The most well-researched compound in turmeric. It inhibits NF-κB — a key inflammatory signalling molecule that activates gene expression across dozens of inflammatory pathways — and also modulates COX-2, LOX, and prostaglandin activity. The bioavailability problem is real: standard curcumin is poorly absorbed. Formulations with piperine (black pepper extract, which inhibits glucuronidation) or phospholipid delivery (phosphatidylcholine complexes) offer meaningfully better plasma levels. Look for products standardised to 95% curcuminoids with at least one bioavailability enhancement strategy.

The resin of the Boswellia tree contains boswellic acids that inhibit 5-lipoxygenase (5-LOX), an enzyme responsible for leukotriene synthesis. Leukotrienes are among the most potent inflammatory signalling molecules in the body, particularly in the respiratory tract and joints. Unlike NSAIDs, which inhibit both COX-1 and COX-2 and thereby damage the protective gut lining, boswellia doesn’t suppress COX-1. This makes it particularly well-suited for long-term use. Clinical trials have shown benefit in osteoarthritis, rheumatoid arthritis, and inflammatory bowel conditions including Crohn’s disease and ulcerative colitis.

Ginger contains gingerols and shogaols — compounds with potent anti-inflammatory and antioxidant effects. Studies show it inhibits COX enzymes similarly to some anti-inflammatory medications, but with a significantly better safety profile for the gastrointestinal tract. Beyond inflammation, ginger supports digestive motility and has demonstrated antiemetic properties. The anti-inflammatory effects appear dose-dependent, with most studies using 1–3 grams of dried ginger powder daily. It pairs well with turmeric for synergistic effect.

EPA and DHA are the structural precursors to resolvins, protectins, and maresins — anti-inflammatory molecules that actively resolve the inflammatory response, rather than simply suppressing it. This is a crucial distinction: most pharmaceutical anti-inflammatories work by blocking inflammatory signals, but omega-3s actually signal the body to begin the resolution phase of inflammation, where damaged tissue is cleared and healing can begin. Low omega-3 intake is associated with higher inflammatory marker levels across virtually every population studied. The most robust evidence supports EPA+DHA for reducing triglycerides, supporting mood regulation, and managing joint inflammation. Aim for at least 1000mg combined EPA/DHA daily for anti-inflammatory effect — higher if you have established inflammatory conditions.

A polyphenol found in grape skins, Japanese knotweed, and red wine, resveratrol activates SIRT1 and AMPK pathways — cellular signalling involved in stress resistance, inflammation resolution, and mitochondrial function. It also modulates NF-κB and inhibits COX-2 expression. The bioavailability of resveratrol is limited (it’s rapidly metabolised), so look for formulations that include piperine or use a nanoparticle delivery system. Trans-resveratrol is the more studied isomer. Beyond inflammation, the SIRT1 activation is of particular interest for longevity researchers, as this pathway is implicated in cellular senescence and metabolic health.

The phenolic compounds in extra virgin olive oil — particularly hydroxytyrosol and oleocanthal — have demonstrated anti-inflammatory effects comparable to ibuprofen in some studies, without the gastrointestinal risks. Oleocanthal inhibits COX enzymes in a dose-dependent manner. The challenge is getting therapeutic doses through diet alone: you’d need to consume several hundred millilitres of high-polyphenol olive oil daily to approach the doses used in studies. Standardised extracts offer a more practical approach for those targeting specific anti-inflammatory benefit from this pathway.