Understanding it
What chronic inflammation actually is
Acute inflammation is the body's healthy, short-term response to injury or infection — it flares, heals, and resolves. Chronic inflammation is different: it's a low-grade, persistent activation that never fully switches off. People experience it as morning stiffness, aches that move from joint to joint, slow recovery from exercise, a sense of being "aged before your time," and lab markers like hs-CRP that sit just above the reference range. Over time, chronic inflammation is the common thread behind most age-related disease — cardiovascular, metabolic, joint, and cognitive. It's not one condition; it's a baseline state the body has settled into.
The roots
What might be causing it
Inflammation genes set your baseline "volume" — how loudly your immune system signals by default. IL-6, TNF, and CRP-related variants influence that baseline. The FADS1 gene decides how efficiently you convert plant-based omega-3 (ALA) into the active EPA and DHA your body uses to resolve inflammation — and many people convert poorly, leaving them functionally low on anti-inflammatory fats even with a "good" diet. Vitamin D status, omega-3 index, magnesium, and antioxidant capacity (SOD2, GST) all decide how quickly an inflammatory signal turns back down. On top of genetics, a Western-style diet, low fibre, poor sleep, chronic stress, gut imbalance, and excess body fat all keep the volume turned up. The combination of a genetically higher baseline and nutrient shortfalls that can't turn it down is what produces the chronic, moving aches and elevated markers.
The standard path
How it's usually treated
The standard medical approach depends on severity and diagnosis. For joint pain and inflammatory arthritis, NSAIDs (ibuprofen, naproxen, celecoxib) are first-line for pain and inflammation. For diagnosed autoimmune inflammation, disease-modifying drugs and biologics that target specific inflammatory pathways (TNF, IL-6) may be prescribed. For cardiovascular inflammation, statins are standard. Each can be effective and sometimes necessary, but they largely suppress the inflammatory signal rather than addressing why the body is producing it. Long-term NSAID use carries gastrointestinal, kidney, and cardiovascular risks, and several are metabolized by CYP2C9 — a gene that varies and changes both effectiveness and risk. None of these approaches address the omega-3, vitamin D, or antioxidant shortfalls that decide how well the body resolves inflammation on its own.
A different angle
How genetic screening can help
Genetic screening maps both your inflammatory baseline and your capacity to resolve it. IL-6, TNF, and CRP variants show your genetic "volume setting." FADS1 reveals whether you convert plant omega-3 poorly — in which case a direct EPA/DHA source is needed, not just flax or chia. SOD2 and GST variants show your antioxidant capacity, guiding targeted support. With that map, support becomes specific: EPA-dominant omega-3 at a meaningful dose for those who convert poorly, vitamin D3 with K2 to status, curcumin and quercetin for inflammatory signaling, and a Mediterranean-style eating pattern that supplies the fibre and polyphenols the microbiome needs to produce its own anti-inflammatory compounds. For many people, closing the omega-3 and vitamin D gaps and matching antioxidants to genetics substantially lowers the inflammatory baseline — reducing joint pain and stiffness and, in some cases, the reliance on daily NSAIDs. Where NSAIDs are still needed, CYP2C9 insight helps your doctor choose a better-tolerated option and dose.
This is educational support, not a diagnosis or a treatment plan. We help you understand genetic tendencies and support them with food, lifestyle and nutrients alongside your doctor.
