Blood Markers: Complete Reference for Bodybuilders

Enzyme primarily found in the liver. Elevated levels indicate liver cell damage.

PED: Oral AAS (especially 17-alpha alkylated compounds like Dianabol, Anadrol, Winstrol) significantly elevate ALT. Intense weight training can also cause mild elevation. Values 2-3x upper limit common on orals. Values up to ~100 U/L on oral AAS are common but should not be ignored long-term.

Enzyme found in liver, heart, and muscles. Elevated by liver damage or muscle breakdown.

PED: Both liver stress and heavy training elevate AST. Post-workout AST can be 2-3x normal. When AST is elevated but ALT is normal, it often indicates muscle damage rather than liver issues. Oral AAS will elevate both. Key diagnostic tip: if AST is high but ALT and GGT are normal, it is almost certainly muscle damage from training -- not liver stress.

Enzyme involved in bile duct function. Sensitive marker for liver/bile duct issues and alcohol use.

PED: Can be elevated by oral AAS. More specific to liver than AST/ALT since it's not affected by muscle damage. Good confirmatory test for liver stress vs training-induced elevation. If GGT is elevated alongside ALT/AST, liver stress is confirmed. If GGT is normal but AST/ALT are elevated, the elevation is likely from muscle damage, not liver.

Enzyme found in liver, bones, and other tissues. Elevated in liver or bone disorders.

PED: Less commonly affected by AAS than ALT/AST. Can be mildly elevated with bone-loading exercise. If elevated with normal GGT, likely bone origin rather than liver.

Waste product from red blood cell breakdown. Elevated in liver disease or Gilbert's syndrome.

PED: Usually not significantly affected by AAS alone. Elevation alongside elevated liver enzymes suggests more serious liver stress. Gilbert's syndrome (benign) is common and causes chronically mild elevation.

Protein made by the liver. Low levels indicate liver dysfunction or malnutrition.

PED: Generally stable in AAS users unless significant liver compromise. High protein diets can support albumin levels. Dehydration can falsely elevate.

Total amount of protein in the blood including albumin and globulins.

PED: High protein diets and training can push toward upper range. Dehydration can artificially elevate. Not a major concern marker for AAS users.

Group of proteins made by the liver and immune system. Includes immunoglobulins.

PED: Generally not significantly affected by AAS. Elevated globulin can indicate chronic inflammation or infection. Calculated as Total Protein minus Albumin.

Enzyme found in most tissues. Elevated levels indicate tissue damage in the heart, liver, kidneys, muscles, or red blood cells.

PED: Commonly elevated in bodybuilders due to intense training (skeletal muscle damage), haemolysis from heavy exercise, and hepatic stress from oral 17-alpha-alkylated AAS. Not specific to any single organ — must interpret alongside organ-specific markers (ALT/AST for liver, CK for muscle, haptoglobin for haemolysis). Post-workout LDH can remain elevated for 24-72 hours.

Calculated ratio of serum albumin to globulin. Reflects the balance between hepatic synthetic function and immune/inflammatory protein production.

PED: Oral 17-alpha-alkylated AAS can increase hepatic albumin synthesis, potentially raising the ratio. If hepatotoxicity progresses, albumin drops and the ratio falls. Intense training stimulates albumin synthesis during recovery. High-protein diets support albumin production. Chronic inflammation from overtraining or joint injuries elevates globulins, lowering the ratio. Dehydration concentrates all proteins but can disproportionately affect the ratio. Interpret alongside albumin, globulin, total protein, and liver function markers.

Waste product from muscle metabolism. Elevated levels may indicate reduced kidney function.

PED: CRITICAL: Creatinine is directly proportional to muscle mass. Heavily muscled athletes will consistently show 'elevated' creatinine that is perfectly normal for their body composition. Creatine supplementation also elevates creatinine. Standard reference ranges are inappropriate for muscular individuals. Values up to 130 umol/L are common and normal. If creatinine is elevated, confirm kidney function with a Cystatin C test -- Cystatin C is not affected by muscle mass and gives a more accurate kidney assessment.

Calculated estimate of kidney filtration rate. Below 60 suggests kidney disease.

PED: Calculated from creatinine, so muscular athletes will show falsely low eGFR. An eGFR of 60-80 in a muscular individual is likely normal. Cystatin C-based eGFR is more accurate for athletes -- request this test to get a true picture of kidney function. If creatinine-based eGFR is low but Cystatin C is normal, kidney function is fine.

Waste product from protein metabolism. Elevated with high protein intake or kidney issues.

PED: High protein diets (common in bodybuilding) will elevate urea. This is expected and not concerning unless accompanied by elevated creatinine and low eGFR. Dehydration also elevates urea.

Product of purine metabolism. High levels can cause gout and kidney stones.

PED: High protein diets can elevate uric acid. AAS can affect uric acid levels. Adequate hydration important for clearance.

Small protein filtered by the kidneys. Unlike creatinine, Cystatin C is not affected by muscle mass, making it a more accurate kidney function marker for muscular individuals.

PED: CRITICAL: The gold-standard kidney marker for athletes with high muscle mass. Creatinine-based eGFR is unreliable in muscular individuals because creatinine scales with muscle mass, giving falsely 'elevated' readings and falsely low eGFR. Cystatin C-based eGFR removes this confounder entirely. If creatinine is elevated but Cystatin C is normal, kidney function is fine — the creatinine elevation is from muscle mass. Request this test whenever creatinine or eGFR results are ambiguous. Especially important when using nephrotoxic compounds (Trenbolone, high-dose orals) or chronic NSAID use.

Albumin in urine. Elevated levels (microalbuminuria) indicate early kidney damage, even before eGFR declines.

PED: Intense training can cause transient proteinuria — collect sample on a rest day for accurate baseline. High-dose AAS, especially trenbolone and oral 17-alpha alkylated compounds, may stress kidney filtration. Elevated urine albumin alongside high creatinine or low eGFR warrants further investigation. NSAIDs (commonly used for joint pain) can also impair renal function.

Creatinine concentration in urine. Used to calculate the albumin/creatinine ratio and assess specimen adequacy.

PED: Urine creatinine is higher in muscular individuals due to greater creatinine production from muscle mass. This is expected and not a concern — unlike serum creatinine, higher urine creatinine reflects normal excretion. A very low urine creatinine may indicate a dilute specimen (over-hydration before collection).

Ratio of urine albumin to creatinine. The primary screening marker for early kidney damage. Normal: <2.5 mg/mmol (males). Microalbuminuria: 2.5-25. Macroalbuminuria: >25.

PED: CRITICAL kidney health marker for PED users. ACR detects kidney damage earlier than eGFR changes. Trenbolone, high-dose orals (especially anadrol), and chronic NSAID use can impair renal filtration. Heavy training can cause transient elevation — always test on rest days. Serial monitoring is important: a single abnormal result should be confirmed with repeat testing. If persistently elevated alongside declining eGFR, nephrologist referral is warranted.

Calculated ratio of blood urea nitrogen to serum creatinine. Differentiates pre-renal (dehydration) from intrinsic renal causes of azotemia.

PED: CRITICAL CONFOUNDER FOR BODYBUILDERS: High muscle mass raises baseline creatinine (lowering the ratio) while high-protein diets elevate BUN (raising it). These opposing effects partially cancel out, making the ratio unreliable in isolation. Creatine supplementation further elevates creatinine. Dehydration during contest prep or weight cuts disproportionately raises BUN. Always interpret alongside individual BUN, creatinine, eGFR (preferably cystatin C-based), and hydration status. A 'normal' ratio does NOT rule out kidney issues in bodybuilders.

Primary male sex hormone. Important for muscle growth, bone density, and mood.

PED: Exogenous testosterone will show supraphysiological levels while on cycle. It suppresses the HPT axis: GnRH from the hypothalamus drops, causing LH and FSH from the pituitary to fall, removing the signal for endogenous production. After cycle without PCT, levels are severely suppressed (often <1 nmol/L) and recovery can take months. TRT doses typically target 20-30 nmol/L. Natural range 8-30 nmol/L.

Testosterone that is free or loosely bound to albumin. Represents the portion available to tissues (free T + albumin-bound T).

PED: Bioavailable testosterone includes both free testosterone and albumin-bound testosterone (which can readily dissociate). It excludes only SHBG-bound testosterone. This is a more comprehensive measure of 'usable' testosterone than free T alone. Common on US lab panels (Quest, LabCorp) where it's reported in ng/dL. On AAS/TRT, bioavailable T will be elevated proportionally to total T, modified by SHBG status.

Unbound, biologically active testosterone. More clinically relevant than total.

PED: More meaningful than total testosterone as it reflects bioavailable hormone. SHBG levels affect free testosterone significantly. AAS that lower SHBG can increase free testosterone disproportionately.

Primary estrogen. Important for bone health, lipids, and cardiovascular protection.

PED: Aromatizable AAS (testosterone, dianabol, nandrolone) increase estradiol. CRITICAL: Elevated E2 in enhanced athletes should be managed by SYMPTOMS, not numbers alone. Estradiol is cardioprotective, neuroprotective, essential for libido, joint health, and lipid profiles -- crashing it causes more harm than running it high. Symptoms of genuinely problematic high E2: sensitive/puffy nipples or gyno onset, excessive water retention and bloating, emotional instability or anxiety, erectile dysfunction or loss of libido, elevated blood pressure from fluid retention. If E2 is elevated but no symptoms are present, do NOT intervene. Optimal TRT range is 70-180 pmol/L but many enhanced athletes run higher without issues.

Pituitary hormone that stimulates testosterone production in testes.

PED: Will be completely suppressed (<0.5) while on any AAS or exogenous testosterone. Used to confirm HPTA suppression/recovery. HCG mimics LH so can maintain testicular function on cycle.

Pituitary hormone important for sperm production.

PED: Suppressed by exogenous AAS. Important for fertility considerations. Recovery of FSH post-cycle indicates HPTA is recovering.

Protein that binds sex hormones, reducing their bioavailability.

PED: Many oral AAS dramatically lower SHBG (especially Proviron, Winstrol, Anavar). Low SHBG increases free testosterone percentage. Very low SHBG can indicate oral AAS use even if testosterone appears 'normal'.

Hormone from pituitary gland. Elevated levels can affect sexual function and mood.

PED: 19-nor compounds (Nandrolone, Trenbolone) can significantly elevate prolactin. High prolactin causes sexual dysfunction (erectile issues, anorgasmia), gyno risk, and in extreme cases lactation. Should be monitored on any 19-nor cycle. If prolactin is elevated without 19-nor use, investigate pituitary function.

Steroid hormone involved in reproductive function, neuroprotection, and immune modulation. In males, produced mainly by the adrenal glands and testes.

PED: Suppressed by exogenous AAS due to HPTA shutdown. Low progesterone on cycle is expected. 19-nor compounds (Nandrolone, Trenbolone) have progestogenic activity and can cause progesterone-like side effects despite low serum levels. Relevant for assessing HPTA recovery in PCT.

Marker for prostate health. Elevated levels warrant investigation for prostate issues.

PED: AAS use, particularly DHT derivatives, can elevate PSA. Important to monitor regularly when using androgens. Elevated PSA doesn't always mean cancer but needs investigation.

Growth factor produced primarily by the liver in response to growth hormone (GH). Reflects overall GH secretion and mediates many of GH's anabolic effects. Age- and sex-specific reference ranges apply.

PED: CRITICAL marker for GH use monitoring. Exogenous GH directly elevates IGF-1 — the primary way to confirm GH is working and dose-response. Supraphysiological IGF-1 (>1.5x upper limit) indicates high GH dosing and increases risk of insulin resistance, soft tissue growth, and long-term cancer risk. AAS alone do not significantly affect IGF-1. Insulin co-administration with GH further amplifies IGF-1 levels. Target for health-conscious GH use: upper-normal range (25-35 nmol/L). Recheck 4-6 weeks after dose changes. Fasting state and time since last GH injection affect levels.

Pituitary hormone that stimulates growth, cell reproduction, and regeneration. Basal fasting levels are typically low; GH is secreted in pulses. Single measurements have limited diagnostic value without stimulation/suppression testing.

PED: Exogenous GH use will elevate random serum GH levels. Basal fasting GH < 1 mIU/L is typical for adult males not on GH. IGF-1 is a more reliable marker for monitoring GH status since it reflects integrated 24h GH secretion. Timing of blood draw relative to last GH injection significantly affects results.

Primary stress hormone produced by the adrenal cortex. Regulates metabolism, immune response, and blood pressure. Levels follow a diurnal pattern (highest in the morning).

PED: Elevated by intense training, caloric deficit, and psychological stress. Chronically elevated cortisol is catabolic and impairs recovery. Some AAS (especially Trenbolone) can increase cortisol-related symptoms. Timing of blood draw significantly affects results -- morning fasting samples are standard.

Adrenal androgen precursor. Most abundant circulating steroid. Declines with age. Reflects adrenal androgen production.

PED: Exogenous AAS suppress HPTA but DHEA-S is primarily adrenal, so it may remain relatively stable on cycle. Low DHEA-S can indicate adrenal insufficiency or chronic stress. Some athletes supplement DHEA as a mild androgen precursor during PCT.

Potent androgen converted from testosterone by 5-alpha reductase. Responsible for male sexual development, prostate growth, and androgenic effects including hair loss.

PED: DHT is 3-5x more androgenic than testosterone. Elevated by exogenous testosterone (more substrate for 5-alpha reductase) and by DHT-derivative compounds (Masteron, Primobolan, Anavar, Winstrol). High DHT drives androgenic side effects: male pattern hair loss, acne, prostate enlargement, and body hair growth.

Ratio of total testosterone to estradiol, converted to conventional units (T ng/dL / E2 pg/mL). Reflects the androgenic-to-estrogenic balance. A low ratio indicates relative estrogen dominance; a very high ratio suggests over-suppressed estradiol.

PED: Auto-calculated when both Testosterone and Estradiol are present in a blood test. IMPORTANT: This ratio is a guide, not a treatment target — E2 management should always be symptom-based. A ratio below 10 suggests significant estrogen dominance and may correlate with gyno risk, water retention, mood issues, and ED. A ratio above 40 suggests E2 may be too low relative to T, risking joint pain, poor libido, worsened lipids, and bone density loss. On TRT doses (100-200mg/week), typical ratios are 20-40. On blast doses, the ratio often drops below 20 because aromatization increases disproportionately at supraphysiological testosterone levels — this is expected and acceptable if asymptomatic. Studies show men with very low E2 (ratio >50) have 3x higher mortality than those with moderately elevated E2 (ratio 15-25). Do not chase a specific number — treat symptoms, not the ratio.

Ratio of total testosterone to SHBG, expressed as a percentage: (Total T / SHBG) × 100. Estimates the proportion of bioavailable testosterone. More useful than total T alone because SHBG status dramatically affects androgen exposure.

PED: Auto-calculated when both Testosterone and SHBG are present in a blood test. Normal male range is 30-150%. On AAS/TRT, FAI is typically very high (>200%) — this is expected and not actionable. The main clinical utility is off-cycle or on TRT: a low FAI (<30%) despite normal total T points to high SHBG as the cause of hypogonadal symptoms (low libido, erectile dysfunction, fatigue, poor recovery). On oral AAS that crush SHBG (Anavar, Winstrol, Proviron), FAI can be extremely high (>500%) even with moderate total T — this means high free androgen exposure and explains androgenic side effects despite 'normal' total T levels.

Total amount of cholesterol in the blood.

PED: AAS generally worsen lipid profiles. Oral AAS are particularly harsh on lipids. Total cholesterol alone is less meaningful than the HDL/LDL ratio and ApoB.

High-density lipoprotein - 'good' cholesterol that protects against heart disease.

PED: CRITICAL: AAS (especially oral compounds) dramatically suppress HDL, often to dangerously low levels (<0.5 mmol/L). This is one of the most significant cardiovascular risks of AAS use. HDL should be monitored closely and given time to recover between cycles. HDL typically takes 4-8 weeks to recover after dropping oral compounds.

Low-density lipoprotein - 'bad' cholesterol associated with heart disease risk.

PED: AAS typically elevate LDL. Combined with suppressed HDL, this creates an atherogenic profile. ApoB is a more accurate measure of atherogenic particle count than LDL alone.

Type of fat in the blood. Elevated levels increase cardiovascular risk.

PED: Can be elevated by high calorie bulking diets, especially high carb. GH use can worsen triglycerides. Fasted blood draw important for accurate reading (12h fast minimum).

Total cholesterol minus HDL. Captures all atherogenic lipoproteins (LDL, VLDL, IDL).

PED: Better predictor of cardiovascular risk than LDL alone. AAS worsen this marker by suppressing HDL and elevating LDL/VLDL. Target <2.5 mmol/L for primary prevention. ApoB is an even more accurate cardiovascular risk marker -- consider requesting alongside lipid panel.

Ratio of total cholesterol to HDL. Lower is better for cardiovascular health.

PED: AAS users often have very unfavourable ratios due to suppressed HDL. Ratio >5.0 indicates elevated cardiovascular risk. Optimal is <4.0.

Protein found on all atherogenic lipoprotein particles (LDL, VLDL, IDL, Lp(a)). Each particle carries exactly one ApoB molecule, making it a direct count of atherogenic particles. Considered a more accurate cardiovascular risk predictor than LDL alone.

PED: Superior to LDL for assessing cardiovascular risk in PED users. AAS worsen ApoB levels -- oral compounds are particularly harmful. Unlike LDL (which measures cholesterol content), ApoB counts the actual number of atherogenic particles, which better predicts arterial plaque buildup. Target <0.9 g/L for primary prevention, <0.7 g/L for high-risk individuals.

Genetically determined lipoprotein particle. Elevated levels are an independent risk factor for cardiovascular disease, aortic stenosis, and stroke. Levels are ~90% determined by genetics and largely unaffected by lifestyle.

PED: Lp(a) is almost entirely genetic -- AAS, diet, and exercise have minimal effect on levels. However, it is a critical cardiovascular risk marker that every PED user should know once. If elevated (>75 nmol/L or >30 mg/dL), it compounds the already elevated cardiovascular risk from AAS-worsened lipids. Test once -- if normal, no need to retest as levels are stable throughout life.

The primary structural protein of HDL particles. Superior predictor of cardiovascular risk compared to HDL-C because it directly quantifies functional HDL particles.

PED: Oral 17-alpha-alkylated AAS devastate ApoA-1. Stanozolol reduced ApoA-1 by 40% in clinical studies — it upregulates hepatic triglyceride lipase (HTGL) by 230% within 3 days, accelerating HDL catabolism. Injectable testosterone at TRT doses has minimal effect. Nandrolone showed no significant change. Compounds ranked worst to least: Stanozolol > Oxandrolone > Oxymetholone > Trenbolone > Boldenone > Testosterone > Nandrolone. Recovery is slow — ApoA-1 had not returned to baseline 6 weeks after a 14-week cycle.

The balance between atherogenic particles (ApoB) and protective particles (ApoA-1). Considered the single most powerful lipid predictor of cardiovascular risk, superior to any cholesterol ratio.

PED: AAS users get a double hit — ApoB rises (more atherogenic particles) while ApoA-1 drops (fewer protective particles), amplifying the ratio dramatically. A baseline of 0.55 can easily reach 1.2+ on an oral AAS cycle. The INTERHEART study (52 countries) found ApoB/ApoA-1 superior to any cholesterol ratio for predicting myocardial infarction, with a population-attributable risk of 54%. This is the most important single lipid marker for PED users to track.

Total number of LDL particles measured by NMR spectroscopy. More predictive of cardiovascular disease than LDL cholesterol concentration alone.

PED: AAS significantly increase LDL particle number, even when LDL-C appears only mildly elevated. Oral 17-alpha-alkylated steroids have the most pronounced effect. Discordance between LDL-C and LDL-P is common in AAS users — LDL-P often reveals higher cardiovascular risk than LDL-C suggests. Combined with HDL suppression, this creates a highly atherogenic particle profile. Trenbolone is particularly harsh on lipoprotein particle counts.

Mean diameter of LDL particles. Pattern A (large buoyant, >20.5 nm) is less atherogenic; Pattern B (small dense, <20.5 nm) is associated with increased cardiovascular risk.

PED: AAS shift LDL toward small dense Pattern B particles, increasing atherogenicity even when total LDL-C is not dramatically elevated. Oral AAS (stanozolol, oxandrolone) cause the most pronounced shift to small dense LDL. Insulin resistance from GH/insulin use compounds this shift. High triglycerides correlate with smaller LDL. Pattern B + elevated LDL-P is the most concerning combination.

Total number of HDL particles. HDL-P is a stronger predictor of cardiovascular protection than HDL cholesterol concentration.

PED: AAS profoundly suppress HDL-P, often more dramatically than HDL-C. Oral AAS cause the most severe suppression. HDL-P is a better measure of reverse cholesterol transport capacity than HDL-C alone. On-cycle HDL-P values of 15-20 umol/L are common (vs normal >30). Recovery of HDL-P after cycle cessation can take 3-6 months.

Concentration of large VLDL particles. Elevated levels indicate triglyceride-rich lipoprotein overproduction and are strongly linked to insulin resistance.

PED: GH use increases hepatic VLDL production, elevating large VLDL-P. Insulin use (common in advanced bodybuilding) and insulin resistance from GH compound this. High-calorie bulking diets (especially high-carb) drive VLDL production. Oral AAS affect hepatic lipid metabolism, contributing to VLDL elevation. Elevated large VLDL-P correlates strongly with the LP-IR score.

Concentration of large HDL particles. These are the most cardioprotective HDL subclass, responsible for the majority of reverse cholesterol transport.

PED: AAS profoundly reduce large HDL-P — these particles are the first to decline on-cycle. Oral AAS have the most severe impact. Large HDL-P is the HDL subclass most associated with cardiovascular protection. On-cycle values often drop to near-zero. Recovery after cycle cessation is slow (3-6 months). Aerobic exercise is the strongest stimulus for large HDL-P production.

Mean diameter of VLDL particles. Larger VLDL particles are more triglyceride-rich and associated with insulin resistance and metabolic dysfunction.

PED: GH use and insulin resistance increase VLDL size by promoting hepatic production of large triglyceride-rich VLDL. High-calorie bulking diets (especially high-carb) increase VLDL size. Larger VLDL particles are a key driver of the LP-IR insulin resistance score. Combined with insulin and GH use in advanced bodybuilding, VLDL size can be significantly elevated.

Mean diameter of HDL particles. Larger HDL particles are more cardioprotective, associated with better reverse cholesterol transport capacity.

PED: AAS shrink HDL particles by reducing the proportion of large cardioprotective HDL. Smaller HDL is less effective at reverse cholesterol transport. Oral AAS have the most pronounced effect on HDL size. Regular aerobic exercise promotes larger HDL particles. HDL size typically recovers post-cycle alongside HDL-C and HDL-P.

NMR-derived composite score (0-100) reflecting insulin resistance based on lipoprotein particle sizes and concentrations. Higher scores indicate greater insulin resistance.

PED: GH use induces insulin resistance, directly elevating the LP-IR score. Exogenous insulin use (common in advanced bodybuilding) creates a complex picture — insulin sensitivity may be adequate but the lipoprotein profile reflects resistance patterns. Bulking phases with high carbohydrate intake worsen LP-IR. AAS themselves have variable effects on insulin sensitivity, but the combined GH + AAS + high-calorie diet profile commonly seen in bodybuilders often produces elevated LP-IR scores. This marker integrates information from VLDL, LDL, and HDL particle sizes and subclass concentrations.

Calculated ratio of LDL to HDL cholesterol. A higher ratio indicates greater atherogenic risk. Useful as a quick cardiovascular risk assessment.

PED: AAS dramatically worsen this ratio through a dual mechanism: elevating LDL while simultaneously suppressing HDL. Oral 17-alpha-alkylated steroids cause the most severe distortion — ratios of 5-10+ are common on-cycle (vs ideal <2.5). Trenbolone is particularly harsh. Even injectable testosterone at supraphysiological doses worsens this ratio. Post-cycle recovery of this ratio depends primarily on HDL recovery, which can take 3-6 months.

Cholesterol carried by VLDL particles, which transport triglycerides from the liver. Usually estimated from triglycerides via the Friedewald equation (Triglycerides / 5 in mg/dL). Elevated levels indicate excess triglyceride-rich lipoprotein production and increased atherogenic risk.

PED: Oral/17-alpha-alkylated AAS (oxandrolone, stanozolol, methandrostenolone) increase hepatic VLDL production while suppressing HDL, creating a broadly atherogenic profile. GH stimulates hepatic VLDL secretion by enhancing lipolysis and promoting insulin resistance. The combination of oral AAS + GH + high-calorie bulking diets creates maximal VLDL elevation through multiple converging pathways. Lipid effects from AAS are generally reversible, normalising 2.5 to 4 months after discontinuation.

Oxygen-carrying protein in red blood cells.

PED: AAS stimulate erythropoiesis (red blood cell production), increasing haemoglobin. This is a significant cardiovascular risk as high haemoglobin increases blood viscosity, raising stroke and heart attack risk. Values >180 g/L are concerning and warrant immediate intervention. EQ (Boldenone) is particularly notorious for raising haemoglobin.

Percentage of blood volume occupied by red blood cells.

PED: Directly related to haemoglobin. AAS increase haematocrit. Values >0.52 increase stroke and cardiovascular risk significantly. EQ (Boldenone) is particularly notorious for raising haematocrit.

Number of red blood cells per liter of blood.

PED: Increased by AAS-stimulated erythropoiesis. Follows haemoglobin and haematocrit trends.

Number of white blood cells. Important for immune function.

PED: Not typically significantly affected by AAS. Intense training can temporarily elevate. Low values may indicate overtraining or immune suppression.

Cell fragments essential for blood clotting.

PED: Generally not significantly affected by AAS. Monitor if using compounds that affect clotting or if taking aspirin/NSAIDs regularly.

Average size of red blood cells. Helps classify types of anemia.

PED: Not typically affected by AAS. Low MCV with low iron suggests iron deficiency from blood donations.

Average amount of haemoglobin per red blood cell.

PED: Not typically affected by AAS. Low MCH with low MCV suggests iron deficiency, common in athletes who donate blood regularly to manage high haematocrit.

Average concentration of haemoglobin in red blood cells.

PED: Not typically affected by AAS. Low MCHC can indicate iron deficiency. Useful alongside MCH and MCV to classify anaemia type.

Measures variation in red blood cell size. Elevated in mixed deficiency states.

PED: Can be elevated when iron is depleted from regular blood donations while AAS are stimulating new red blood cell production. A high RDW with normal MCV may indicate early iron deficiency.

Most abundant white blood cell type. First responders to bacterial infection.

PED: Can be transiently elevated after intense training. Chronic elevation may indicate infection or inflammation. Not typically directly affected by AAS.

White blood cells important for adaptive immunity (B cells, T cells, NK cells).

PED: Can be suppressed by overtraining or extreme caloric restriction during contest prep. Chronic low lymphocytes may indicate immune suppression.

White blood cells that differentiate into macrophages. Part of innate immunity.

PED: Not typically significantly affected by AAS. May be elevated with chronic inflammation or infection.

White blood cells involved in allergic responses and parasitic infections.

PED: Not typically affected by AAS. Elevation may indicate allergic reaction, parasitic infection, or certain medications.

Rarest white blood cell type. Involved in allergic and inflammatory responses.

PED: Not typically affected by AAS. Usually present in very small numbers. Rarely clinically significant in isolation.

Average size of platelets. Larger platelets are younger and more reactive. Can indicate bone marrow activity.

PED: Not directly affected by AAS. May increase when platelet turnover is high (e.g. from heavy training-induced microtrauma). Persistently elevated MPV with low platelets warrants investigation.

Immature red blood cells released from bone marrow. The absolute count is the most reliable indicator of bone marrow erythropoietic activity.

PED: AAS stimulate erythropoiesis via increased EPO production, suppressed hepcidin, and direct bone marrow stimulation — reticulocyte counts are typically elevated on cycle. Boldenone (EQ) has particularly marked erythropoietic effects. After blood donation (common for managing high haematocrit), reticulocytes spike within 3-6 days and normalise by 9-12 days. EPO use produces dramatic elevations — counts doubling from baseline is characteristic.

Percentage of immature granulocytes (metamyelocytes, myelocytes, promyelocytes) in peripheral blood. Normally near zero; elevation indicates bone marrow stimulation or infection.

PED: AAS stimulate granulopoiesis — stanozolol has been shown to accelerate neutrophil precursor maturation in bone marrow. EPO use stimulates broad haematopoiesis including granulocyte production. Intense training itself can cause transient elevation via exercise-induced bone marrow stimulation. Mild elevation (0.5-2%) is common in enhanced athletes and usually benign. Values >3% warrant investigation for infection or bone marrow pathology regardless of PED use.

Red blood cell precursors normally confined to bone marrow. Their presence in peripheral blood indicates severe erythropoietic stress, bone marrow pathology, or extramedullary haematopoiesis.

PED: EPO use and AAS-driven erythropoiesis can push NRBCs into peripheral blood, especially at high doses. High-dose testosterone, trenbolone, and equipoise (boldenone) are strongly erythropoietic. NRBCs are rare even in enhanced athletes — their presence at >1/100 WBC is always clinically significant and warrants investigation. Combined AAS + EPO use increases risk. Severe polycythaemia (HCT >54%) can be accompanied by NRBCs.

Amount of iron circulating in the blood.

PED: AAS-driven increased red blood cell production increases iron demand. Regular blood donors (recommended for high haematocrit) may develop iron deficiency. Monitor iron studies regularly if donating blood.

Protein that stores iron. Low levels indicate depleted iron stores.

PED: Regular blood donation (recommended for AAS users with high haematocrit) depletes ferritin. Also an acute phase reactant so can be falsely elevated with inflammation. Optimal for athletes: 50-150 ug/L.

Protein that transports iron in the blood.

PED: Rises when iron stores are depleted. Good indicator of iron status alongside ferritin.

Percentage of transferrin bound with iron. Indicates iron availability.

PED: Low saturation with low ferritin confirms iron deficiency. Monitor in regular blood donors.

Measures the maximum capacity of transferrin to bind iron. Elevated in iron deficiency, reduced in iron overload or chronic inflammation.

PED: AAS-driven erythropoiesis plus regular blood donation creates high iron throughput. Each donation removes ~250mg of iron. The liver responds by producing more transferrin, raising TIBC. Interpret alongside ferritin, serum iron, and transferrin saturation — high TIBC + low ferritin + low TSAT confirms true iron deficiency (most common from donation). Low TIBC + high ferritin + low iron suggests anemia of chronic disease or inflammation (ferritin falsely elevated).

Reflects total erythropoietic activity and cellular iron demand. Unlike ferritin, it is NOT affected by inflammation, making it the most reliable iron marker in inflammatory states.

PED: The most valuable iron marker for AAS users because unlike ferritin, it is NOT an acute phase reactant — unaffected by inflammation, liver stress from oral AAS, or intense training. When ferritin appears normal but the athlete has iron deficiency symptoms (fatigue, poor recovery), sTfR reveals whether tissue iron demand is being met. The sTfR/log ferritin index (sTfR ÷ log10 ferritin) >1.8 indicates iron-deficient erythropoiesis — this should be the gold standard for AAS users who donate blood regularly.

Pituitary hormone that controls thyroid gland output.

PED: T3 supplementation (cytomel, common in contest prep) will suppress TSH. Prolonged suppression can take weeks to recover. Trenbolone may affect thyroid function in some individuals.

Active thyroid hormone. Controls metabolic rate.

PED: May be affected by severe caloric restriction during contest prep. T3 supplementation reduces T4 production through feedback. Important to check alongside TSH.

Most active thyroid hormone. Directly affects metabolic rate.

PED: Exogenous T3 use will show elevated Free T3 with suppressed TSH and T4. Contest prep caloric restriction naturally lowers T3 (metabolic adaptation). GH can improve T4-to-T3 conversion.

Autoantibodies against thyroid peroxidase. Elevated levels are the hallmark of Hashimoto's thyroiditis (autoimmune hypothyroidism).

PED: AAS reduce thyroxine-binding globulin (TBG), causing total T3/T4 to appear low while free hormones remain unchanged — this is not autoimmune. GH increases T4-to-T3 conversion and can unmask latent thyroid insufficiency if anti-TPO is borderline. Exogenous T3 (Cytomel) suppresses TSH, which can mask rising anti-TPO. If symptoms like fatigue, weight gain, or poor recovery persist post-cycle, check anti-TPO alongside TSH and Free T4 to rule out Hashimoto's.

Autoantibodies against thyroglobulin, a protein produced by the thyroid gland. Elevated levels indicate autoimmune thyroid disease, most commonly Hashimoto's thyroiditis. Also used in thyroid cancer monitoring, where TgAb interferes with thyroglobulin tumour marker assays.

PED: AAS are broadly immunosuppressive and may suppress autoantibody production, so TgAb may appear deceptively low on-cycle. Check during off-cycle or cruise periods for a more accurate reading. GH increases T4-to-T3 conversion and may unmask latent autoimmune thyroiditis in susceptible individuals. Exogenous T3 (Cytomel) profoundly suppresses TSH, which can mask a developing autoimmune process. After T3 discontinuation, TSH rebound can amplify the autoimmune response and temporarily spike TgAb.

Essential electrolyte for fluid balance, nerve and muscle function.

PED: Water manipulation during contest prep can affect sodium levels. Generally stable on AAS. Stay hydrated and maintain electrolyte balance.

Essential electrolyte for heart function and muscle contraction.

PED: Diuretic use during contest prep can dangerously deplete potassium. Critical for heart function -- low potassium can cause fatal cardiac arrhythmias. Monitor closely if using diuretics.

Electrolyte that helps maintain fluid balance and acid-base status.

PED: Generally stable on AAS. Can be affected by dehydration or excessive fluid intake. Follows sodium trends in most cases.

Key buffer in the blood that maintains acid-base balance. Low levels indicate metabolic acidosis.

PED: Can be affected by intense exercise (lactic acidosis lowers bicarbonate transiently). Generally not affected by AAS. Low values with high anion gap may indicate kidney issues.

Calculated value (Na - Cl - HCO3) that helps identify causes of metabolic acidosis.

PED: Can be transiently elevated after intense training due to lactic acid accumulation. Persistent elevation warrants investigation. Not directly affected by AAS.

Essential mineral for bones, muscles, and nerve function.

PED: Generally stable on AAS. Adequate vitamin D and calcium intake important for bone health and muscle function.

Calcium level adjusted for albumin concentration. More accurate than total calcium when albumin is abnormal. Formula: Corrected Ca = Total Ca + 0.02 × (40 - Albumin).

PED: More clinically meaningful than uncorrected calcium when albumin is low (e.g., during illness or liver stress from oral AAS). If total calcium appears normal but albumin is low, corrected calcium may reveal true hypercalcemia. Generally stable on AAS.

Essential mineral involved in hundreds of enzymatic reactions.

PED: Many athletes are deficient despite adequate diet. Important for recovery, sleep, muscle function, and over 300 biochemical reactions. Heavy sweating depletes magnesium.

Mineral important for energy production and bone health.

PED: Generally not significantly affected by AAS or training. Part of the ATP energy system.

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.

Blood sugar level. Elevated levels indicate diabetes risk.

PED: GH use can elevate fasting glucose and potentially cause insulin resistance. Important to monitor on GH, especially at higher doses. High carb diets can affect non-fasting values.

Average blood sugar over 2-3 months. Best marker for long-term glucose control.

PED: GH use can worsen HbA1c over time, indicating insulin resistance. More reliable than single glucose readings as it reflects 2-3 months average. High haematocrit from AAS can affect accuracy of some HbA1c assays. Target <5.5% for optimal metabolic health.

IFCC-standardised HbA1c measurement. Same marker as HbA1c % but in SI units. Normal: <42 mmol/mol. Pre-diabetes: 42-47. Diabetes: >=48. Conversion: mmol/mol = (% - 2.15) x 10.929.

PED: Equivalent to HbA1c % — same clinical significance. GH use can worsen HbA1c over time, indicating insulin resistance. High haematocrit from AAS can affect accuracy of some HbA1c assays. Australian labs report both units; mmol/mol is the IFCC standard.

Hormone that controls blood sugar. High levels indicate insulin resistance.

PED: GH use increases insulin resistance, requiring more insulin to control blood sugar. Some athletes use exogenous insulin (extremely dangerous -- can cause fatal hypoglycaemia). Low fasting insulin with normal glucose is optimal and indicates good insulin sensitivity.

Calculated index of insulin resistance derived from fasting glucose and fasting insulin. Lower values indicate better insulin sensitivity. The most practical tool for detecting early GH/peptide-induced metabolic dysfunction.

PED: Auto-calculated when both Fasting Glucose and Fasting Insulin are present in a blood test. Formula: (Glucose mmol/L x Insulin mIU/L) / 22.5. Lean, muscular athletes typically have lower baseline HOMA-IR (0.5-1.0) than sedentary adults. This means even 'normal' values (1.5-2.0) can represent a meaningful shift on GH or MK-677. Track the trend, not just the absolute number. A HOMA-IR that doubles from 0.8 to 1.6 over a GH cycle is a stronger signal than a single reading of 1.6 in isolation. GH, MK-677, and other GH-releasing peptides are the primary drivers of HOMA-IR elevation in this population. The index catches insulin resistance weeks before fasting glucose alone would flag a problem.

Total volume of ejaculate. Low volume may indicate obstruction, retrograde ejaculation, or hormonal insufficiency.

PED: AAS use suppresses gonadotropins (LH/FSH) which can reduce seminal fluid production from accessory glands. Volume may decrease on cycle but is typically the least affected semen parameter. HCG use on cycle helps maintain testicular contribution to volume. Recovery is usually relatively quick post-PCT compared to concentration and motility.

Number of spermatozoa per milliliter of ejaculate. WHO 6th edition lower reference limit is 16,000,000/mL (16 million/mL).

PED: CRITICAL: AAS cause profound suppression of spermatogenesis via HPT axis shutdown. FSH suppression removes the primary signal for Sertoli cells to support sperm development. Most AAS users become severely oligospermic (<5 million/mL) or azoospermic (zero sperm) within 2-3 months of cycle start. HCG maintains intratesticular testosterone but does not fully preserve spermatogenesis without FSH. Recovery post-PCT is highly variable: 6-12 months typical, but some users experience prolonged or incomplete recovery. Values near zero on cycle are expected and not alarming if temporary.

Percentage of sperm showing any movement (progressive + non-progressive). WHO 6th edition lower reference limit is 42%.

PED: Motility is severely impaired by AAS-induced hormonal disruption. Even residual sperm during AAS use often show poor motility due to disrupted epididymal maturation from low intratesticular testosterone. During recovery post-PCT, motility typically lags behind concentration recovery — sperm may return before quality does. HCG on cycle provides some protection. Values near zero on cycle are expected.

Percentage of sperm moving actively forward. WHO 6th edition lower reference limit is 30%. Most clinically relevant motility parameter for natural conception.

PED: Progressive motility is the most functionally important parameter for fertility — sperm must swim forward to reach the egg. AAS suppress this severely. During recovery, progressive motility is often the slowest parameter to normalise. A semen analysis showing adequate concentration but poor progressive motility still indicates impaired fertility. Monitor this marker closely during PCT and recovery if fertility is a goal.

Percentage of sperm with normal shape and structure (strict Kruger criteria). WHO lower reference limit is 4%.

PED: Morphology reflects the quality of spermatogenesis. AAS-disrupted hormonal milieu produces abnormal sperm forms (teratozoospermia). Even naturally, only a small percentage of sperm are morphologically normal — the 4% threshold is already low. During AAS use, morphology typically drops below this threshold. Recovery of normal morphology post-PCT can take 3+ months after concentration recovers, as it reflects a full spermatogenic cycle (~74 days). Persistently abnormal morphology after prolonged recovery may warrant fertility specialist referral.

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.