Why Don’t Women Have Prostates? A Biological Explanation

Women do have prostates, or at least the biological equivalent of one. The small cluster of glands and ducts surrounding the female urethra, long known as Skene’s glands, are now formally recognized as the female prostate. In 2002, the international body responsible for anatomical terminology officially adopted the term “female prostate gland” for these structures. The real story is not that women lack a prostate but that the same embryonic tissue develops along different paths depending on hormonal signals during fetal life.

A Shared Starting Point in the Womb

Every human embryo, regardless of genetic sex, begins with the same basic plumbing. Early in development, a structure called the urogenital sinus sits at the base of the bladder. In both male and female embryos, this tissue has the potential to become prostate tissue. What determines the outcome is hormones, specifically testosterone and its more potent derivative, dihydrotestosterone (DHT).

In a male fetus, the testes begin producing testosterone, which is then converted into DHT by an enzyme in the surrounding tissue. DHT acts on the urogenital sinus mesenchyme and triggers a cascade of events: epithelial buds push outward, branch into ducts, and eventually form the glandular architecture of the male prostate. This process depends on signaling molecules expressed in the urogenital sinus in a testosterone-dependent manner.¹ The conversion of testosterone to DHT creates a feed-forward loop: even trace amounts of DHT stimulate production of more of the enzyme that makes it, amplifying the signal and driving rapid prostate growth.²

In a female fetus, without the surge of testosterone from testes, the urogenital sinus follows a different path. The same tissue that would have become a full-sized prostate instead develops into much smaller paraurethral glands, the Skene’s glands. These glands retain many of the structural and functional features of prostate tissue, just on a far smaller scale. The critical point is that the tissue itself was always capable of becoming a prostate. What it lacked was the hormonal signal to do so. Researchers have demonstrated this directly by grafting human fetal female urethral tissue into a DHT-rich environment, where it developed into recognizable prostatic tissue.³

What the Female Prostate Looks Like

Skene’s glands sit on either side of the urethral opening in women. They are tiny compared to the male prostate, which in an adult man is roughly the size of a walnut and weighs around 20 grams. The female version consists of a small number of glandular ducts embedded in the tissue surrounding the urethra. But under a microscope, the resemblance to male prostate tissue is striking.

The first detailed electron-microscopy study of these glands found that they contain both secretory cells and basal cells, the same two cell types that define the male prostate. The researchers concluded that the female prostate functions as a genuine genitourinary organ, not a vestigial leftover.⁴ Other studies have found prostatic-type tissue appearing not only around the urethra but occasionally in unexpected locations, including the vaginal wall and vulva, where it still tests positive for prostate-specific markers.⁵

The variation between women is worth noting. Not every woman has the same amount of paraurethral glandular tissue, and in some women it may be nearly absent. This variability likely reflects differences in androgen exposure during development and possibly genetic factors that influence how the tissue responds to hormonal signals.

Why the Name Changed

For centuries, Skene’s glands were treated as minor anatomical curiosities with no clear function. Alexander Skene described them in 1880, and medical textbooks largely ignored them afterward. The push to rename them came from accumulating evidence that these glands are biochemically, structurally, and functionally equivalent to the male prostate.

The key biochemical finding was that Skene’s glands produce prostate-specific antigen, or PSA, the same protein used as a screening marker for prostate cancer in men. In women, the Skene’s glands are the principal source of PSA. This discovery, combined with the structural parallels and the shared embryonic origin, led the Federative International Committee on Anatomical Terminology to officially add “female prostate gland” to the list of recognized anatomical structures in 2002.⁶ The reasoning was straightforward: an organ that shares the same embryonic origin, the same cell types, the same biochemical markers, and similar disease patterns as the male prostate deserves the same name.⁷

PSA in Women and What It Means

Most people associate PSA exclusively with men, so the fact that women produce it catches people off guard. About 90 percent of histological studies examining Skene’s gland tissue have found expression of PSA and prostatic acid phosphatase, another classic prostate marker.⁸ The concentrations are far lower than in men, which is why PSA is not used as a clinical screening tool in women. But the protein is there, and when female prostate tissue becomes diseased, PSA levels can rise measurably.

This has practical implications. In case reports of women who developed adenocarcinoma of the Skene’s glands, elevated PSA was a consistent finding. In one systematic review covering cases from 1974 to 2022, PSA was measured in eight patients and found elevated in all of them, with levels ranging from 0.8 to over 60 ng/mL.⁹ After treatment, PSA returned to normal in every case, mirroring the pattern seen in male prostate cancer treatment. The fact that PSA functions as a disease marker in the female prostate the same way it does in the male prostate is one of the strongest arguments that these are fundamentally the same organ.

What the Female Prostate Does

In men, the prostate’s primary job is to produce a fluid that nourishes and protects sperm. That function obviously has no purpose in a woman’s body, which raises the question of why the female prostate exists at all. The honest answer is that researchers are still working this out, and the female prostate may not have a single clear-cut function the way the male prostate does.

The most discussed role involves female ejaculation. The fluid secreted by the Skene’s glands during orgasm is a small volume of thick, milky fluid that contains PSA, distinguishing it chemically from urine or vaginal lubrication.¹⁰ Whether this secretion serves a reproductive, antimicrobial, or other function is not yet clear. Some researchers have speculated that the fluid could play a role in urethral defense against infection, given the glands’ location and secretory nature, but firm evidence for this is thin.

From an evolutionary standpoint, the female prostate may simply be a byproduct of shared developmental biology. Male and female mammals develop from the same embryonic blueprint, and some structures persist in both sexes even when they serve a primary function in only one. The male nipple is the most commonly cited parallel. The female prostate may exist for a similar reason: the genetic program for building prostate tissue is shared, and without strong evolutionary pressure to eliminate it in females, it persists in a reduced form.¹¹

How Hormones Can Change the Picture

Because the female prostate develops from the same androgen-sensitive tissue as the male prostate, it retains the ability to respond to androgens throughout life. This is not just a theoretical possibility. Animal studies have shown that exposing adult female rats to testosterone causes their prostatic tissue to grow substantially, taking on the appearance of an adult male prostate’s ventral lobe.¹² In gerbils, testosterone stimulated both the growth and secretory activity of the female prostate, with the tissue expressing androgen receptors and a PSA-related protein.¹³

Estrogen exposure also affects the tissue. In gerbil studies, treatment with ethinyl estradiol (the synthetic estrogen found in many oral contraceptives) caused glandular hyperplasia, increased cell proliferation, and upregulated both androgen and estrogen receptors in the female prostate. Combined estrogen-progestogen treatment produced more concerning changes, including precancerous lesions and signs of cellular degeneration.¹⁴ These are animal findings and cannot be directly extrapolated to human contraceptive use, but they demonstrate that the female prostate is a hormonally responsive organ, not an inert remnant.

In clinical practice, the hormonal responsiveness of the female prostate most commonly surfaces in conditions that alter androgen levels. Women with polycystic ovary syndrome, for instance, have elevated androgen levels, and while large-scale studies specifically examining Skene’s gland changes in these patients are lacking, the basic biology suggests that increased androgen exposure could stimulate this tissue.

When Things Go Wrong

Because the female prostate is real glandular tissue, it can develop the same general categories of disease as any gland: cysts, inflammation, overgrowth, and even cancer. These conditions are uncommon enough that they are often initially misdiagnosed.

Skene’s gland cysts are the most frequently reported problem. They typically present as a tender, swollen mass near the urethral opening and can cause painful urination, discomfort during sex, urinary tract infections, or difficulty voiding.¹⁵ Other benign conditions documented in the female prostate include hyperplasia (tissue overgrowth), leiomyomas, adenofibromas, and even tiny stones forming within the gland ducts.¹⁶ MRI has become the preferred imaging tool for evaluating these lesions, because its soft-tissue contrast allows clinicians to see how a mass relates to surrounding structures before deciding on treatment.¹⁷

The most striking parallel with the male prostate is cancer. Adenocarcinoma of the female prostate is rare, but when it occurs, it looks remarkably like prostate cancer in men. The tumor cells test positive for PSA and prostatic acid phosphatase, the same markers used to identify male prostate cancer. Under the electron microscope, the cancer cells are structurally comparable to those of male prostate carcinoma, and the cancer likely originates from the same secretory (luminal) cell type.¹⁸

In the systematic review mentioned earlier, covering 15 cases of metastatic Skene’s gland adenocarcinoma, the typical patient was an older woman (median age 71) whose tumor was often found incidentally as a painless lesion near the urethra. Treatment ranged from local excision to radical surgery to radiation. One patient even received androgen deprivation therapy, the standard hormonal treatment for male prostate cancer, and it worked. No recurrences or cancer-related deaths were recorded during follow-up.⁹ The rarity of the disease makes it impossible to draw broad conclusions from such a small series, but the pattern reinforces just how biologically similar the male and female prostates are, right down to how they go wrong.

Not Just Humans

The female prostate is not a quirk unique to our species. It has been identified in several mammalian groups, including rodents, rabbits, bats, and dogs.¹¹ In rodents, where the most detailed comparative studies have been done, the female prostate shows strong macroscopic and microscopic similarities to the ventral lobe of the male prostate. It responds to the same hormones, expresses the same receptors, and develops from the same embryonic tissue.¹⁹

The fact that the female prostate is conserved across multiple mammalian lineages makes it harder to dismiss as meaningless. If the organ served absolutely no function, evolutionary pressure might have eliminated it over millions of years. Its persistence suggests either a subtle function that has not been clearly identified yet, or that the developmental program for building prostate tissue is so deeply embedded in mammalian biology that eliminating it in females would require disrupting pathways that are needed for other things. Probably both explanations contain some truth.

Why Textbooks Still Get It Wrong

Despite the 2002 official name change and decades of supporting research, most medical and anatomy textbooks still either omit the female prostate entirely or mention Skene’s glands only in passing as minor structures of unclear significance. This matters for patient care. When a woman develops a cyst, mass, or unexplained urinary symptoms originating from paraurethral tissue, clinicians who are unaware that this tissue is prostatic in nature may not order PSA testing, may not recognize adenocarcinoma patterns, and may not consider treatments known to work for male prostate disease.

The educational gap also feeds the misconception that prostate problems are exclusively a men’s health issue. While male prostate disease is vastly more common and more clinically significant, due to the sheer size difference between the organs, the female prostate can and does develop pathology that requires recognition and appropriate management. The knowledge that female and male prostates share an embryonic origin, biochemical identity, hormonal responsiveness, and disease spectrum is not a curiosity. It is clinically relevant information that still has not fully made it into mainstream medical training.

Researchers studying the female prostate have noted this disconnect with some frustration. One group of reviewers put it bluntly: the expression of PSA in Skene’s glands, combined with structural, functional, and pathological parallels to the male prostate, provides “convincing evidence of the existence of a prostate in women and definitive preference of the term ‘prostate’ over that of Skene’s glands and ducts.”⁷ Whether the broader medical community catches up is another question, but the science has been settled for some time.