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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 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 + + + + + + + + + + + ? + + + + + ? ? + ? + + + + + + + + + + ? 50% 20% 33% 60% ~20% - + = 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.