Chronic
Allostasis
Oxidative
stress
Immune
Defense
‘Metaflammation’
Insulin
Resistance
Disease
‘DysMetab
Olism’
Inflammation
Classical, Acute,
Infectious Response
Ref: Egger G, Dixon J. Obes Rev 2009 (in press)
Modern, Chronic.
Non-infectious Response
Inflammation (“metaflammation”) in chronic disease
Ref: Lamon BD, Hajar DP. Am J Pathol 2008;173(5):1253-1264
‘Inducers’ of Metaflammation
ENVIRONMENT
Lifestyle
Smoking
OverNutrition
Starvation
Inactivity
Drug use
Pollution Overexercise
Excess
Alcohol
Diet
Sleep
Obesity
Stress/
Depression
Metaflammation
+ Other Mechanisms(eg. oxidative stress, insulin resistance etc)
Chronic (Non-Communicable) Disease
Ref: Egger G, Dixon J. Ob Rev 2009;10:237-249.
ANTI-Inflammatory ‘Inducers’
PRO-Inflammatory ‘Inducers’
A. LIFESTYLE
Exercise/Physical activity/fitness
Intensive lifestyle change
Nutrition
- 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. LIFESTYLE
Exercise
- too little / too much
Nutrition
- 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
- starvation
Obesity
Smoking
Sleep deprivation
Stress/Anxiety/Depression
- mono-unsaturated fats/olive oil
- nuts
- soy protein
- tea/green tea
- vinegar
Smoking cessation
Weight loss
B. ENVIRONMENT
Air pollution (indoor/outdoor)
Atmospheric CO2
Perceived organisational injustice (low)
Second hand smoke
SE Status
-100,000
~1800
Egger G, Dixon J.
Ob Rev (in press)
today
Range of ‘Metaflammatory’ Effects
Affected Organs
• Endothelium
(atherosclerosis)
•Lung
(COPD)
• Brain
(Alzheimer’s/
Dementia)
• Joints
(arthritis)
• Bowel
(IBD)
Ref: Libby P. Nature, 2010
• Neuron/Glia
(neuropathic/
‘gliapathic’? pain)
Modulation of the Neurovascular Unit by Pain
Ref: Willis CL, Davis TP. Current Pharmaceutical Design, 2008, 14, 1625-1643
Glia – More Than Just Brain Glue
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
Ref: Fields D. ‘The Other Brain’, 2009
Glia
Glia
Glia
Neuron
Glia
Glia
Neuron
Neuron
The Potential Impact of Glia on Central Pain Signaling
The links between Chronic Pain and Lifestyle
Lifestyle Factors and Chronic Pain – SE Factors
Ref: Saastamoinen P et al., Pain, 2008
Number of Pain Sites by
Lifestyle Behaviours –
Norway
N=2926
Ref: Kalameri et al., Eur J Pain, 2008
Lifestyle, ‘Metaflammation’ and Chronic Pain
Metaflam- Endothelial Chronic Chronic
mation
Dysfunction Disease Pain
Prevalence
Lifestyle processes
Inactivity
Smoking
Passive smoking
Poor sleep
Overweight/Obesity
Stress
Nutrition
Sat/trans fat intake
High GI load
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50%
20%
33%
60%
~20%
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+ = positive effect
? = not sufficient
evidence
Ref: Shiri R et al. Eur Spine J, 2007;16:2043-2054
Why nutrition & chronic pain?
obesity
diabetes
Nutrition
CVD
M E T A F L A M M A T I O N!!! cancer
insulin
resistance
aging
C H R O N I C P A I N???
immune function
arthritis
gut health
”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
Why exercise & chronic pain?
Exercise
obesity
diabetes
CVD
M E T A F L A M M A T I O N!!! cancer
insulin
resistance
aging
C H R O N I C P A I N???
immune function
arthritis
gut health
” 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
Can we unknowingly contribute to the
persistence of pain ?
Inflammatory
actions
Inflammatory
attitudes
• stress
• anger
• bitterness
Tissue inflammation
• over doing
• under doing
• poor sleep
Neural sensitisation
Inflammatory
eating
• excess starchy
carbohydrate
Inflammatory
environment
Inflammatory
relationships
• toxins
• smoking
• medication
Models in Pain Management
Traditional (dualistic) Model
Emerging (Holistic) Model
• Medical or psychological focus
• More clinician centred
• Limited benefits for limited time
• Individual treatment approach
• Patient as recipient of treatment
• Potential dependency/ complications
• Distracts recipient from active
management
• “Siloed” health system approach
• Neural plasticity disregarded
• Ongoing/discontinued biomedical
treatment
• Individual health perspective only
• Little or no attention to lifestyle
• + Social and environmental focus
• More patient centred
• Significant, long term benefits
• individual + group treatment
• Patient as partner in treatment
• Limited dependency/complications
• Involves recipient in active selfmanagement
• Integrated health system approach
• Neural plasticity vital for treatment
• ‘Tapered’ biomedical treatment
• Population health perspective
• Significant attention given to lifestyle
change
The Australian Lifestyle
Medicine Association
(ALMA)
www.ALMA.net.au
Thank you
Chronic Pain and Lifestyle Medicine
Garry 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.