Inflammation is one of the most misunderstood concepts in medicine. Acute inflammation, the redness, swelling, heat, and pain following a cut, a sprain, or an infection, is a beneficial, precisely orchestrated response that clears pathogens and initiates tissue repair. It resolves within days to weeks. Chronic low-grade inflammation is a different phenomenon: a persistent, subclinical activation of the immune system that operates below the threshold of obvious symptoms but produces ongoing damage to tissues, vessels, and organs over months and years. It is this chronic inflammatory state that is mechanistically implicated in virtually every major non-communicable disease.
The Inflammatory Markers
The primary clinically available markers of systemic inflammation are C-reactive protein, particularly high-sensitivity CRP, interleukin 6, and fibrinogen. Elevated hsCRP, even within the standard normal range, is an independent predictor of cardiovascular events, metabolic disease progression, and all-cause mortality in prospective studies. The JUPITER trial, which enrolled adults with normal LDL cholesterol but elevated hsCRP above 2mg per litre, found that statin treatment significantly reduced cardiovascular events and all-cause mortality, suggesting that inflammatory reduction, not just lipid lowering, is a therapeutic target.
What Drives Chronic Inflammation
Chronic inflammation has multiple causes that often operate simultaneously. Visceral adiposity, excess fat stored around internal organs, is metabolically active and releases inflammatory cytokines including TNF-alpha, interleukin 6, and leptin continuously. Gut dysbiosis and intestinal permeability allow bacterial products including lipopolysaccharide into systemic circulation, producing ongoing innate immune activation. Chronic psychological stress elevates cortisol, which initially suppresses inflammation but in the context of glucocorticoid resistance drives pro-inflammatory gene expression. Poor sleep amplifies all of these pathways simultaneously.
Inflammaging: The Intersection with Ageing
The term inflammaging, coined by immunologist Claudio Franceschi, describes the chronic pro-inflammatory state that characterises ageing and appears to be the common mechanism underlying age-related disease. Centenarians, those who reach 100 in good health, consistently show lower inflammatory markers than typical older adults, and this appears to be a key feature that distinguishes exceptional longevity. Reducing chronic inflammation is therefore not only relevant for disease prevention but for the rate of biological ageing itself.
- Request hsCRP testing as part of a routine health screen: it is inexpensive and clinically informative
- Reduce visceral fat: it is the most potent endogenous driver of systemic inflammation
- Prioritise sleep: chronic sleep restriction raises interleukin 6 and CRP measurably within weeks
- Adopt a Mediterranean dietary pattern: it reduces CRP by an average of 30 to 40 percent in clinical trials
- Address chronic psychological stress: it drives glucocorticoid resistance and pro-inflammatory gene expression
Sources
- Ridker, P.M., et al. (2008). Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. New England Journal of Medicine, 359(21), 2195-2207.
- Franceschi, C., et al. (2000). Inflammaging and anti-inflammaging: a systemic perspective on aging and longevity. Mechanisms of Ageing and Development, 121(1-3), 153-166.