Hormones Blood Markers

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.