LH (luteinising hormone)
LH is a pituitary gonadotrophin. In men, it stimulates the Leydig cells to produce testosterone. Individual readings can vary, so the result is interpreted in conjunction with testosterone, follicle-stimulating hormone (FSH) and the laboratory-specific reference range.
Auch bekannt als: LH
What LH measures
Luteinizing hormone, LH for short, is a gonadotropin from the pituitary gland. In men, it stimulates the Leydig cells in the testicles to produce testosterone. In women, LH controls the menstrual cycle; the preovulatory surge triggers the release of the egg.
LH is not released evenly, but in pulses. In a small human physiological study with ten healthy men, three 24-hour profiles were examined at intervals of 14 days and three months. The maximum individual coefficient of variation of a pulse parameter was 78.4 percent; The median coefficients of variation were between 9.7 and 37.7 percent, depending on the parameter. The study involved healthy young men, not users of anabolic-androgenic steroids (AAS) or men with hypogonadism. A single measured value should therefore not be read as a permanent property of the axis without context.
Which reference values apply?
Reference ranges depend on the laboratory, the measurement method, gender and, for women, the phase of the cycle. For the Roche-cobas assay, Labcorp states 1.7 to 8.6 mIU/mL in men. In women, 2.4 to 12.6 mIU/mL in the follicular phase, 14.0 to 95.6 mIU/mL at ovulation, 1.0 to 11.4 mIU/mL in the luteal phase and 7.7 to 58.5 mIU/mL after menopause are reported.
These values are assay-specific reference information and are not a universal limit for each laboratory. The reference range based on your own findings is decisive.
What happens after the LH signal in the Leydig cell
A mechanistic overview describes the following chain: LH binds to the LH receptor of the Leydig cell, activates cyclic AMP (cAMP) signaling and promotes the transport of cholesterol into the mitochondria. Testosterone is produced via the enzyme CYP11A1 and other steroidogenic enzymes. The overview combines findings from human, cell and other models. It therefore explains a plausible biological pathway, but does not prove that a single LH value predicts later axis recovery or specific testosterone development.
How exogenous testosterone administration suppresses LH
A human randomized controlled trial in 51 healthy men compared a control period of six months of intramuscular testosterone enanthate at doses of 25, 50, 100, or 300 mg per week. Testosterone enanthate resulted in dose-dependent suppression of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and sperm production. At 50 mg per week, LH was 65 percent of the control value, at 100 mg it was 32 percent; 300 mg was no more effective than 100 mg for this endpoint. These data show suppression during controlled testosterone exposure, not the course after discontinuation, and not the effect of each heterogeneous AAS use.
The strength of the suppression is not the same for every man. In a retrospective cohort of 227 men with testosterone deficiency, 73 percent had LH below 1.0 IU/mL at least once during follow-up, but only 22 percent remained below this threshold throughout treatment. Intramuscular administration was associated with a higher likelihood of suppression, with an adjusted odds ratio of 2.44. The limit of 1.0 IU/mL was the study definition and not a general target value.
How long recovery can take after AAS
A systematic review with meta-analysis evaluated four studies with a total of 35 men comparing gonadotropins during versus after AAS and three studies with 17 men comparing before versus after AAS. In the included data, gonadotropins increased gradually toward baseline after discontinuation and reached this within 13 to 24 weeks. AAS exposures and follow-up were heterogeneous, and standardized post-cycle therapy (PCT) was not tested.
A retrospective cohort included 641 men examined with a single non-fasting random blood test between 2015 and 2022 within less than 36 months of AAS discontinuation. A combined normalization of LH, FSH and total testosterone reached 48.2 percent. With self-reported PCT, the median time to this composite endpoint was 13.0 versus 26.0 weeks without PCT. In the group that had discontinued three months or less previously, PCT was associated with a higher likelihood of combined normalization, with an adjusted odds ratio of 3.80. The association was not randomized and does not demonstrate efficacy or safety of PCT; No corresponding association was observed with discontinuation more than three months ago. A general rule that LH must be normal four to six weeks after the end of PCT cannot be derived from this.
What LH means along with testosterone and FSH
For men with recurrent low testosterone, a clinical guideline recommends LH and FSH to clarify the cause. Low gonadotropins with low testosterone is more consistent with secondary hypothalamic-pituitary hypogonadism. Elevated gonadotropins are more consistent with a primary testicular disorder. For the classification, symptoms, repeated morning testosterone measurements, sex hormone binding globulin (SHBG) or free testosterone as well as, depending on the findings, prolactin, iron saturation and, if necessary, a pituitary MRI are also taken into account.
Low testosterone together with low LH is therefore a diagnostic constellation, but not proof that the axis is simply “sleeping” after a PCT. Additionally, available data does not make a single LH value a reliable individual timer of recovery. Conversely, low testosterone and elevated LH are more likely to indicate a disorder at the testicular level. Both patterns need clinical context and joint evaluation with FSH and testosterone.
What tamoxifen, human chorionic gonadotropin (hCG) and prolactin cannot be derived from the LH value
Tamoxifen can increase hormone levels, but does not prove AAS recovery
A small double-blind cross-over study in 16 infertile men with idiopathic oligozoospermia compared tamoxifen 20 mg daily for six months and placebo for six months. Tamoxifen significantly increased LH, FSH, estradiol and testosterone, each with p less than 0.001. However, sperm analysis did not differ significantly. The population did not have an AAS or PCT context, and a biochemical LH surge therefore cannot be read as evidence of better long-term axis recovery.
Despite sharing a receptor, human chorionic gonadotropin (hCG) is not the same as LH
LH and hCG act on the common LH/CG receptor. However, a mechanistic overview describes differences in molecular properties, half-lives and signaling profiles. The common receptor therefore proves neither a biological equivalence nor a specific suppression of endogenous LH or a later recovery of the hypothalamic-pituitary-testicular axis in the context of strength training.
Prolactin works depending on duration and context
A narrative review of men with hyperprolactinemia describes that chronically elevated prolactin can inhibit the pulsatile release of gonadotropin-releasing hormone (GnRH), thereby lowering LH, FSH, and testosterone. In a small human physiological study in nine healthy men, a short-term increase in prolactin over 1.5 to 3 hours to approximately two to three times, from 10.5 to 30.9 or from 9.5 to 17.4 µg/L, depending on the protocol, resulted in no significant change in LH, FSH, or thyrotropic hormone (TSH). It does not follow from the chronic mechanism described and the acute null finding that a single elevated prolactin value automatically means chronic hyperprolactinemia with LH suppression.
What energy availability and training can contribute
A narrative review describes possible negative changes in sex hormones with limited energy availability in male endurance athletes, but emphasizes that data in men are limited. There is a lack of reliable data for male strength athletes and an isolated LH endpoint; The question of whether “overtraining” permanently lowers LH has also not been answered. A severe calorie deficit or overtraining cannot therefore be reliably identified as the cause of a permanently low LH in strength athletes.
How the value is practically classified
- Use the reference range of your own laboratory and take gender and, for women, the cycle phase into account. A range from a single assay is not a universal cutoff.
- Interpret individual values carefully because of the pulsatile distribution instead of deriving a permanent property of the axis from them.
- If testosterone is repeatedly low, do not look at LH in isolation, but rather classify it together with FSH and the additional information recommended by the guidelines.
- LH suppression has been proven in controlled human studies when exogenous testosterone is administered, but its extent is variable. A value close to zero is therefore not a generally valid finding; Based on the available data, no reliable statement about subsequent recovery can be derived from this alone.
- Do not assume a fixed four to six week time point as the target value after stopping AAS. The available data describe group-related courses over weeks to months and do not describe a reliable individual LH schedule.
LH is therefore a signal of hormonal control, the value of which depends on pulsatility, physiological context and exposure at the time of blood sampling. The data presented do not demonstrate that a single LH value reliably predicts subsequent axis recovery.
Sources
- MedlinePlus. Luteinizing Hormone (LH) Levels Test. U.S. National Library of Medicine. Open source
- Labcorp. 004283: Luteinizing Hormone (LH) Information. Open source
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