Why this panel
Testosterone replacement isn’t a set-and-forget therapy. The HPG axis is a feedback loop, and dropping exogenous testosterone into it has predictable downstream effects: LH and FSH suppress, estradiol rises (because aromatase converts T to E2), and red-cell production increases. The point of routine bloodwork isn’t to chase a single “ideal” testosterone number — it’s to keep the whole system in a tolerable equilibrium and catch the slow drifts (E2 creep, polycythemia) that don’t feel like anything until they’re a problem.
The same panel is useful if you’re not on TRT but you’re running peptides that affect the axis — kisspeptin (which raises endogenous T), high-dose GHRPs (which can shift SHBG), or a long GH-axis stack (CJC-1295 + ipamorelin + tesamorelin) where IGF-1 trends matter alongside the sex hormones.
The core markers
Total testosterone
The headline number. On TRT, target ranges depend on the protocol your clinician picked — some target the upper end of standard, some sit comfortably in the middle. Above-range total T isn't automatically bad; sub-range total T on TRT means the dose isn't doing what you think it is.
Free testosterone
The unbound, biologically active fraction. Most clinicians read this one over total T because it's what your tissues actually see. Free-T-by-equilibrium-dialysis is the gold standard; calculated free T from total T + SHBG + albumin is the common cheaper alternative and is reasonable.
SHBG (sex-hormone binding globulin)
Carrier protein — high SHBG means more total T is bound and unavailable. SHBG rises with thyroid hormone and dropping insulin; falls with insulin resistance, NAFLD, and high-dose testosterone. A high SHBG with a normal total T can still leave you symptomatic because free T is low.
Estradiol (E2, sensitive assay)
Aromatase converts testosterone to estradiol. On TRT, E2 rises proportional to T dose — for most men this is fine and helpful (libido, mood, joints). Above ~50 some men feel bloated or moody. Below ~15 (often from over-aggressive aromatase inhibition) you'll feel terrible — joint pain, low libido, low energy. Order the SENSITIVE assay; the standard assay isn't accurate at male E2 levels.
LH + FSH
Pituitary gonadotropins. On exogenous TRT, both will be suppressed (often < 0.5) — that's the loop closing. Useful if you're on a peptide that targets the axis directly (kisspeptin, hCG) or if you're planning a PCT/restart and need to see if the pituitary is recovering.
Hematocrit (HCT)
Red-cell percentage. Testosterone stimulates erythropoiesis; on TRT, HCT drifts up and can cross into polycythemia (commonly defined as > 52% in men, sometimes > 54%). High HCT is the most consistent TRT-related risk worth monitoring — thick blood means clot risk. Donating blood (or therapeutic phlebotomy if needed) brings it back down.
Hemoglobin (HGB)
Tracks with hematocrit. Clinicians watch the pair together; HGB > 17.5 paired with HCT > 52 is the polycythemia signal.
PSA (men 40+)
Testosterone doesn't *cause* prostate cancer (the saturation model is well-established) but it does grow whatever's there. Baseline PSA before starting TRT and yearly thereafter is standard. A rising trend matters more than any single number.
When to draw
- Time of day matters. Endogenous testosterone peaks in the morning. Draw between 7–10am for repeatable numbers. Inconsistent timing produces wide swings that look like “my dose isn’t working” but is actually circadian noise.
- Fasted is preferred. Not strictly required for sex hormones, but if your panel includes metabolic markers (HbA1c, lipids, fasting glucose) you want fasted anyway.
- Inject-day timing matters on injectable TRT. Trough (right before next injection) is the conventional draw point — gives you the worst-case T level on the protocol. Some clinicians prefer mid-cycle (~3.5 days into a weekly schedule). Pick one and stick to it so successive draws compare cleanly.
- Wait 6–8 weeks after a dose change for steady state on a long ester (cypionate, enanthate). Any earlier and you’re measuring transient state, not the equilibrium your protocol actually produces.
Reading the results
Optimal vs standard. The lab’s printed reference range is a population statistic — the middle 95% of whoever they sampled. Functional-medicine optimal ranges are tighter and reflect where most people feel best. The standard range is what flags on your lab report; the optimal range is what to discuss with a clinician you trust.
Don’t chase one number. If total T is mid-range but free T is low, the SHBG number is the story. If E2 is high but HCT is creeping up, the dose may be too high overall. Hormone bloodwork is a system, not a list — read it together.
Trends beat snapshots. Two readings on different mornings will disagree even if nothing has changed. Three or four data points across months tell you what your protocol actually produces. Juno’s lab history view (under /account/labs) plots your readings over time per marker and flags drift.
How often to retest
- Starting / changing TRT: at 6–8 weeks (steady state on long ester), then every 3 months for the first year.
- Stable on TRT: every 6 months. Some clinicians do annual once the protocol is dialed in.
- If symptoms change: retest sooner, no matter how recent the last draw was. Symptoms are real data; ranges are noisy.
What about the rest of a comprehensive panel?
The hormone panel above is the focused subset for TRT and HPG-axis monitoring. A complete annual workup also covers metabolic markers (fasting glucose, HbA1c, lipid panel), inflammation (hs-CRP), kidney (creatinine, eGFR), liver (ALT, AST), and thyroid (TSH at minimum, free T4 + T3 if you want the full picture). Those are out of scope for this guide — they’ll get their own write-ups as the lab-guide library expands.
What Juno can do with these values
Paste any of these readings into /account/labs and the lab-anomaly analyst surfaces plausible contributors — including which peptides in your active stack are documented to affect that marker. It does not diagnose; it shows what’s worth discussing with your clinician, with citations.
For total testosterone specifically, the analyst already knows about kisspeptin, semaglutide / tirzepatide / retatrutide (free T can rise modestly with significant fat loss), and any direct exogenous T you list as a medication. For E2, it knows about aromatase inhibitors and any peptide that might shift SHBG. For HCT, it knows the testosterone link is well-established and will flag the polycythemia threshold.