What hsCRP is
C-reactive protein (CRP) is an acute phase protein produced by the liver in response to interleukin-6 (IL-6) and other pro-inflammatory cytokines. It serves as a sensitive signal of systemic inflammation. Standard CRP assays can only detect levels above 3–5 mg/L, making them useful for detecting acute infections but blind to the chronic low-grade inflammation relevant to metabolic health and longevity.
High-sensitivity CRP (hsCRP) uses a more sensitive immunoassay that detects levels down to 0.1 mg/L — enabling detection of the subtle, persistent elevation in chronic disease, metabolic syndrome, and accelerated ageing. Always specify hsCRP when ordering this test.
Why chronic low-grade inflammation matters
The concept of "inflammaging" — chronic low-grade inflammation as a driver of ageing — is one of the most important frameworks in longevity medicine. Persistent inflammation at levels that cause no obvious symptoms drives:
- Atherosclerosis — inflammatory cells infiltrate arterial walls; hsCRP independently predicts cardiovascular events beyond LDL-C
- Insulin resistance — inflammatory cytokines impair insulin receptor signalling
- Neurodegeneration — neuroinflammation is a primary mechanism in Alzheimer's and Parkinson's
- Sarcopenia — chronic inflammation accelerates muscle protein breakdown
- Cancer — inflammatory microenvironments promote tumour development and progression
- Immune senescence — chronic activation exhausts immune surveillance
hsCRP ranges — clinical vs longevity
| hsCRP Level | Category | Primary Drivers in India | Intervention Response |
|---|---|---|---|
| <0.5 mg/L | Optimal (longevity target) | Lean, well-sleeping, low-stress, anti-inflammatory diet | Maintain with ongoing lifestyle |
| 0.5–1.0 mg/L | Low-normal | Minor lifestyle suboptimalities | Omega-3, sleep, dietary refinement |
| 1.0–3.0 mg/L | Moderate — investigate | Visceral fat, poor sleep, high-glycaemic diet, air pollution | Omega-3 high dose; curcumin; sleep improvement; weight loss |
| 3.0–10.0 mg/L | Elevated — significant | Metabolic syndrome, insulin resistance, gut dysbiosis | Comprehensive lifestyle overhaul; physician evaluation; consider metformin |
| >10 mg/L | Acute elevation | Active infection, autoimmune flare, acute injury | Do not interpret for chronic inflammation — retest when resolved |
What raises hsCRP in India
- Visceral fat — adipose tissue (especially visceral/omental fat) actively secretes IL-6 and TNF-alpha; the strongest modifiable driver of hsCRP
- Poor sleep — less than 7 hours dramatically elevates cytokines overnight; sleep is an anti-inflammatory process
- High-glycaemic diet — refined carbohydrates spike glucose and insulin, triggering inflammatory cascades
- Seed oils and trans fats — high omega-6 linoleic acid in seed oils (sunflower, soybean, corn oil) shifts eicosanoid balance toward pro-inflammatory pathways
- Psychological stress — cortisol acutely suppresses inflammation but chronic HPA activation ultimately drives it
- Air pollution — PM2.5 particulate matter in Indian metro cities (Delhi, Mumbai, Bengaluru) directly activates inflammatory pathways; a major underappreciated driver
- Alcohol — even moderate alcohol intake raises hsCRP over time
- Gut dysbiosis — leaky gut allows bacterial LPS to enter circulation, triggering systemic inflammatory response
What lowers hsCRP
- Omega-3 EPA+DHA — best evidence; 2–4g/day reduces hsCRP 20–40%; converts to resolvins and protectins that actively resolve inflammation
- Curcumin BCM-95 — 500–1000mg/day; multiple RCTs show 15–30% hsCRP reduction; BCM-95 or phospholipid complex for bioavailability
- Exercise — both aerobic and resistance training reduce hsCRP; effect is primarily mediated through fat loss and improved insulin sensitivity
- Weight loss — every kg of visceral fat lost reduces hsCRP measurably
- Vitamin D correction — deficiency is pro-inflammatory; correcting to 50+ ng/mL reduces hsCRP in deficient individuals
- Berberine — addresses the metabolic syndrome drivers of inflammation; indirect but significant hsCRP reduction
- Sleep optimisation — the most underrated anti-inflammatory intervention; 7.5–9 hours consistently
- Mediterranean-style dietary pattern — abundant olive oil, fatty fish, vegetables, legumes, minimal processed food
Always test hsCRP when you are not acutely ill. An active cold, wound, or flu will spike hsCRP to 50–200 mg/L — rendering the chronic inflammation reading meaningless. Wait 2–3 weeks after recovery. If hsCRP is above 10 mg/L without explanation, investigate for underlying infection or autoimmune condition before interpreting as metabolic inflammation.
How often to test
Include hsCRP in your annual metabolic panel. If elevated and actively intervening: retest at 3 months to assess response. Always pair with ApoB, ferritin, and homocysteine for a full inflammatory and cardiovascular risk picture.
Frequently asked questions
What is a good hsCRP level in India?
Below 0.5 mg/L is the longevity optimal. Clinical "low risk" is below 1.0 mg/L. Most urban Indians test between 1.0–3.0 mg/L, driven largely by visceral fat, poor sleep, high-glycaemic diet, and air pollution.
How do I lower CRP inflammation markers?
Omega-3 EPA+DHA 2–4g/day has the strongest evidence (20–40% reduction). Curcumin BCM-95 (500–1000mg/day), regular exercise, visceral fat reduction, sleep optimisation, and Vitamin D correction all contribute meaningfully.
What is the difference between CRP and hsCRP?
Standard CRP only detects levels above 3–5 mg/L — useful for acute infections, useless for chronic metabolic inflammation. hsCRP detects levels down to 0.1 mg/L, capturing the low-grade inflammatory state relevant to cardiovascular disease, metabolic syndrome, and longevity. Always specify hsCRP.
Does omega-3 lower CRP?
Yes — consistently shown across multiple RCTs. 2–4g/day EPA+DHA reduces hsCRP by 20–40%. Mechanism involves conversion to anti-inflammatory resolvins, protectins, and maresins. Use triglyceride-form omega-3 for superior bioavailability.