What biological mechanisms have recent studies proposed for female ejaculation and squirting?
Executive summary
Recent studies separate two related phenomena: “female ejaculation” (small, whitish prostatic secretions from Skene’s/paraurethral glands that contain PSA) and “squirting” (larger-volume transurethral emission that is largely urine). Multiple recent reviews and case studies report that ejaculate can include prostate-like secretions with PSA while ultrasonography and dye tests show squirting largely empties the bladder [1] [2] [3] [4].
1. Anatomy under the microscope: the Skene’s (female prostate) story
Anatomical and biochemical work finds a paraurethral glandular tissue—often called Skene’s glands or the female prostate—that can produce a small, milky secretion containing prostate‑specific antigen (PSA) and other prostatic markers; authors cite this as the origin of the classic, low‑volume “female ejaculation” [1] [5]. Reviews that re‑examined historical and modern dissections conclude the female prostate is real and can expel scant, prostatic‑type fluid during orgasm [1] [2].
2. Two phenomena, two mechanisms: why scientists separate FE and SQ
Narrative reviews and systematic analyses explicitly treat female ejaculation (FE) and squirting (SQ) as etiologically different: FE is a small mechanical extrusion of paraurethral secretions, while SQ is a substantial transurethral expulsion sourced mainly from the bladder [2] [6] [5]. Authors argue they differ by source, quantity, biochemical signature, and expulsion mechanics [5] [6].
3. Imaging and dye tests: evidence that squirting comes from the bladder
Ultrasound bladder monitoring and dye‑injection protocols have directly visualized bladder filling before squirting and bladder emptying afterward; studies that injected marker dye into the bladder found the expelled fluid carried the dye, supporting a urinary origin for most squirting fluid [4] [3]. Okayama University’s visualization study echoed this: the main component of squirt fluid was urine, with occasional contribution from Skene’s secretions [3] [7].
4. Biochemistry: PSA vs. urea/creatinine signatures
Biochemical assays show a pattern: fluids classified as FE often contain PSA and lower creatinine/urea consistent with prostatic secretions, while squirting samples show urea/creatinine values like diluted urine. Several reviews and case reports point to PSA as a distinguishing marker for true prostatic secretions and to urea/creatinine as markers of urinary origin [1] [6] [4].
5. Mechanistic hypotheses for how squirting happens physiologically
Studies propose squirting occurs when intense anterior vaginal wall stimulation and pelvic floor muscle activity trigger involuntary relaxation/strain and transient bladder filling during arousal, then forceful transurethral expulsion at orgasm — essentially an orgasm‑linked, non‑pathological emission of urine possibly mixed with paraurethral secretions [8] [9] [4]. Ultrasonography showing bladder refilling during stimulation underpins this mechanical explanation [4].
6. Open questions and contested interpretations
Despite converging evidence, disagreement remains. Some researchers emphasize the female prostate’s role and argue FE and SQ may sometimes co‑occur or blend; others stress that many reported squirts are biochemically urine and caution against treating all urethral emissions as a unique ejaculatory fluid [10] [2] [4]. Reviews note that sample sizes are small, methodologies vary (self‑report vs. lab visualization), and definitions differ across studies, which fuels the debate [11] [1].
7. Why the debate matters: physiology, stigma and research gaps
The distinction matters clinically and culturally: labeling squirting as urinary has implications for how clinicians counsel patients about continence and sexual function, while recognizing a female prostate secretion reframes ejaculatory phenomena as part of reproductive‑tract biology [12] [1]. Authors repeatedly call for standardized definitions, larger controlled studies with imaging and biochemical panels, and attention to participant selection to settle remaining uncertainties [11] [1].
Limitations and provenance of this summary: this article relies only on the provided literature, which includes narrative reviews, case studies, ultrasound/dye experiments, and biochemical analyses. Available sources do not mention population‑scale, long‑term cohort studies that would estimate prevalence or causes definitively beyond the cited ranges and lab demonstrations [11] [6].