Chronic low-grade systemic inflammation — sometimes called "inflammaging" in the longevity science literature — is now understood to be the shared pathological substrate of cardiovascular disease, type 2 diabetes, Alzheimer's disease, and a growing list of cancers. It is not the acute inflammation of a sprained ankle or a fever. It is a slow, persistent, sub-threshold activation of the immune system that produces none of the obvious signs of inflammation — no swelling, no redness, no pain — while quietly causing progressive tissue and vascular damage.

The key markers

hsCRP (high-sensitivity C-reactive protein) is produced by the liver in response to inflammatory cytokines. Unlike standard CRP (which detects acute, high-level inflammation), hsCRP is sensitive enough to detect the chronic, low-level inflammatory state associated with cardiometabolic disease. A JUPITER trial involving 17,802 participants showed that statin therapy reduced cardiovascular events in individuals with normal LDL but elevated hsCRP — confirming inflammation as an independent cardiovascular risk factor.

IL-6 (interleukin-6) is a pro-inflammatory cytokine produced by macrophages, adipose tissue, and vascular endothelial cells. Elevated IL-6 is strongly associated with progression to type 2 diabetes (the Whitehall II study showed a 3-fold elevated risk in the highest IL-6 quartile), with Alzheimer's disease neuropathology, and with cardiovascular mortality independent of other risk factors.

What drives chronic inflammation?

Intervention: what the evidence supports

The interventions with the most robust evidence for reducing hsCRP and IL-6 include: omega-3 supplementation (reducing hsCRP by 20–30% in RCTs), vigorous aerobic exercise (sustained effect over 12+ weeks), Mediterranean dietary pattern, sleep optimisation, and addressing vitamin D deficiency — a direct immune modulator.

None of this is possible if you do not first know your baseline. And the standard check-up does not measure it.

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