Pain serves a protective function: it signals tissue damage and motivates protective behaviour. Acute pain is proportional to tissue damage and resolves as healing progresses. Chronic pain, defined as pain persisting beyond three to six months, often has a different underlying biology. The initial injury may have healed, but the nervous system has undergone changes, a process called central sensitisation, that maintain pain signalling in the absence of ongoing damage. Systemic and neuroinflammation play central roles in establishing and maintaining this sensitised state.
Central Sensitisation
Central sensitisation involves plastic changes in the central nervous system that amplify pain signals, reduce the threshold at which stimuli are perceived as painful, and cause normally non-painful stimuli to be interpreted as painful. It is maintained in part by microglial activation in the spinal cord and brain. Microglia are the resident immune cells of the central nervous system, and when chronically activated, they release pro-inflammatory cytokines including interleukin 1 beta and TNF-alpha that increase neuronal excitability and perpetuate the sensitised state. Systemic inflammation feeds microglial activation and therefore sustains central sensitisation.
The Role of Peripheral Inflammation
Persistent peripheral inflammation, even at low levels, continuously signals the central nervous system and prevents the downregulation of pain pathways that would otherwise occur as healing completes. Adults with chronically elevated inflammatory markers are significantly more likely to develop and maintain chronic pain conditions. A large epidemiological study in the Annals of Rheumatic Disease found that elevated CRP independently predicted the development of chronic widespread pain at five-year follow-up in adults who were initially pain-free.
Anti-Inflammatory Strategies in Chronic Pain
A comprehensive anti-inflammatory approach to chronic pain includes dietary modification toward a Mediterranean pattern, omega-3 supplementation at 2 to 3g EPA and DHA per day, sleep prioritisation, stress reduction through breathwork and mind-body practices, and regular moderate exercise. Each of these reduces systemic inflammatory markers and may reduce the neuroinflammatory load that maintains central sensitisation. None replaces specialist pain management, but the evidence for their adjunctive benefit is meaningful and the risk is negligible.
- Adopt a Mediterranean dietary pattern and eliminate refined vegetable oils: this reduces systemic inflammatory load significantly
- Supplement with 2 to 3g of EPA and DHA daily: omega-3 fatty acids reduce neuroinflammatory cytokine production
- Prioritise sleep: sleep deprivation raises pain sensitivity and inflammatory markers simultaneously
- Engage in regular moderate exercise: it reduces systemic inflammation and promotes endogenous pain inhibition through endorphin release
- Consider slow breathing and mind-body practices: they reduce the sympathetic activation that amplifies central sensitisation
Sources
- Woolf, C.J. (2011). Central sensitization: implications for the diagnosis and treatment of pain. Pain, 152(3 Suppl), S2-15.
- McBeth, J., et al. (2004). Musculoskeletal pain is associated with a long-term increased risk of cancer and cardiovascular-related mortality. Rheumatology, 48(1), 74-77.