
Peter Humaidan answers a practical question: which women in ART programmes truly need LH supplementation, and which do not. The answer cannot be reduced to a single lab value.
The first thesis: there is no single threshold for "low" serum LH. Moreover, the blood LH level does not equal the bioactivity of the molecule or receptor sensitivity — so relying on the lab value alone is wrong.
Humaidan identifies four proven groups that benefit from adding LH: hypogonadotropic hypogonadism; deep LH suppression under GnRH antagonists; POSEIDON 1–4 poor responders; and carriers of FSHR/LHR polymorphisms and the β-LH variant.
The POSEIDON concept (Patient-Oriented Strategies Encompassing Individualized Oocyte Number) frames the personalisation of stimulation in patients with a poor or suboptimal response — it is in these groups that LH support matters most.
A separate emphasis is genetics. FSH-receptor polymorphisms occur in roughly 20% of patients; the β-LH variant is a frequent but under-diagnosed cause of a "strange" response to a standard protocol.
Hence a specific strategy: for a suspected FSHR polymorphism — a higher FSH dose; for the β-LH variant — adding LH activity (hCG or recombinant LH). Different mechanisms call for different decisions.
In practice this means moving from "one dose for all" to choosing the form and the very presence of LH support according to age, ovarian reserve, the suppression protocol and the patient's genetic background.
Hypogonadotropic hypogonadism is the extreme case where follicles do not grow at all without exogenous LH; deep suppression under antagonists is a reversible but clinically meaningful mid-stimulation LH dip that is reasonable to compensate.
For POSEIDON patients the decision on LH rests not on dogma but on a combination of clinical and, where available, genetic data — this is the essence of individualisation, not a mechanical addition of LH to everyone.
Why the blood level is deceptive: the biological activity of LH depends on the molecule's isoforms, its glycosylation and the receptor sensitivity of the individual patient. Two women with the same "normal" LH may respond differently to one protocol — and the lab figure will not show it.
Humaidan therefore builds the LH-support decision as multifactorial: first, whether the patient falls into one of the four proven groups; then which mechanism predominates (LH deficiency, its suppression, or a receptor feature); and only then the choice between hCG and recombinant LH and their dose. This algorithm replaces the habit of "adding LH just in case."
The lecture's closing message is simple and practical: "don't treat everyone the same." LH supplementation is a tool for properly selected patients, not a universal add-on; its value is revealed only with a precise indication.
Is the LH you measure the same as the LH the follicle actually receives? Serum levels do not capture bioactivity or receptor function — and yet most stimulation decisions are made on a single number. A look at three patient groups where LH supplementation moves the cycle: congenital deficiency, antagonist-induced suppression and the over-35 ovarian profile.
Professor Peter Humaidan is Professor in Reproductive Endocrinology at the Fertility Clinic, Skive Regional Hospital, Aarhus University, Denmark. He is internationally recognized for his work in individualized ovarian stimulation, ovulation triggering, and luteal phase physiology, and is co-founder of both the POSEIDON concept and the APHRODITE criteria.
Author of the lecture "Personalizing LH supplementation in female infertility: which patients may benefit"