What physiological mechanisms cause female ejaculation and how are they measured?
Executive summary
Research distinguishes two related but different phenomena: “female ejaculation” — a small, whitish secretion from paraurethral (Skene’s or “female prostate”) glands that can contain prostate-specific antigen (PSA) — and “squirting” (or gushes) — often a larger-volume, bladder-derived transurethral fluid that can be diluted urine [1] [2] [3] [4]. Studies link ejaculation-type fluids to orgasmic pelvic-muscle contractions and autonomic/brainstem control similar to micturition, and investigators measure these effects using biochemical assays (PSA, creatinine), urodynamics, imaging, and pelvic electromyography [5] [2] [3] [1].
1. Anatomy at the center of the debate: Skene’s glands vs bladder
Contemporary reviews and case reports present a consistent anatomical hypothesis: a “real” female ejaculation is secreted by paraurethral/Skene’s glands (sometimes called the female prostate) and produces a small, thick, whitish fluid; in contrast, squirting is described as a large-volume expulsion of fluid originating in the urinary bladder that exits transurethrally [1] [2] [4] [3]. Authors advising clinical clarity emphasize distinguishing ejaculation from coital incontinence and vaginal transudate because the organs and mechanisms differ [2] [5].
2. Physiological mechanisms proposed: neuromuscular and glandular drivers
Multiple sources frame the physiology as involving supraspinal (brainstem/pontine) orchestration of pelvic organs, with orgasmic pelvic muscle contractions and autonomic activity producing voiding-like events; this neural pattern resembles micturition control and can trigger glandular secretion or bladder expulsion depending on anatomy and arousal [5] [3]. The clitourethrovaginal complex — the anatomical/functional unit that includes clitoral tissues, urethra and paraurethral glands — is invoked to explain how anterior vaginal wall stimulation or clitoral stimulation can activate glands or reflex pathways resulting in ejaculate or squirting [6] [4].
3. What researchers measure to tell fluids apart
Investigators use biochemical markers and physiological testing. Biochemical assays detect PSA and other prostate-associated markers consistent with Skene’s gland secretions; they also measure creatinine or other urine markers to identify bladder-derived fluid in squirting episodes [3] [1] [4]. Urodynamic studies and cystography or imaging during sexual stimulation have demonstrated transurethral bladder expulsion in squirting cases, while pelvic electromyography and observation of orgasm-associated pelvic contractions support a neuromuscular triggering mechanism across both phenomena [5] [2] [1].
4. Prevalence, variability and clinical framing
Systematic reviews report wide prevalence estimates — female ejaculation (as defined narrowly) appears in roughly 10–54% of women in various studies — a range reflecting inconsistent definitions, self-report bias and methodological differences [2]. Clinical reviewers caution that orgasmic fluid can be misidentified as urinary incontinence; when women report ejaculation without other lower urinary tract symptoms, many studies find normal voiding patterns and no pathological detrusor overactivity, supporting a physiological (not necessarily pathologic) interpretation [5] [2].
5. Points of disagreement and limitations in the literature
The literature is contentious: some historical commentators and critics argue evidence is weak or conflated with other phenomena, while biochemical and imaging work has provided counterevidence that large-volume squirting is bladder-derived and small-volume ejaculate is glandular [7] [1] [4]. Reviews note limited sample sizes, variability in stimulation methods, and ethical/practical constraints on in vivo sexual physiology research; therefore consensus on function, precise neural circuitry and prevalence remains incomplete [3] [2].
6. Practical takeaways and what remains unmeasured
Available studies establish two measurable pathways — Skene’s gland secretion (PSA-positive, small-volume) and bladder transudate (creatinine/urine markers, large-volume) — and show pelvic-muscle and pontine/micturition-like control during orgasm [1] [3] [5]. What current reporting does not mention in detail is a definitive mapping of the exact neural circuit differences between glandular ejaculation and bladder squirting in large human cohorts; available sources do not mention a standardized, large-scale protocol that simultaneously combines neuroimaging, urodynamics, biochemical assays and EMG in many participants to resolve remaining uncertainties [5] [2] [3].
Sources cited above are the literature syntheses, case reports and systematic reviews summarized in PubMed and related reviews [6] [1] [5] [2] [3] [4].