Other Blood Markers

Free PSA expressed as a percentage of total PSA. Used to separate benign prostate enlargement from cancer when total PSA sits in the borderline range.

PED: Its whole purpose is to add information when total PSA is equivocal, typically 4 to 10 ug/L, where an elevated result could be benign enlargement or could be cancer. Cancerous tissue produces proportionally more bound PSA, so a LOW ratio is the concerning direction, which is the opposite of how most markers on this site read. Roughly, above 25% is reassuring and below 10% carries substantially higher cancer risk. It matters here because androgens drive prostate growth and both testosterone therapy and long-term AAS use raise total PSA, so enhanced athletes hit that equivocal range more often and more often face an unnecessary biopsy decision. Note this ratio is only interpretable alongside total PSA: it is meaningless when total PSA is normal, and it does not replace urological assessment.

The pressure in your arteries when the heart contracts. The upper number in a blood pressure reading, and the stronger predictor of cardiovascular risk in adults over 50.

PED: Blood pressure is the most commonly neglected marker in enhanced athletes, and one of the few that can cause harm silently for years. Almost every AAS raises it, through some combination of water and sodium retention (oestrogenic and mineralocorticoid activity), raised haematocrit thickening the blood, reduced arterial compliance, and direct effects on the renin-angiotensin system. Trenbolone, oral 17-alpha-alkylated compounds, and anything driving haematocrit hard are the usual offenders. Stimulants (clenbuterol, ephedrine, high-dose caffeine) and GH stack on top of that. The bodybuilder target is NOT more lenient than the general target: hypertension damages kidneys, heart, and eyes at the same rate regardless of how much muscle you carry. Measure seated, after five minutes rest, arm supported at heart level, and take the average of two or three readings rather than reacting to a single spike.

The pressure remaining in your arteries between heartbeats, while the heart refills. The lower number in a blood pressure reading, and the more informative of the two in adults under 50.

PED: Diastolic pressure reflects baseline arterial resistance, so a raised diastolic in a younger lifter often shows up before systolic drifts and is an early sign of reduced arterial compliance. AAS use is associated with increased aortic stiffness independent of the absolute pressure reading. Rising diastolic alongside a normal systolic still deserves attention. As with systolic, the target for enhanced athletes is the standard target: carrying more muscle does not protect the kidneys or the retina.

How many times your heart beats per minute at rest. Reported by most home blood pressure monitors as the third number alongside systolic and diastolic.

PED: Resting heart rate is the cheapest early warning system an enhanced athlete has. It rises before most lab markers move, and a jump of 10-15 bpm above your own baseline is meaningful even when the absolute number still reads normal, which is why tracking your own trend beats comparing against a population range. Trenbolone is the compound most associated with a raised resting pulse, often alongside night sweats and poor sleep. Clenbuterol and other beta-2 agonists raise it directly, as do T3 and T4, ephedrine, yohimbine and high-dose caffeine. Non-drug causes matter just as much: rising resting heart rate is a classic sign of accumulated fatigue and inadequate recovery, and it also rises with dehydration, a heavy cut, illness, and anaemia (where the heart compensates for reduced oxygen-carrying capacity). Note that a well-trained athlete legitimately sits in the 40s and 50s, so the enhanced-athlete range here is wider at the bottom than the standard clinical range. Measure it the same way each time, seated after five minutes rest, ideally first thing in the morning.

Total body mass. Recorded to give context to other markers rather than judged on its own, since there is no clinically meaningful reference range for what a person should weigh.

PED: Weight is deliberately left without a reference range here. What a person should weigh depends entirely on height, frame, training age and what phase they are in, so flagging a bodyweight as high or low would be meaningless. It is tracked because it changes how other numbers are read. Creatinine scales with muscle mass, which is exactly why a lean 110kg lifter can show a creatinine that looks alarming on a standard range and why Cystatin C is the better kidney marker in this population. Several compounds are dosed per kilogram, so a weight recorded alongside your bloods makes those doses reconstructable later. On GLP-1 medications weight is the outcome measure, and pairing it with HbA1c and lipids shows whether the metabolic improvement tracked the weight loss. Blood pressure falls by roughly 1 mmHg per kilogram lost in people carrying excess weight. Read the trend rather than any single reading: day-to-day swings of 1-3kg are water, glycogen and gut content, not tissue. Weigh yourself the same way each time, ideally first thing in the morning after the toilet and before eating or drinking.

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).

Folate concentration inside red blood cells. Reflects tissue folate status over the previous 3-4 months (the RBC lifespan), making it a more stable marker of long-term folate stores than serum folate, which mirrors recent dietary intake.

PED: Most athletes do not need this test if serum folate is adequate. It becomes useful when serum folate is borderline, when macrocytic anaemia is present, or when long-term folate status needs confirmation independent of recent supplementation. Heavy training and AAS-driven erythropoiesis increase folate demand for DNA synthesis in new red cells. Methylfolate and folic acid both raise this marker, although MTHFR polymorphisms affect how efficiently folic acid is converted. Pair with B12 (cobalamin) and homocysteine for a full one-carbon metabolism picture, since isolated folate repletion can mask B12 deficiency and worsen neurological symptoms.

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.

A protein normally produced by the fetal liver and yolk sac that falls to low levels after birth. In adults it is used as a tumour marker, principally for hepatocellular carcinoma (primary liver cancer) and for certain testicular germ-cell tumours, and it can also rise with benign liver injury.

PED: Relevant to long-term AAS users because of liver risk. Oral 17-alpha-alkylated steroids are associated with cholestasis, hepatic adenomas, peliosis hepatis, and, rarely, hepatocellular carcinoma; AFP is one screening tool for liver tumours alongside imaging. Note that AFP also rises modestly with ordinary hepatocyte regeneration, so a mild elevation during a period of raised liver enzymes may reflect benign liver stress rather than cancer. In men it is also part of the germ-cell tumour panel alongside beta-hCG and LDH.

A glycoprotein produced in fetal gut tissue and present at low levels in healthy adults. It is used mainly as a tumour marker for colorectal cancer, where it helps monitor treatment response and detect recurrence, and can also rise with several other cancers and with benign conditions.

PED: Not a PED-specific marker, but it appears on broad screening panels that athletes sometimes order. The single most important interpretive point for this group is smoking: cigarette smokers have higher baseline CEA, so the non-smoker cutoff (about 3 ng/mL) should be relaxed to roughly 5 ng/mL in smokers. CEA is a monitoring tool, not a screening test for healthy people, and mild elevations are far more often benign (smoking, inflammation, liver or lung disease) than malignant.

A carbohydrate tumour-associated antigen used chiefly as a marker for pancreatic and biliary tract cancers, and sometimes to monitor other gastrointestinal malignancies. It is most useful for monitoring a known cancer rather than screening healthy people.

PED: Appears on comprehensive panels but has little PED-specific relevance. The key interpretive caveats: individuals who are Lewis-antigen negative (roughly 5-10% of people) cannot produce CA 19-9 at all, so a normal value never excludes disease in them, and benign obstructive or inflammatory conditions of the bile ducts, pancreas, or liver can raise it substantially. Treat a mild isolated elevation in a healthy athlete as far more likely benign than sinister.

A tumour-associated glycoprotein antigen used mainly as a marker for gastric (stomach) cancer, and sometimes ovarian and other gastrointestinal cancers. It is chiefly used to monitor known disease rather than to screen.

PED: Uncommon on athlete panels and with no PED-specific link. Its practical quirks: CA 72-4 can be transiently raised by benign gastrointestinal conditions and, notably, by some medications and supplements (proton pump inhibitors and colchicine have been reported to affect levels), so a mild isolated elevation is usually not meaningful. It is most often ordered alongside CEA and CA 19-9 for gastric cancer monitoring.

A tumour-associated antigen (a subfraction of TA-4) used as a marker for squamous cell carcinomas, most notably of the uterine cervix, and also of the head and neck, lung, and oesophagus. It is used to monitor known squamous cancers rather than to screen.

PED: Rare on athlete panels and without PED relevance. The main interpretive trap is that benign skin and mucosal conditions raise it: psoriasis, eczema, and other dermatoses, as well as benign lung and liver disease and renal impairment, can all elevate SCC antigen. Given how common skin conditions are in gym-going populations (including acne and steroid-related skin changes), a mild isolated elevation is usually benign.

The biologically active fraction of vitamin B12, bound to transcobalamin and available for uptake by cells. It differs from the standard total Vitamin B12 test, which also measures B12 bound to haptocorrin that cells cannot use. Active B12 is considered a more sensitive early indicator of true B12 status.

PED: Useful when total B12 is borderline or gives a confusing picture. Bodybuilders commonly supplement or inject B12 for energy and recovery, which raises total B12 and can mask an underlying functional deficiency; measuring active B12 (holotranscobalamin) alongside functional markers like homocysteine and methylmalonic acid gives a truer read of whether tissues are actually getting enough. Vegan or plant-heavy athletes, and those on metformin or long-term acid suppression, are at higher risk of true deficiency.

The serum level of retinol, the circulating form of vitamin A. Vitamin A is a fat-soluble vitamin essential for vision, immune function, skin and epithelial health, and cellular differentiation. Both deficiency and excess cause clinical problems.

PED: Two angles matter for this population. First, vitamin A supports skin turnover and immune function, and its derivatives (retinoids like isotretinoin) are widely used for the acne that AAS often worsen; that overlap raises the risk of stacking retinoid exposure. Second, vitamin A is fat-soluble and accumulates: high-dose supplementation or heavy liver/organ-meat intake can cause hepatotoxic vitamin A excess, which is a concern in users who already stress the liver with oral steroids. Do not megadose vitamin A on top of a hepatotoxic cycle.

The serum level of selenium, an essential trace element and cofactor for antioxidant selenoenzymes (glutathione peroxidases) and for the deiodinases that convert thyroid hormone T4 to active T3. This entry tracks the measured blood level, distinct from selenium taken as a supplement.

PED: Selenium is frequently recommended as a supplement on this platform for thyroid support and antioxidant defence, so athletes who follow that advice may want to confirm they are in range rather than over-supplementing. The therapeutic window is narrow: enough selenium supports T4-to-T3 conversion and glutathione peroxidase activity, but chronic excess (selenosis) causes hair and nail loss, garlic breath, and neuropathy. High-dose 'thyroid' or 'antioxidant' stacks can push intake into the toxic range.

The main copper-carrying protein in blood, holding roughly 90% of circulating copper and also acting as a ferroxidase in iron metabolism. It is measured chiefly to help diagnose Wilson's disease (copper overload) and to assess copper status, and it behaves as an acute-phase reactant.

PED: Not a routine PED marker, but it interacts with two things athletes care about. It is an acute-phase reactant, so it rises with inflammation and can also be elevated by high oestrogen states, which matters for AAS users running aromatising compounds or those with elevated oestradiol. It also links copper and iron handling, relevant to enhanced athletes who supplement iron heavily or run copper peptides. A low ceruloplasmin in a young person with liver or neurological symptoms should prompt evaluation for Wilson's disease.

The main antibody class guarding mucosal surfaces (gut, respiratory, and urogenital tracts) and also present in serum. Total serum IgA is measured to assess humoral immune status and, importantly, to check for selective IgA deficiency before interpreting IgA-based coeliac antibody tests.

PED: The most practical reason this shows up alongside athlete panels is coeliac testing. The standard coeliac screen (tissue transglutaminase IgA and endomysial IgA) relies on the person making normal amounts of IgA; selective IgA deficiency, which affects roughly 1 in 500 people, produces falsely negative coeliac antibodies. So a total IgA is often drawn with those tests. IgA can also rise with chronic mucosal inflammation, liver disease, and infections.

An antibody test used in the diagnosis of coeliac disease. It detects IgG antibodies against deamidated gliadin peptides, a component of gluten. It is especially valuable because it works even in people who are IgA-deficient, in whom the standard IgA-based coeliac tests can be falsely negative.

PED: Gut symptoms, bloating, and unexplained fatigue or anaemia are common complaints in dieting athletes, and coeliac disease is an under-recognised cause. This IgG-based test is the go-to when total IgA is low (selective IgA deficiency makes tTG-IgA and endomysial IgA unreliable). For accurate results the person must be eating gluten in the weeks before testing; a self-imposed gluten-free diet, common among physique athletes, can normalise the antibodies and hide the diagnosis.

The first-line blood test for coeliac disease. It measures IgA antibodies against tissue transglutaminase, the enzyme targeted by the autoimmune response to gluten. It has high sensitivity and specificity, but depends on the person producing normal amounts of IgA.

PED: The standard coeliac screen, relevant to athletes with unexplained GI symptoms, iron-deficiency anaemia, or difficulty gaining weight. Two caveats matter for this group. First, the test is only valid if the person is eating gluten: physique athletes who have already cut gluten can test falsely negative. Second, it must be interpreted alongside total IgA, because selective IgA deficiency (about 1 in 500 people) makes tTG-IgA falsely negative, in which case an IgG-based test (deamidated gliadin IgG) is used instead.

A highly specific confirmatory test for coeliac disease, reported qualitatively as positive, negative, or equivocal. It detects IgA antibodies against endomysium (connective tissue around muscle fibres) using an immunofluorescence method, and a positive result is very strongly associated with coeliac disease.

PED: Usually ordered as a confirmatory step after a positive tissue transglutaminase IgA, because its specificity for coeliac disease is very high. Like the other IgA-based coeliac tests, it is only valid while eating gluten and is unreliable in people with selective IgA deficiency (check total IgA). For athletes, the same rule applies: do not go gluten-free before the coeliac workup is complete, or the test can turn falsely negative.

A non-invasive test for active Helicobacter pylori stomach infection. After swallowing urea labelled with carbon-13, the test measures the change in labelled carbon dioxide in the breath (the 'delta' value); H. pylori splits urea and releases the labelled CO2, so a high delta indicates active infection. It is the preferred non-endoscopic test for both diagnosis and confirmation of eradication.

PED: Worth knowing about for athletes with reflux, dyspepsia, or ulcer symptoms, which can be aggravated by heavy NSAID use (common for training aches) and by the gastric stress of very high food volumes. Two practical points: recent proton pump inhibitors, antibiotics, or bismuth can suppress the bacteria and cause a false-negative, so PPIs should be stopped roughly 2 weeks and antibiotics 4 weeks before testing; and the same test is used 4+ weeks after treatment to confirm the infection is cleared.

A protein (MUC16) shed from certain epithelial surfaces, used chiefly as a tumour marker for monitoring epithelial ovarian and peritoneal cancer. It is reported in kIU/L (numerically equivalent to the older U/mL). It is primarily a female-relevant marker.

PED: CA 125 is mainly a female marker: its established role is monitoring known ovarian or peritoneal cancer and following treatment response, not general screening. It has poor specificity, being raised by many benign conditions in women, including menstruation, endometriosis, ovarian cysts, pelvic inflammation, pregnancy, and any cause of peritoneal irritation or ascites. Because of that, it is not a useful screen in people at average risk. In men it has very limited relevance and is only occasionally elevated (for example with peritoneal or pleural inflammation, liver disease with ascites, or heart failure); it appears here because broad wellness panels sometimes include it. For enhanced athletes there is no meaningful PED-specific interpretation. Any genuinely elevated or rising value should be assessed clinically rather than self-interpreted.

A metabolite that accumulates when vitamin B12 is insufficient at the tissue level, because B12 is a required cofactor for the enzyme that converts methylmalonyl-CoA onward. It is a sensitive functional marker of B12 status that can reveal a true deficiency even when serum B12 looks normal.

PED: MMA answers a question serum B12 often cannot: is there enough B12 where the cells actually use it. Serum B12 can sit in the normal range while tissue B12 is inadequate, and in that situation MMA rises early, making it the better test for suspected functional deficiency (fatigue, tingling or numbness, balance or memory changes, unexplained macrocytosis). It complements the Vitamin B12 and Active B12 (holotranscobalamin) markers already in this knowledge base: Active B12 estimates the usable fraction, MMA shows the downstream metabolic consequence of running short. Relevant to bodybuilders because frequent B12 injections are common in the community (which normalise MMA), while strict plant-based diets and metformin use (common with GH/insulin protocols) deplete B12 and can raise MMA. Note MMA also rises with impaired kidney function, so interpret alongside renal markers.

A toxic heavy metal with no safe biological role. Blood lead reflects recent and ongoing exposure, and chronic low-level exposure is linked to hypertension, cardiovascular and kidney harm, and neurological effects. There is no threshold below which lead is known to be completely safe.

PED: For enhanced athletes there is a genuine, often overlooked harm-reduction angle here: underground, gray-market, and unregulated supply chains have no meaningful quality control, and heavy-metal contamination has been documented in some unregulated supplements, imported or counterfeit products, and poorly manufactured underground-lab preparations. Anyone using such products, especially oral compounds or high-volume dosing, carries a real (if variable) contamination risk, and blood lead is a reasonable check. General environmental sources still dominate for most people: old paint and plumbing, contaminated soil and water, some traditional remedies and cosmetics, and occupational exposure (shooting ranges, battery work, renovation). The CDC blood lead reference value is 3.5 mcg/dL, a statistical threshold flagging higher-than-background exposure rather than a safety cut-off. Rising or elevated values should prompt a search for the source.

A toxic heavy metal measured in blood to assess recent exposure, most often to methylmercury from dietary fish and seafood. Chronic elevation is associated with neurological effects and, at higher levels, cardiovascular and renal toxicity.

PED: The dominant source of an elevated blood mercury in a healthy adult is diet, specifically high intake of large predatory fish (tuna, swordfish, king mackerel, shark). That is directly relevant to physique athletes who eat very large amounts of fish for lean protein: someone eating multiple tins of tuna daily can accumulate a genuinely raised mercury over time. Some contaminated or unregulated supplements can also contribute. The fish angle is nuanced, because oily fish also supply the EPA/DHA that benefit cardiovascular and metabolic health, so the goal is smarter species selection rather than cutting fish out. Practical mitigation is to favour low-mercury sources (salmon, sardines, mackerel, shrimp) and rotate protein sources. Reference ranges are lab dependent; toxicity concern rises well above the general-population reference.

Measures arsenic exposure in whole blood. Blood arsenic reflects recent exposure (it clears within a couple of days as arsenic redistributes to tissues), so urine is usually preferred for confirming exposure. Arsenic is a toxic metalloid linked to skin, neurological, and cardiovascular effects and to cancer at chronic exposure.

PED: Arsenic is a genuine contamination concern for enhanced athletes. Underground-lab (UGL) gear, some imported peptides, and low-quality supplements are not always tested for heavy metals, and contaminated products have been documented. Certain protein powders, greens powders, and seafood-derived supplements can also carry arsenic (though dietary organic arsenic from seafood is far less toxic than inorganic arsenic and transiently raises blood levels). A low or undetectable level is normal and healthy, so only high values are meaningful. The bodybuilder range equals the standard range; the difference for PED users is a higher likelihood of exposure through contaminated products, not a different healthy target.

Measures cadmium exposure in whole blood, reflecting relatively recent and ongoing exposure. Cadmium is a toxic heavy metal that accumulates in the kidneys and bones over decades and is strongly associated with cigarette smoke and some contaminated foods and supplements.

PED: Cadmium is not produced by AAS, GH, or peptides, but it is a contamination and lifestyle concern for enhanced athletes. Smoking is by far the biggest driver: smokers typically run several times higher than non-smokers. Some untested supplements (certain plant-based proteins, greens powders, cocoa and shellfish-derived products) and low-quality UGL products can also contribute. Because cadmium concentrates in and damages the kidneys over time, and PED users already stress the kidneys (high protein, high blood pressure, high muscle mass affecting creatinine), keeping cadmium exposure low is sensible harm reduction. A low value is normal; only high values are meaningful. The bodybuilder range equals the standard range.

Plasma ascorbate (vitamin C), a water-soluble antioxidant essential for collagen synthesis, immune function, and iron absorption. Deficiency causes scurvy; it is not stored in large amounts, so status depends on regular intake.

PED: Vitamin C is not directly altered by AAS, GH, or peptides, but low status is common and relevant to lifters. Vitamin C is required for collagen synthesis, so adequacy supports tendon, ligament, and connective-tissue integrity, which matters for athletes under heavy mechanical load and for recovery from injury. Restrictive contest-prep diets low in fruit and vegetables can drive intake down, and smoking and high oxidative stress increase requirements. Vitamin C also enhances non-haem iron absorption, useful for those managing iron status around blood donation. Both low and high results are worth understanding, though high values are usually benign. The bodybuilder range equals the standard range.