LH and FSH: what they show during suppression and during recovery

LH and FSH are the difference between "my testosterone is fine" and "my testosterone is fine because I am injecting it". On therapy they are expected to be low; after it, they are how recovery is confirmed.

What they do

Luteinising hormone and follicle-stimulating hormone are pituitary gonadotrophins. LH drives testosterone production by the Leydig cells; FSH, with intratesticular testosterone, drives spermatogenesis in the Sertoli cells. Both are released in pulses under hypothalamic control, and both are suppressed by negative feedback from testosterone and estradiol.

Established clinical use That feedback loop is why they matter here. Exogenous testosterone suppresses LH and FSH, which switches off endogenous production and — because intratesticular testosterone collapses along with it — impairs spermatogenesis. This is expected physiology on therapy rather than a side effect of it, and it is why guidelines direct that fertility be discussed before treatment starts.¹

Reading them on therapy

On adequate testosterone therapy, LH and FSH at or below the bottom of the reference interval are the expected finding. A suppressed LH alongside a good total testosterone tells you the testosterone is exogenous, which you already knew — the value of measuring is in the cases where it is not suppressed, or where it is being deliberately maintained.

Established clinical use The pair also does diagnostic work before therapy that it cannot do after. Low testosterone with low or inappropriately normal LH and FSH points to a secondary, pituitary or hypothalamic, cause; low testosterone with high LH and FSH points to a primary testicular one. Those are different conditions with different workups, and once exogenous testosterone is on board the distinction can no longer be made.¹

Anyone using hCG or a SERM alongside or instead of therapy has a further reason to watch these. hCG acts at the LH receptor rather than raising LH itself, so it will not show up as a rising LH — which surprises people. SERMs and enclomiphene work by blocking feedback, and there LH and FSH are exactly the markers that show whether the drug is doing anything.

Reading them after stopping

Off-label or community practice The timing point in that note is the one people get wrong. Measuring LH and FSH while a long-acting ester is still releasing tells you about the ester, not about your recovery: the axis is still suppressed because there is still exogenous testosterone in circulation. The app's Levels tab models exactly this decay, and the practical rule community practice has landed on is to wait out the ester before drawing anything you intend to interpret as recovery.

Recovery, when it happens, generally shows as LH and FSH rising first and testosterone following. A rising LH with a still-low testosterone is a different picture from a low LH with a low testosterone, and distinguishing the two is most of the reason to measure the pair rather than testosterone alone.

How long recovery takes, and whether anything should be done to assist it, varies with how long and how heavily the axis was suppressed and with individual factors nobody can read off a chart. That belongs with a clinician, with a timeline and the actual numbers in front of them.

Units, and why the numbers look odd

LH and FSH are reported in mIU/mL or the numerically identical IU/L, so most reports agree without conversion. A report in mIU/L is a thousand-fold different and the converter handles it, but a value that looks wildly out of range is worth checking against the unit before anything else.

Both are pulsatile, so a single value is a snapshot of a rhythm. That matters less on therapy — suppressed is suppressed — and more during recovery, where a single low reading is weaker evidence than a trend.

What the app records for this marker

Compounds whose monitoring panel includes this marker

Generated by matching this marker's own aliases against the monitoring note on every compound in the app's reference, so the list is the app's, not an author's.

• Kisspeptin-10 Total T, LH, FSH, E2 every 4 weeks. LH surge 30-60 min post-injection confirms receptor response.
• Tamoxifen Total T, LH, FSH, E2 at end of PCT. Goal: LH/FSH recovering, T returning toward baseline.
• Clomiphene LH, FSH, Total T, E2 throughout PCT and 4 weeks post-completion.
• HCG E2 (HCG aromatizes significantly), Total T. LH/FSH will be suppressed — this is expected.
• Enclomiphene Total T, Free T, LH, FSH, E2, Semen analysis (if fertility is goal), every 6-8 weeks when adjusting.
• Kisspeptin-54 LH, FSH, Total T, E2 every 4 weeks. LH surge 45-60 min post-injection confirms receptor response.
• Gonadorelin LH, FSH (will show some activity unlike HCG protocols), Total T, E2, testicular volume assessment. LH response 30-60 min post-injection confirms pituitary response.
• Estriol Estradiol (E2); Estriol (E3); Progesterone; FSH / LH; Bone density annually; Breast exam / mammogram

Questions people actually ask

My LH is zero on TRT. Is that bad?

It is the expected consequence of exogenous testosterone rather than a finding. What it means practically is that your own production is switched off for as long as you are on therapy, which is the trade the therapy involves. Whether that matters to you depends mostly on fertility plans, and that is worth settling with a prescriber before starting rather than after.

Will hCG raise my LH?

No, and expecting it to is a common misreading. hCG acts at the LH receptor — it substitutes for LH rather than stimulating its release — so LH stays suppressed while the downstream effect happens anyway. The markers that move are testosterone and, over time, testicular volume.

How long after stopping should I test?

Long enough that the ester has cleared, or the result is measuring the drug rather than you. The app's Levels tab models the decay for the compound and dose you logged, which is the least arbitrary way to pick a date. What to do with the result once you have it is a clinical conversation.

Sources

Every claim above that is not a definition is either labelled by evidence tier or carries a numbered reference to one of these.

1. Bhasin S et al., Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline, J Clin Endocrinol Metab 103(5):1715 (2018) The role of LH and FSH in separating primary from secondary hypogonadism, and fertility counselling before therapy.
2. Handelsman & Wartofsky, Requirement for Mass Spectrometry Sex Steroid Assays, J Clin Endocrinol Metab 98(10):3971 (2013) Why the testosterone measured alongside these gonadotrophins needs a stated method.
3. ADLM (formerly AACC), Optimal Testing: laboratory test utilisation guidance Test-selection guidance for the hormone panel these sit in.