Inflammation is not a disease — it is a process. The problem begins when it never switches off
Acute inflammation is one of the body's most important healing tools. Chronic low-grade inflammation is a shared mechanism underlying cardiovascular disease, type 2 diabetes, Alzheimer's and cancer. Diet is one of the most direct variables in the difference between the two.
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When you cut your finger, inflammation is the cascade that begins healing it. Blood vessels dilate, immune cells flood the area, cytokines signal for repair, and within days the tissue is restored. This is acute inflammation — precise, localised, time-limited and essential. It is regulated by a balance between pro-inflammatory signals (prostaglandins, leukotrienes, cytokines like IL-1β and TNF-α) and pro-resolving signals (lipoxins, resolvins, protectins) derived largely from the fatty acids in your cell membranes.
Chronic low-grade inflammation is a different state entirely. It is systemic rather than localised, persistent rather than time-limited, and subclinical — it produces no obvious symptoms until it has been silently damaging tissue for years. It is characterised by chronically elevated levels of inflammatory markers — CRP, IL-6, fibrinogen — that sit above normal but below the levels associated with acute infection. This is the inflammatory state that underlies the majority of chronic Western disease, and it is driven in significant part by diet.
The to ratio in the diet directly determines the balance between pro-inflammatory and pro-resolving signalling molecules. arachidonic acid is the precursor to pro-inflammatory eicosanoids; EPA and DHA are the precursors to pro-resolving resolvins and protectins. The evolutionary ratio was approximately 2:1 to 4:1. The modern Western ratio is 15:1 to 20:1 — meaning the cellular environment is continuously biased toward inflammatory signalling
Ultra-processed foods drive chronic inflammation through multiple simultaneous mechanisms: the load from seed oils used in production, the advanced glycation end products formed during high-temperature processing, emulsifiers like carrageenan and maltodextrin that increase gut permeability, and the absence of the polyphenols and that would otherwise modulate inflammatory tone
Visceral fat — the fat stored around the abdominal organs — is itself an endocrine organ that continuously secretes pro-inflammatory adipokines including leptin, resistin and TNF-α. This creates a self-reinforcing cycle: chronic inflammation promotes visceral fat accumulation; visceral fat amplifies inflammation. This is one reason why waist circumference predicts cardiovascular and metabolic disease risk more accurately than BMI
Dietary polyphenols — from berries, dark chocolate, olive oil, leafy greens, tea and coffee — do not act primarily as direct anti-inflammatory agents. They activate Nrf2 and NF-κB regulatory pathways, upregulating the body's endogenous anti-inflammatory enzymes and resolution pathways. This indirect, gene-expression-level effect is far more sustained and powerful than the temporary direct quenching that isolated antioxidant supplements attempt to replicate
A 2025 umbrella review of systematic reviews and meta-analyses found that dietary patterns emphasising minimally processed foods rich in polyphenols, and fatty acids — the Mediterranean, DASH and Nordic diets — consistently reduced hs-CRP, IL-6 and other inflammatory biomarkers across diverse populations. The common denominator was food quality and variety, not any single anti-inflammatory ingredient
Sleep deprivation is one of the most potent and underappreciated activators of chronic inflammation. A single night of poor sleep raises IL-6 and TNF-α measurably the following day. Chronic sleep restriction produces sustained elevation of inflammatory markers that dietary intervention alone cannot fully reverse. This is why addressing sleep is inseparable from addressing inflammation — the dietary work and the sleep work reinforce each other or undermine each other.
The most important practical insight is that chronic inflammation is not managed by adding anti-inflammatory supplements on top of an inflammatory diet and lifestyle. It is managed by removing the primary drivers — excess ultra-processed food, refined inadequate sleep, chronic stress and sedentary behaviour — and replacing them with inputs that support resolution: diversity, sources, polyphenol-rich plant foods, adequate and sleep. The goal is not suppressing inflammation but allowing it to resolve — which is what the body is designed to do when the conditions support it.