Inflammation Blood Markers

Non-specific marker of inflammation. Elevated in infection, injury, or chronic disease.

PED: Training-induced inflammation can elevate CRP. Some AAS may increase systemic inflammation. High-sensitivity CRP (hs-CRP) is more useful for cardiovascular risk assessment -- target <1.0 mg/L for low cardiovascular risk. Rest 48-72h before blood draw for accurate baseline.

Non-specific marker of inflammation that measures how quickly red blood cells settle in a tube. Elevated in infection, autoimmune conditions, and chronic inflammation. Slower to rise and fall than CRP.

PED: Complementary to CRP — ESR rises more slowly but stays elevated longer, making it useful for detecting chronic/ongoing inflammation. AAS-induced polycythemia (high RBC/haematocrit) can actually lower ESR because more packed red cells settle slower. If ESR is elevated despite high haematocrit, it suggests significant inflammation. Not typically a primary monitoring marker for PED users, but useful alongside CRP for a complete inflammatory picture.

Amino acid in the blood. Elevated levels are an independent risk factor for cardiovascular disease, stroke, blood clots, and cognitive decline. Metabolised by B-vitamins (B6, B12, Folate).

PED: An often-overlooked cardiovascular risk marker for PED users. Elevated homocysteine damages blood vessel walls and promotes clotting -- compounding the cardiovascular risk from AAS-worsened lipids and elevated haematocrit. Some AAS may affect homocysteine metabolism. Target <10 umol/L for optimal cardiovascular protection.

NMR-derived composite inflammatory biomarker reflecting glycosylation of acute phase proteins. More stable than CRP with lower intra-individual variability, providing a better measure of chronic systemic inflammation.

PED: Chronic PED use causes sustained low-grade systemic inflammation reflected by GlycA. Unlike CRP which spikes acutely and normalises quickly, GlycA captures chronic inflammatory burden — more relevant for long-term health monitoring in enhanced athletes. AAS-induced hepatic acute phase protein production elevates GlycA. Intense training, joint stress, and chronic muscle damage from heavy lifting contribute. GH may reduce GlycA through anti-inflammatory effects, partially counteracting AAS-driven elevation. GlycA independently predicts cardiovascular events and all-cause mortality.