Other Blood Markers

Essential vitamin for bone health, immune function, and hormone production.

PED: Many athletes are deficient despite supplement use. Important for testosterone production, immune function, bone health, and mood. Aim for 75-150 nmol/L for optimal performance and hormonal health.

Essential vitamin for nerve function and red blood cell production.

PED: Important for energy, recovery, nerve function, and red blood cell production. Deficiency causes fatigue, neurological symptoms, and elevated homocysteine (cardiovascular risk). Critical for homocysteine metabolism alongside Folate and B6.

B vitamin essential for DNA synthesis and red blood cell production.

PED: Important for red blood cell production, DNA synthesis, and homocysteine metabolism. Adequate levels support recovery. Critical alongside B12 and B6 for keeping homocysteine levels in check (elevated homocysteine is an independent cardiovascular risk factor).

Enzyme found predominantly in skeletal muscle, cardiac muscle, and brain. The most sensitive marker of skeletal muscle damage, used to diagnose rhabdomyolysis and myopathies.

PED: Heavy resistance training routinely elevates CK to 500-2000 U/L within 24-72 hours. This is physiological, not pathological. AAS can potentiate exertional rhabdomyolysis — case reports document AAS-induced myopathy with extreme CK (>10,000 U/L). Trenbolone is particularly associated with higher muscle damage. Athletes on statins (prescribed for AAS-worsened lipids) face compounded CK elevation risk. Always draw CK after 48-72 hours of rest for a meaningful baseline.

Cardiac biomarker released from cardiomyocytes in response to myocardial wall stress. Highly sensitive for detecting heart failure, left ventricular hypertrophy, and cardiac dysfunction.

PED: Critical marker for AAS users. AAS cause concentric left ventricular hypertrophy — thickening of the heart wall from chronic hypertension and direct androgen receptor stimulation in cardiac tissue. The HAARLEM study showed 4.9% decline in LV ejection fraction after a 16-week cycle. 58% of AAS users show cardiac remodelling on echo. Trenbolone (BP elevation, severe lipid disruption), boldenone (erythrocytosis increasing cardiac workload), and GH+insulin (cardiomegaly) are the most concerning compounds. Always draw after 48+ hours of rest — intense training transiently elevates NT-proBNP.

Digestive enzyme produced exclusively by pancreatic acinar cells. More specific for pancreatic pathology than total amylase. Elevation suggests pancreatic injury or pancreatitis.

PED: 17-alpha-alkylated oral AAS can cause both hepatic and pancreatic injury. Case reports document acute pancreatitis from methandrostenolone (Dianabol) and trenbolone acetate — one case showed recurrence on re-exposure, confirming causation. GH stimulates pancreatic enzyme production; at bodybuilding doses (4-10 IU/day) risk is elevated. Exogenous insulin increases pancreatic amylase by ~61% and lipase by ~47%. The GH + insulin combination is the most concerning protocol for pancreatic health. GLP-1 agonists (semaglutide) have also been investigated for pancreatitis risk.

Pancreatic enzyme that hydrolyses triglycerides. More sensitive and specific for pancreatic pathology than amylase. The preferred diagnostic marker for acute pancreatitis.

PED: GLP-1 receptor agonists (semaglutide, tirzepatide, retatrutide) cause pharmacological lipase elevations of 28-31% without clinical pancreatitis in the vast majority of users. Up to 8.3% of GLP-1 users will exceed 3x the upper limit of normal. GH at bodybuilding doses (4-10 IU/day) stimulates pancreatic enzyme production; exogenous insulin increases lipase by approximately 47%. Oral 17-alpha-alkylated AAS can cause pancreatitis through cholestatic and direct toxic mechanisms. Hypertriglyceridemia above 11.3 mmol/L is an independent pancreatitis risk factor, relevant for athletes on lipid-worsening compounds.