Neuroendocrine effects of androgens in adult polycystic ovary syndrome and female puberty.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanistic hypothesis without systematic search or original human data
PubMed 17710731 · doi:10.1055/s-2007-984741
What was done
This narrative review summarizes the neuroendocrine mechanisms linking hyperandrogenism, altered gonadotropin-releasing hormone (GnRH) pulsatility, and ovulatory dysfunction in adult polycystic ovary syndrome (PCOS) and female puberty. It synthesizes evidence regarding hypothalamic progesterone resistance and responses to androgen receptor blockade.
What was found
The abstract provides no quantitative data or effect sizes. It describes a mechanistic pathway in which reduced hypothalamic sensitivity to progesterone negative feedback accelerates GnRH pulse frequency, biasing pituitary secretion toward luteinizing hormone (LH) over follicle-stimulating hormone (FSH). This neuroendocrine defect is reported to be reversible with the androgen receptor antagonist flutamide, and similar progesterone insensitivity and elevated LH pulse frequency are noted in a subset of peripubertal girls with elevated androgens.
Why it matters
The review outlines how peripubertal androgen excess may initiate hypothalamic-pituitary-ovarian axis dysregulation, offering a developmental framework for the transition from adolescent hyperandrogenemia to adult PCOS.
Limits
As a narrative review, it lacks a systematic search methodology, quality assessment, and quantitative synthesis. The abstract presents a theoretical model and general pathophysiological claims without reporting sample sizes, study designs, or statistical precision.
Cited by
- supports In PCOS, rapid GnRH pulsatility from the hypothalamus shifts gonadotropin balance so that LH is approximately double the level of FSH, stimulating ovarian theca cells to overproduce androgens.