Chronic low-grade inflammation is increasingly linked to heart disease, diabetes, cancer, and accelerated ageing. This panel measures key inflammatory and immune markers to help you identify hidden inflammation and strengthen your immune defences.
hs-CRP reveals hidden inflammation that drives chronic disease. This sensitive marker helps identify cardiovascular risk and guides anti-inflammatory interventions for optimal health.
Optimal Range
<1.0 mg/L low risk
1.0-3.0 mg/L moderate risk
>3.0 mg/L high risk
optimal <0.5 mg/L
ESR measures systemic inflammation and serves as a valuable screening tool for inflammatory conditions and monitoring treatment response.
Optimal Range
Men: <15 mm/hr
Women: <20 mm/hr
optimal <10 mm/hr for both
Inflammation & Immunity
Inflammation & Immunity
Inflammation & Immunity
Inflammation & Immunity
Inflammation & Immunity
Inflammation & Immunity
Inflammation & Immunity
Inflammation & Immunity
Inflammation & Immunity
Inflammation is the immune system's fundamental defence mechanism — a complex cascade of cellular and molecular events that eliminates pathogens, clears cellular debris, and initiates tissue repair. In its acute form, inflammation is lifesaving. The problem arises when the inflammatory response fails to fully resolve, producing a state of chronic low-grade inflammation — sometimes called 'inflammageing' — that silently promotes arterial plaque formation, insulin resistance, neurodegeneration, and malignant cell transformation.
Research over the past two decades has established chronic inflammation as the underlying mechanism linking obesity, sedentary behaviour, poor diet, sleep deprivation, and psychological stress to virtually all major non-communicable diseases. Inflammatory biomarkers like hs-CRP, homocysteine, and ESR are not just markers of existing disease — they are predictive of future cardiovascular events, cognitive decline, and all-cause mortality, making them powerful tools for preventive health assessment.
Inflammation health does not exist in isolation — it is deeply intertwined with every major system.
Atherosclerosis is now understood as an inflammatory disease of the arterial wall. Oxidised LDL triggers endothelial NF-κB signalling, upregulating adhesion molecules that recruit circulating monocytes into the subendothelial space. These monocytes mature into macrophages, engulf lipid, and become foam cells — the building blocks of plaque. Plaque rupture, driven by macrophage-secreted metalloproteinases, causes the acute thrombosis that produces heart attacks and strokes. Elevated hs-CRP reflects this process and predicts cardiac events independently of LDL-C, while IL-6 is increasingly recognised as a causal mediator of cardiovascular disease.
Visceral adipose tissue acts as an endocrine-inflammatory organ, secreting TNF-α, IL-6, and resistin that directly impair insulin receptor signalling in muscle, liver, and fat cells — driving insulin resistance and type 2 diabetes. Conversely, hyperglycaemia and advanced glycation end-products (AGEs) activate inflammatory pathways, creating a self-reinforcing cycle between metabolic dysfunction and inflammation. Reducing visceral fat through diet and exercise measurably lowers hs-CRP and improves insulin sensitivity simultaneously.
Neuroinflammation — inflammation within the central nervous system driven by activated microglia — is now recognised as central to Alzheimer's disease, Parkinson's disease, and major depression. Systemic inflammation drives neuroinflammation through multiple pathways: inflammatory cytokines breach the blood-brain barrier, activate microglia, and reduce BDNF (brain-derived neurotrophic factor) production. Elevated hs-CRP correlates with reduced hippocampal volume and increased dementia risk in longitudinal studies. Depression is associated with elevated IL-6 and TNF-α even without other organic disease.
The immune system maintains balance between attacking pathogens and tolerating self-tissues. When this balance breaks down, autoimmune diseases develop — conditions where immune cells erroneously target the body itself. Over 80 autoimmune diseases are recognised, affecting 5–8% of the population. ESR and ferritin often reflect disease activity in autoimmune conditions. ANA and specific autoantibodies provide diagnosis, while WBC differential shows the pattern of immune cell involvement. Chronic unresolved inflammation from any source increases autoimmune risk by promoting loss of self-tolerance through molecular mimicry and bystander activation.
Clinical Note
hs-CRP should be measured in a resting state and not during or within two weeks of an acute infection or injury, which causes transient spikes unrelated to chronic baseline. An optimal baseline hs-CRP below 1.0 mg/L, in the context of normal metabolic markers and healthy lifestyle, suggests well-controlled systemic inflammation. Elevated hs-CRP with otherwise normal markers warrants investigation of occult infection, autoimmune condition, or sleep disordered breathing.
Acute inflammation is the immune system's rapid, short-term response to injury or infection — characterised by redness, swelling, heat, and pain. It is protective and resolves within days to weeks. Chronic low-grade inflammation is a sustained, low-level immune activation that persists without an obvious cause. It produces no obvious symptoms but drives the pathology of cardiovascular disease, type 2 diabetes, neurodegenerative disease, and several cancers. Blood markers like hs-CRP, IL-6, and homocysteine detect this silent inflammatory state.
High-sensitivity C-reactive protein (hs-CRP) is a protein produced by the liver in response to inflammation signals, primarily interleukin-6 (IL-6). Unlike standard CRP used to detect acute infection, the high-sensitivity assay detects the low-level elevation associated with chronic inflammatory states. According to the American Heart Association, hs-CRP below 1.0 mg/L represents low cardiovascular risk; 1.0–3.0 mg/L is moderate risk; above 3.0 mg/L is high risk. Optimal functional medicine targets hs-CRP below 0.5 mg/L. Infections and acute illness can temporarily spike hs-CRP — test after recovery for accurate baseline assessment.
Homocysteine is an amino acid produced during methionine metabolism. Elevated levels (above 10 µmol/L) damage the inner lining of blood vessels, promote platelet aggregation, and increase risk of cardiovascular disease, stroke, dementia, and deep vein thrombosis. Deficiencies in B6, B12, and folate impair homocysteine clearance — which is why elevated homocysteine often responds dramatically to B-vitamin supplementation. Optimal homocysteine is below 7 µmol/L for cardiovascular and cognitive protection.
The most evidence-backed anti-inflammatory interventions are: (1) a Mediterranean-style diet rich in olive oil, fatty fish, vegetables, and polyphenols, which reduces hs-CRP by 20–35% in clinical trials; (2) regular moderate exercise — as few as 150 minutes per week of moderate aerobic activity significantly reduces inflammatory markers; (3) adequate sleep — below 6 hours per night raises IL-6 and hs-CRP; (4) stress management via mindfulness and relaxation techniques; (5) smoking cessation, which reduces chronic oxidative stress; and (6) omega-3 fatty acid supplementation (EPA+DHA), which reduces triglycerides and inflammatory eicosanoids.
ESR measures how quickly red blood cells settle to the bottom of a test tube over one hour. When inflammation is present, abnormal proteins cause red cells to clump and settle faster, raising the ESR. ESR is a non-specific marker — it can be elevated by infections, autoimmune diseases (rheumatoid arthritis, lupus), inflammatory bowel disease, and cancer. Unlike hs-CRP, which can rise and fall within hours, ESR changes more slowly and is more useful for monitoring the course of chronic inflammatory conditions over weeks.
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