LH & FSH
Luteinizing Hormone and Follicle-Stimulating Hormone
Evidence grade 5 of 5, Settled. Read how the Atlas grades evidence.
The written rationale for this grade is still being prepared.
- FDA
- Endogenous hormones (not a product)
Reference only. Not medical advice.
What can go wrong
LH and FSH are diagnostic markers, not treatments, so the risk lies in misinterpretation. Exogenous testosterone suppresses both gonadotropins, which is why men on TRT typically show very low LH/FSH and reduced sperm production. A single elevated or borderline value should be interpreted alongside a morning total testosterone, SHBG, and clinical picture rather than in isolation.
This is something to take to a clinician. The Atlas can tell you what is known about lh & fsh in general. It cannot tell you what is happening in your body, and the difference matters most for exactly the symptoms that bring people to this page.
Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are the gonadotropins secreted by the anterior pituitary that drive testicular function. LH stimulates Leydig cells to produce testosterone; FSH stimulates Sertoli cells to support spermatogenesis. Their pattern is central to distinguishing primary from secondary hypogonadism: high LH/FSH with low testosterone points to a testicular (primary) problem, while low or inappropriately normal LH/FSH with low testosterone points to a pituitary/hypothalamic (secondary) problem.
The two pituitary signals that run the testes.
What people take it for
What it is taken for. Approval, where it exists, covers only some of these.
How it works
GnRH from the hypothalamus reaches the anterior pituitary in pulses and triggers release of LH and FSH. LH binds Leydig cell receptors to upregulate steroidogenesis and testosterone output; FSH acts on Sertoli cells to promote sperm maturation and inhibin B production. Testosterone and inhibin B feed back negatively on the pituitary and hypothalamus to keep the system in balance.
What it does to fertility
LH and FSH are themselves the drivers of fertility. Exogenous testosterone suppresses LH and FSH, shutting down intratesticular testosterone and spermatogenesis; agents like hCG (an LH analog) and FSH-based therapy are used to restart or preserve fertility.
What has to be monitored
The bloodwork this needs, and the reason it belongs with a clinician rather than a website.
- Serum LH
- Serum FSH
- Morning total testosterone
- SHBG
- Inhibin B or semen analysis where fertility is relevant
What people get wrong
Nothing recorded here yet. There is almost certainly something people get wrong about this one, and the blank space means we have not written it down, not that the record is clean.
Who profits, and who pushes back
Nobody is named here yet, because we have not done that work on this entry. Read that as unfinished. Somebody almost certainly sells this, and somebody almost certainly disputes it. Assume both until we have checked.
Set against the alternatives
Where total testosterone tells you the output, LH and FSH tell you where the problem sits along the axis. Elevated gonadotropins implicate the testes; suppressed gonadotropins implicate the brain or exogenous androgen exposure.
At a glance
- LH target
- Leydig cells (testosterone)
- FSH target
- Sertoli cells (sperm)
- Measured by
- Serum immunoassay, mIU/mL
What this entry does not yet cover
What follows is unfinished work on our side, not a finding about LH & FSH. A short entry is not a safe entry.
- Timeline. We have not built the dated record of research and regulatory events.
- Cost and market. We have not documented what it sells for or who sells it.
- Supply chain. We have not mapped where it is made.
- Who uses it. We have not documented the user groups.
- What could change. No forward-looking summary yet.
- Children and teenagers. We have not checked what is known about younger people.
- Where we land. We have not taken a position on this yet.
Sources
The studies below are named and described, but not linked. You cannot open them from here and check our reading against them, which means this page is our summary of the literature rather than a document you can verify. Weigh it accordingly until the links exist.
The studies that matter
Endocrine Society Clinical Practice Guideline on testosterone therapy2018
Recommends LH/FSH to classify hypogonadism as primary or secondary after confirming low morning testosterone on two occasions