Key Benefits

• See how well LH signals your ovaries or testes to function.
• Spot ovulation problems when cycles are irregular, absent, or hard to predict.
• Clarify possible PCOS when LH is high relative to FSH and symptoms.
• Differentiate testicular versus pituitary causes of low testosterone and fertility issues.
• Flag premature ovarian insufficiency when LH is high with low estradiol.
• Explain early or delayed puberty by gauging pituitary-driven reproductive signaling.
• Guide fertility care by timing ovulation induction, trigger shots, or assisted reproduction.
• Best interpreted with FSH, estradiol, testosterone, prolactin, and your symptoms.

What is Luteinizing Hormone (LH)?

Luteinizing hormone (LH) is a protein messenger made in the front part of the pituitary gland (anterior pituitary) under signals from the brain’s control center (hypothalamus via gonadotropin‑releasing hormone, GnRH). Once released into the bloodstream, LH travels to the reproductive organs (gonads) and binds to specific cells there. It is one of the two key pituitary “gonadotropins” that coordinate human reproduction, alongside follicle‑stimulating hormone (FSH).

LH acts as the body’s reproductive timing signal. In women, a sharp rise in LH triggers the release of an egg (ovulation) and converts the emptied follicle into a hormone‑producing gland (corpus luteum) that supports progesterone and estrogen production. In men, LH stimulates cells in the testes (Leydig cells) to produce testosterone, which enables sperm development and male reproductive function. Because it links brain signals to ovarian and testicular hormone output, LH reflects the activity of the hypothalamic‑pituitary‑gonadal axis (HPG axis) and helps orchestrate puberty, menstrual cycles, and fertility.

Why is Luteinizing Hormone (LH) important?

Luteinizing hormone (LH) is the brain’s go signal to the gonads. Released by the pituitary, it triggers ovulation in ovaries and drives testosterone production in testes. Through these sex steroids, LH influences fertility, menstrual rhythm, libido, muscle and bone maintenance, red blood cell production, mood, and metabolism.

Patterns vary by sex and life stage. In cycling women, LH is low early, surges mid‑cycle to trigger ovulation, then moderates. In men, it remains fairly steady. It is very low before puberty, suppressed in pregnancy, and chronically high after menopause. Outside the ovulatory surge, mid‑range values generally indicate a well‑tuned axis.

When LH is low, the brain‑pituitary drive is muted (hypogonadotropic hypogonadism). Ovaries may not ovulate and estrogen falls: irregular or absent periods, vaginal dryness, hot flashes, low bone density, and infertility. In men, testicular testosterone drops: low libido, erectile difficulty, fatigue, loss of muscle, anemia, and reduced sperm. In teens, puberty is delayed. Low LH is expected in pregnancy.

When LH is persistently high, the pituitary is compensating for under‑responsive gonads (primary ovarian or testicular insufficiency): sex hormones fall and fertility declines; the postmenopausal pattern reflects this. A brief spike is normal at ovulation. Chronically higher LH relative to FSH can accompany polycystic ovary syndrome with irregular cycles and excess androgens. In children, high LH can signal early puberty.

Big picture: LH is a real‑time readout of the hypothalamic–pituitary–gonadal axis. Because it governs estrogen and testosterone, it links to bone strength, body composition, metabolic and cardiovascular health, cognition, and lifelong reproductive capacity; pairing LH with FSH, estradiol or testosterone, prolactin, and thyroid tests clarifies where the axis is disrupted.

What Insights Will I Get?

Luteinizing hormone (LH) is a pituitary signal that coordinates the brain–gonad axis. In ovaries it triggers ovulation and luteal progesterone; in testes it drives testosterone from Leydig cells. Through these sex steroids, LH influences fertility, bone and muscle, metabolism, cognition, and mood.

Low values usually reflect reduced hypothalamic–pituitary drive (secondary hypogonadism). Common suppressors include stress or illness, low energy availability, high prolactin (hyperprolactinemia), obesity, and certain drugs; pregnancy and hormonal contraception also lower LH. In women this impairs ovulation and cycles. In men it reduces testosterone, affecting energy, libido, and body composition. In youth it can delay puberty.

Being in range suggests an intact brain–gonad feedback loop with adequate sex-steroid output. In reproductive‑age women, LH is low‑to‑moderate except for a brief mid‑cycle surge; in men, values are steady. Optimal typically sits mid‑range, supporting stable mood, bone turnover, red cell production, and metabolic balance.

High values usually reflect reduced gonadal responsiveness (primary hypogonadism) or a normal life‑stage transition. In women, LH rises in perimenopause/menopause and premature ovarian insufficiency; it may be disproportionately high in polycystic ovary syndrome. In men, high LH with low testosterone signals testicular failure; high LH with normal testosterone suggests compensated dysfunction.

Notes: LH is pulsatile and cycle‑dependent; single measurements vary by time of day and menstrual phase. Interpretation depends on age/puberty, pregnancy, acute illness, and drugs (sex steroids, GnRH analogs, opioids). Assays differ; pairing LH with FSH, estradiol or testosterone, and prolactin refines localization.