What studies have specifically investigated female ejaculation (squirting) and urinary tract infection rates?
Executive summary
Female ejaculation—the phenomenon sometimes called “squirting”—has been hypothesized to originate from Skene’s (female prostate) glands and to possibly carry antimicrobial properties that could protect the urethra, but the peer‑reviewed literature providing direct, population‑level studies tying female ejaculation events to urinary tract infection (UTI) rates is essentially absent in the provided reporting; the main explicit scientific treatment is a speculative/propositional analysis rather than an epidemiologic demonstration [1] [2]. Broad evidence shows sexual activity can increase UTI risk by moving bacteria toward the urethra, but multiple consumer and clinical sources caution that sperm or semen themselves are not the causative agents of UTIs and that proven links between ejaculation (male or female) and UTI incidence depend on bacterial transmission mechanisms rather than on ejaculate composition alone [3] [4] [5] [6].
1. The core study and its claim: a hypothesis, not an epidemiologic result
A focal piece in the scholarly discussion proposes that glandular tissue homologous to the male prostate (often called Skene’s glands or the “female prostate”) can secrete a viscous fluid during sexual stimulation and that this secretion might serve an antimicrobial, UTI‑protective role, but the article frames this as a hypothesis about function rather than reporting controlled trials or cohort data showing lower UTI rates in women who ejaculate [1] [2]. Both PubMed and ScienceDirect records summarize the same line: researchers describe anatomical and biochemical plausibility and explicitly hypothesize protection from UTIs, rather than presenting direct empirical evidence of reduced infection incidence following female ejaculation [1] [2].
2. What the clinical and consumer health literature actually measures
Clinical sources and mainstream health reporting focus on well‑established UTI risk factors—female anatomy, bacterial transfer from the perianal area during sexual activity, use of spermicides, and other behaviors—and emphasize that sexual activity generally can trigger UTIs by mechanically moving bacteria toward the urethra; these accounts do not present studies showing female ejaculation reduces or increases UTI rates [3] [7] [5] [4]. Several consumer‑facing pages specifically note that sperm/semen components are unlikely to be direct causes of UTIs and that prevention strategies target bacterial transmission (hygiene, urination after sex, avoiding spermicides), underscoring that the causal mechanism is microbial movement rather than ejaculate chemistry per se [6] [4].
3. Evidence gaps and diagnostic limitations highlighted by advocacy and specialist sources
Advocacy and specialist resources underscore a practical barrier: there is no standard test for bacterial load in female ejaculate, and urine tests may fail to detect Skene’s gland infections (skenitis), meaning observational data that would link female ejaculate microbiology to clinical UTI diagnoses are sparse or inconsistent; consequently, misclassification and underdetection are real problems for researchers attempting to measure any protective or harmful effect [8]. LiveUTIFree explicitly states a lack of standardized bacterial assays in female ejaculate and warns that skenitis can mimic or be misidentified as bladder UTI, which complicates cleanly attributing infection outcomes to ejaculatory secretions [8].
4. How to read the current state of the science
Taken together, the literature in the provided reporting shows a plausible biological hypothesis (Skene’s gland secretions might be antimicrobial) and robust evidence that sexual activity can move bacteria to the urethra and cause UTIs, but it does not include controlled clinical trials or epidemiological studies that measure UTI incidence in relation to female ejaculation frequency, composition, or microbial content; therefore the hypothesis remains unproven and understudied in the sources provided [1] [2] [3] [5] [8]. Alternative viewpoints exist in mainstream health reporting that place causal emphasis on mechanical bacterial transfer and behavioral risk factors rather than on any protective ejaculatory chemistry, an agenda consistent with public‑health prevention messaging [6] [4].
5. Bottom line and research priorities
The bottom line is clear in these sources: researchers have proposed that female ejaculation might have an antimicrobial function, but there are no specific, readily cited studies in the provided reporting that empirically measure female ejaculation (squirting) and compare UTI rates longitudinally or in randomized designs; future research needs standardized assays of ejaculate microbiology, careful clinical differentiation of Skene’s gland pathology from bladder infection, and epidemiologic designs to test whether ejaculation frequency correlates with UTI risk [1] [2] [8] [3].