Luteinizing Hormone (LH)

GnRH is released from the hypothalamus in pulses, driving pulsatile LH release from the pituitary. The pulsatile nature of LH secretion is physiologically important — continuous GnRH stimulation (as with GnRH analogues used pharmacologically) actually suppresses LH release via receptor downregulation.

Circulating testosterone and oestradiol exert negative feedback on both the hypothalamus (reducing GnRH pulse frequency) and the pituitary (reducing LH response to GnRH). This closed-loop system maintains testosterone within a physiological range in healthy men.

LH secretion follows a mild diurnal pattern in young men, with somewhat higher levels in the morning. This pattern attenuates with ageing. Sleep — particularly slow-wave sleep — is associated with augmented LH pulsatility and overnight testosterone release.

Serum LH in adult men: 1.7-8.6 IU/L (units are international units per litre, consistent across most laboratories). Values should always be interpreted in context with total testosterone.

Elevated LH with low testosterone indicates primary hypogonadism — the testes are failing to respond to adequate or elevated gonadotropin stimulation. Conditions include Klinefelter syndrome, testicular torsion history, orchitis, chemotherapy damage, and idiopathic primary hypogonadism.

Low or inappropriately normal LH with low testosterone indicates secondary (hypogonadotrophic) hypogonadism — the pituitary or hypothalamus is not generating adequate stimulation. Causes include pituitary tumours, hyperprolactinaemia, haemochromatosis, exogenous testosterone or anabolic steroid use, obesity, opioid use, and functional hypothalamic dysfunction.

LH is most informative when drawn simultaneously with FSH and total testosterone. Together, this trio maps the entire HPG axis. The pattern — low T + high LH = primary; low T + low/normal LH = secondary — guides both investigation and treatment.

Men using exogenous testosterone or anabolic steroids suppress endogenous LH to near-zero, causing testicular atrophy and impaired spermatogenesis. Monitoring LH during TRT discontinuation (and use of LH-stimulating agents such as hCG or clomiphene) helps assess HPG axis recovery.

Stimulation testing: a GnRH stimulation test evaluates pituitary LH reserve, and an hCG stimulation test assesses testicular Leydig cell capacity. These are useful in complex or ambiguous hypogonadism cases.

High LH (>8-10 IU/L with low testosterone) is a strong indicator of primary gonadal failure. Klinefelter syndrome (47,XXY) is the most common genetic cause and is frequently undiagnosed in adulthood. LH testing is part of the standard work-up for infertility.

Low LH in the context of hypogonadism has a broader differential diagnosis and generally requires pituitary MRI and prolactin measurement. Functional causes (obesity, sleep apnoea, opioids, high-dose cannabis) are more common than structural pituitary pathology.

Clomiphene citrate and enclomiphene — selective oestrogen receptor modulators (SERMs) — block oestrogen feedback at the hypothalamus and pituitary, raising LH (and FSH), and thereby stimulating endogenous testosterone production. These are used off-label in secondary hypogonadism to maintain fertility.