Last reviewed: August 2026

DHEA and the Vulva: What Human Studies Show—and What Hasn't Been Studied

DHEA is often discussed as if it were simply another hormone supplement. Its biology is more interesting than that.

Dehydroepiandrosterone, or DHEA, is a naturally occurring steroid precursor: a molecule that hormone-responsive tissues can use to make active hormones - androgens and estrogens - locally.

That process is known as intracrine metabolism.

Human vaginal tissue has been shown directly to possess the enzymatic machinery needed to convert DHEA into active androgens.[1] Prescription intravaginal DHEA, called prasterone, has also been studied in randomized clinical trials and is FDA-approved for moderate-to-severe dyspareunia associated with menopause.[2]

But there is an important anatomical problem hidden inside that evidence.

The established treatment is delivered inside the vagina.

Yet studies that have actually mapped pain in postmenopausal women with painful penetration have found that the tissue most consistently tender is often not the vaginal wall. It is the vulvar vestibule—the ring of tissue immediately surrounding the vaginal opening.[3,4]

And the vagina, vestibule and external vulva are not one interchangeable absorptive surface.

This creates a surprisingly unanswered question:

What happens when DHEA is delivered directly to vulvar and vestibular tissue rather than placed inside the vagina?

The existing science provides several important pieces of that answer.

It does not provide all of them.

What Is DHEA?

DHEA is produced naturally in the human body, primarily by the adrenal glands in midlife.

Unlike estradiol or testosterone, DHEA acts largely as a precursor. Tissues containing the appropriate enzymes can convert it through local steroidogenic pathways into active androgens—including testosterone and dihydrotestosterone (DHT)—and estrogens, including estradiol and estrone.

Importantly, this shows that these active hormones do not have to be produced in an endocrine gland and then delivered to the tissue through the bloodstream.

They can be made inside peripheral tissues themselves.

This is the principle of intracrinology.

Human vaginal tissue can make androgens from DHEA

Cellai and colleagues examined human vaginal tissue and cultured human vaginal cells and identified multiple enzymes involved in steroid hormone synthesis.

Using mass spectrometry, the investigators demonstrated that human vaginal cells could synthesize active androgens from DHEA.[1]

This provides direct human evidence that vaginal tissue can metabolize DHEA locally.

It does not prove that every genital tissue behaves identically.

That distinction becomes important when we move from the vagina to the vulva and vestibule.

The Vulva Is Not the Vagina

The terms vulva and vagina are frequently used interchangeably in everyday language.

Anatomically, they are different structures.

The vagina is the internal muscular canal.

The vulva comprises the external genital structures.

Between them lies the vulvar vestibule, the tissue surrounding the vaginal and urethral openings inside the labia minora.

These tissues also differ structurally.

An ultrastructural study comparing normal human vulvar, vaginal and keratinized perineal tissue found that vulvar epithelium resembled partially keratinized, mucosal-like tissue rather than ordinary keratinized skin.[5]

But even “the vulva” is not one uniform skin type.

The more external tissues have greater cutaneous characteristics, while tissue approaching the vaginal entrance becomes increasingly mucosal. The vestibule is a specialized mucosal region with its own innervation, vascular supply and hormone responsiveness.

Human vestibular-biopsy studies have demonstrated steroid-receptor expression and hormone-associated changes in vestibular morphology.[6,7]

This means we should not think of the lower genital tract as one continuous piece of tissue with one absorption profile.

Why the Vestibule Matters in Painful Sex

This anatomical distinction becomes particularly important when we ask a basic clinical question:

Where does postmenopausal pain with penetration actually hurt?

For decades, menopausal dyspareunia - pain with sex - has often been discussed in terms of “vaginal dryness” and vaginal atrophy.

When researchers have actually mapped tenderness structure by structure, however, a more specific pattern has emerged.

In one study, 91% had significant vestibular tenderness. Vaginal tenderness was found in 2%.

In 2022, Goetsch and colleagues performed systematic genital pain mapping in 55 postmenopausal women with moderate-to-severe dyspareunia.[3]

Nearly all—98%—had physical findings of vulvovaginal atrophy.

But the atrophy and the pain did not map to the same places.

Fifty of 55 women, or 91%, had clinically significant tenderness at one or more sites in the vulvar vestibule.

Only one of 55 women, or 2%, had significant lateral vaginal-wall tenderness.

Median pain scores at the most sensitive vestibular locations were 4–5 out of 10.

Median pain on both vaginal sidewalls was: 0.

The investigators concluded that although atrophic changes affected both the vulva and vagina, tenderness was predominantly localized to the vulvar vestibule.[3]

Pain localization in the 2022 study

Examined structure	Women with significant tenderness
Vulvar vestibule	50/55 — 91%
Labia minora/majora	1/55 — 2%
Lateral vaginal wall	1/55 — 2%
Superficial perineal muscles	8/55 — 15%
Deeper pelvic-floor muscles	Up to 31% depending on muscle
Bladder	4/55 — 7%
Uterus	2/55 — 4%

These findings do not mean that every woman's dyspareunia originates in the vestibule. Pelvic-floor dysfunction, dermatologic disorders, inflammation, infection, deeper pelvic pathology and other causes of pain must still be considered.

But they demonstrate that vaginal atrophy and vaginal pain are not necessarily the same phenomenon.

For a broader look at why sex can become painful in midlife, see Why Does Sex Hurt in Midlife?

An earlier study found the same anatomical separation

In a 2014 study of 49 estrogen-deprived breast-cancer survivors with moderate-to-severe dyspareunia, every woman had vulvar vestibular tenderness.[4]

49 of 49: vestibular tenderness.

Only one had significant vaginal mucosal tenderness.

All of the women had clinical evidence of vulvovaginal atrophy.

In other words, the vaginal tissue could be markedly atrophic without being the tissue that was tender during examination.

When topical 4% lidocaine was applied to the painful vestibular sites, the vestibular tenderness was dramatically reduced.[4]

A subsequent randomized, double-blind trial tested the same principle during penetration. Forty-six estrogen-deficient breast-cancer survivors with severe dyspareunia applied either aqueous 4% lidocaine or saline to the vulvar vestibule before penetration.

Median penetration pain was:

1.0 with vestibular lidocaine

versus

5.3 with saline placebo.[8]

This does not establish that vestibular sensitivity explains every form of menopausal dyspareunia.

It does provide functional evidence that, in appropriately selected women, the vestibule itself can be a major generator of penetration pain.

This Changes the DHEA Question

The pain-localization findings make the DHEA literature much more interesting.

The established pharmaceutical DHEA treatment is placed inside the vagina.

But a major site of provoked pain in several carefully examined postmenopausal cohorts lies outside the vaginal canal, in the vestibule.

So the scientific question is no longer simply:

Does vaginal DHEA improve menopausal dyspareunia?

We already know that it can.

A second question becomes important:

What effect does DHEA have on the vestibule?

And there is now preliminary human evidence addressing exactly that.

What Has Actually Been Proven With Vaginal DHEA?

Prasterone is pharmaceutical DHEA.

A 6.5 mg prasterone vaginal insert is FDA-approved for moderate-to-severe dyspareunia due to menopause.

These tissue changes sit within the broader clinical syndrome known as genitourinary syndrome of menopause (GSM).

Its clinical evidence base is meaningful—but it is specifically an evidence base for intravaginal administration.

In a large randomized, double-blind, placebo-controlled phase III trial, daily intravaginal 6.5 mg DHEA significantly:

decreased parabasal vaginal cells;
increased superficial vaginal cells;
lowered vaginal pH;
reduced pain during sexual activity;
improved vaginal dryness; and
improved clinical measures of vaginal secretions, epithelial integrity, epithelial thickness and tissue color.[2]

These findings establish that intravaginal DHEA produces measurable biological and clinical effects in postmenopausal women.

But the classical trial endpoints were predominantly vaginal endpoints: vaginal maturation, vaginal pH and patient-reported dyspareunia.

They did not establish where the pain itself originated.

And they did not directly study DHEA applied externally to the vestibule.

Then Researchers Looked at the Vestibule

In 2023, Goldstein, Goldstein and Kim conducted a prospective study specifically asking whether intravaginal prasterone could also affect vestibular tissue.[9]

Eleven menopausal women with moderate-to-severe dyspareunia used a 6.5 mg intravaginal prasterone insert daily for 20 weeks.

Unlike the pivotal prasterone trials, the investigators examined the vestibule separately.

They assessed:

vestibular cotton-swab pain;
vestibular tissue appearance;
vaginal tissue appearance;
vulvoscopic photographs; and
pain associated with sexual activity.

Vestibular cotton-swab pain progressively decreased and reached statistical significance at 16 weeks.

Vestibular tissue-health scores improved significantly by week 4 and remained improved through week 20.

All 11 participants showed reductions in photographed vestibular erythema and pallor by the end of the study.[9]

The study was small and open-label, so these findings require confirmation.

But anatomically, the observation is important:

DHEA was placed inside the vagina, yet measurable changes occurred in the vestibule outside the vaginal canal.

The investigators proposed that prasterone leaving the vagina passed across the vestibule and produced a local effect there.[9]

That hypothesis leads directly to the next question.

What Happens If the Target Tissue Is Treated Directly?

The concept of treating the vestibule itself is not unprecedented.

A 2023 pilot randomized comparative trial assigned 50 postmenopausal women with moderate-to-severe dyspareunia to one of two doses of estradiol cream applied directly to the vulvar vestibule nightly for 12 weeks, together with precoital silicone lubricant.[10]

Forty-seven women completed the study.

Across the two treatment groups, median intercourse pain declined by approximately 75% at 12 weeks, and tenderness at the vulvar vestibule—the most tender anatomical region—improved substantially.[10]

Because the trial compared two active estradiol doses and included lubricant rather than a placebo-only group, it cannot by itself establish the size of the estradiol-specific treatment effect.

But it supports an important anatomical principle:

the vestibule can be evaluated and treated as a specific target tissue rather than merely as an extension of the vagina.

That distinction matters when considering DHEA.

The Critical Pharmacology: Vaginal Delivery Is Not Vulvar Delivery

It is tempting to compare doses of DHEA simply by looking at milligrams.

That is pharmacologically misleading.

A milligram placed inside the vagina is not automatically equivalent to a milligram placed on the external vulva or vestibule.

The relevant chain is:

amount applied → amount crossing the epithelial barrier → local tissue concentration → local metabolism → amount reaching systemic circulation

Every step can change with anatomical route and formulation.

The vagina is a large mucosal delivery surface.

The vulva is a heterogeneous external structure containing regions with different degrees of keratinization and mucosal character.

The vestibule represents yet another epithelial micro-environment.

Human vaginal mucosa has been experimentally demonstrated to be permeable to small molecules, and vaginal delivery is a recognized route capable of producing both local and systemic exposure.[11]

That does not mean vulvar absorption is necessarily negligible.

It means it must be studied separately.

Vaginal, Vestibular and Vulvar DHEA Are Different Exposure Questions

Site / route	What is exposed	What the evidence tells us	What it does not tell us
Intravaginal DHEA	Vaginal mucosa	Randomized trials demonstrate biological and clinical activity; pharmacokinetic data exist	Does not establish external vulvar PK or dose equivalence
Vestibule exposed secondarily to vaginal DHEA	Vestibular mucosa as material leaves vagina	Pilot data show improvement in vestibular appearance and pain	Does not determine the effect of intentionally dosing the vestibule
Direct vestibular treatment	Vestibular target tissue	Estradiol studies support the vestibule as a clinically relevant treatment target	Does not establish DHEA efficacy
External vulvar DHEA	Heterogeneous vulvar and vestibular surfaces depending on application	Biologically plausible and testable	Controlled efficacy and route-specific PK remain inadequately characterized
A specific topical DHEA formulation	Depends on formulation, dose and application pattern	Must be characterized directly	Cannot be inferred from a vaginal insert simply by comparing milligrams

This is why the nominal dose alone cannot tell us whether two routes produce equivalent exposure.

What About Systemic Absorption?

“Local” administration should not be interpreted to mean that absolutely nothing reaches the circulation.

The FDA's review of intravaginal prasterone found that vaginal administration produced additional systemic exposure to DHEA metabolites, including estrogens and androgens, above endogenous exposure, although concentrations generally remained in the postmenopausal range.[12]

Importantly, the FDA pharmacology program also found that absorption changed with treatment.

The Agency noted that DHEA absorption appeared greater after the first dose than after repeated dosing and proposed that this could reflect changing permeability as initially thin postmenopausal vaginal mucosa responded to treatment.[12]

That observation reinforces the central point:

epithelial condition itself can influence uptake.

And those data describe vaginal mucosal administration.

They cannot be used to calculate systemic exposure from a product distributed externally across the vestibule and vulva.

Applied dose is not absorbed dose

Prescription prasterone contains 6.5 mg DHEA per vaginal insert.

An external vulvar formulation may contain a larger nominal amount of DHEA.

That does not mean local tissue exposure—or systemic exposure—is proportionally greater.

The correct scientific comparison is not:

6.5 mg vaginally versus X mg externally.

It is:

What local and systemic exposure results from this dose, in this formulation, applied to this anatomical site?

That requires direct testing.

Preliminary External-Route Exposure Testing at The Vulva Co

Because vaginal prasterone pharmacokinetics cannot answer the external-route question, The Vulva Co has conducted a small exploratory internal assessment of systemic hormone exposure following external vulvar application of its DHEA formulation.

At exposures of up to six times the intended dose, we observed an increase in circulating DHEA to slightly above typical postmenopausal levels.

We did not observe corresponding increases in circulating estradiol or testosterone.

These observations are preliminary.

This was a small internal assessment, not a randomized clinical trial, and the findings have not been peer reviewed. They should therefore not be interpreted as proof of clinical safety, efficacy, absence of systemic exposure, or exclusive localization of DHEA within vulvar tissue.

They are early formulation-specific exposure data.

Their relevance is narrower—but important:

The systemic exposure of an externally applied vulvar DHEA formulation should be measured directly rather than inferred from intravaginal prasterone.

Larger controlled pharmacokinetic studies are needed.

The Evidence So Far

Scientific question	Current evidence	Evidence level
Can human genital tissue convert DHEA locally?	Human vaginal cells and tissue contain steroidogenic machinery and can synthesize androgens from DHEA.[1]	Direct human mechanistic evidence
Is the vestibule hormone-responsive tissue?	Human vestibular biopsies demonstrate steroid-receptor expression and hormone-associated morphological differences.[6,7]	Direct human tissue evidence
Where is tenderness found in many postmenopausal women with dyspareunia?	In one systematic study, 91% had significant vestibular tenderness versus 2% with significant vaginal-wall tenderness; median vaginal mucosal pain was zero.[3]	Direct human clinical mapping
Is this vestibular localization reproducible in another estrogen-deficient cohort?	All 49 breast-cancer survivors studied had vestibular tenderness; significant vaginal mucosal tenderness occurred in one.[4]	Direct human clinical mapping
Can selectively anesthetizing the vestibule reduce penetration pain?	Vestibular lidocaine reduced median pain to 1.0 versus 5.3 with saline in a randomized trial.[8]	Randomized clinical evidence
Does vaginal DHEA improve menopausal dyspareunia and vaginal biology?	Multiple randomized prasterone trials demonstrate improvement.[2]	Strong randomized clinical evidence
Can vaginal DHEA affect the vestibule?	A prospective pilot found improved vestibular tissue measures and pain after intravaginal prasterone.[9]	Preliminary clinical evidence
Can the vestibule itself be treated as a target?	Direct vestibular estradiol studies support this principle.[10]	Clinical evidence, still limited
Does direct external vulvar DHEA improve symptoms?	Comparable controlled clinical studies have not yet established this.	Anecdotal yes; evidence gap
Can vaginal prasterone PK predict external vulvar DHEA PK?	No. Route, epithelium and formulation differ.	Requires direct measurement
What is the optimal external vulvar DHEA dose?	Not established.	Anecdotal; Evidence gap

Why This Matters

The usual model of menopausal genital symptoms often collapses several distinct things into one concept:

low estrogen → vaginal atrophy → vaginal dryness → painful sex.

Those relationships are real.

But they are not the whole story.

Pain-mapping studies show that a woman can have widespread vulvovaginal atrophy while provoked tenderness is highly localized to the vestibule.[3,4]

The vestibule is also hormone-responsive tissue.[6,7]

Vaginal DHEA has established clinical activity.[2]

And when researchers deliberately looked beyond the vagina, vaginally administered DHEA was associated with measurable improvement in vestibular tissue and vestibular pain.[9]

That produces a more precise scientific sequence:

Where is the pain?

Frequently, in the carefully mapped cohorts studied so far, the vestibule.

↓

Is the vestibule hormone-responsive?

Yes.

↓

Can DHEA affect it?

Preliminary human evidence suggests that intravaginal prasterone can.

↓

Was the DHEA in those studies delivered directly to the vestibule?

No.

↓

Can vaginal absorption be assumed to represent vulvar or vestibular absorption?

No.

↓

Has direct external vulvar DHEA been adequately characterized?

Not yet.

That is the evidence gap.

This is also why estrogen can improve symptoms without necessarily addressing every component of vulvar and vaginal tissue function.

Read: Why Estrogen Alone Isn’t Enough for Vaginal Tissue Health.

Is DHEA an Estrogen?

No.

DHEA is not estradiol, and it is not testosterone.

It is a steroid precursor that can be converted locally into both androgenic and estrogenic sex steroids in tissues containing the necessary enzymes.

It participates directly in sex-steroid biology, but in itself it is not active.

Its particular biological interest lies in the ability of target tissues to generate active hormones locally, like in the vulva.

Is Prasterone the Same as DHEA?

Chemically, prasterone is DHEA.

But a prescription vaginal prasterone insert is not pharmacologically equivalent to every other preparation containing DHEA.

Does DHEA Help the Vulva?

The most accurate evidence-based answer today is:

We have strong evidence that intravaginal DHEA works in postmenopausal dyspareunia and changes vaginal biology.

We also have preliminary human evidence that vaginally administered DHEA can improve the vestibule.

We do not yet have equivalent controlled evidence establishing the clinical effect of DHEA deliberately applied directly to the external vulva and vestibule.

That distinction matters.

The existing evidence creates a strong biological rationale for studying direct delivery.

What We Know—and What We Still Need to Know

We know:

Human vaginal tissue can metabolize DHEA into active androgens.[1]
The vulvar vestibule is hormonally responsive tissue.[6,7]
In carefully mapped postmenopausal dyspareunia cohorts, provoked tenderness has been concentrated predominantly at the vestibule rather than the vaginal wall.[3,4]
Selectively anesthetizing the vestibule can markedly reduce penetration pain in selected women.[8]
Intravaginal DHEA improves menopausal dyspareunia and vaginal biological endpoints.[2]
Intravaginal DHEA has also been associated with improvement in vestibular tissue and vestibular pain.[9]
Vaginal and external vulvar administration cannot be assumed to produce equivalent absorption.

We do not yet know:

the pharmacokinetics of DHEA delivered directly to different external vulvar regions;
the local tissue concentrations produced in the vestibule after direct external delivery;
the pattern of local DHEA metabolism within human vestibular tissue after topical dosing;
whether direct external DHEA changes vestibular morphology or biological markers;
whether direct external DHEA improves pain, dryness or other symptoms in controlled clinical trials;
the optimal external dose and dosing interval; or
which women are most likely to benefit.

These are not unanswerable questions.

They are the next research questions.

The Next Scientific Question Is Route × Tissue × Formulation

The scientific rationale for investigating external vulvar DHEA does not require pretending that the clinical research has already been completed.

It rests on a more interesting observation:

the biological pieces already exist, but they have not yet been assembled around the external vulvar route.

Human genital tissue can use DHEA.

A clinically important site of menopausal penetration pain can be the vestibule.

The vestibule is hormonally responsive.

Vaginal prasterone improves dyspareunia.

Vaginal prasterone can also affect vestibular tissue.

But the established delivery route targets the vagina first, while pain in carefully mapped populations is often concentrated at the vestibule.

And vaginal mucosal uptake cannot simply be used as a proxy for external vulvar or vestibular uptake.

The next question is therefore specific:

What happens when DHEA is formulated for external vulvar use and delivered directly to the tissues being targeted?

That is the question direct clinical and pharmacokinetic studies need to answer.

Frequently Asked Questions

What is DHEA?

DHEA, or dehydroepiandrosterone, is a naturally occurring steroid precursor. Tissues possessing the appropriate enzymes can convert it locally into active androgens and estrogens.

Is vaginal DHEA the same as vulvar DHEA?

The molecule may be the same, but the route is not. Vaginal administration exposes vaginal mucosa. External vulvar administration exposes different epithelial tissues, including the vestibule. Dose, absorption and tissue exposure cannot therefore be assumed to be equivalent.

Is the vestibule part of the vagina?

No. The vulvar vestibule is the tissue immediately surrounding the vaginal and urethral openings, inside the labia minora. It is part of the vulvar anatomy and is distinct from the vaginal canal.

Why does the vestibule matter in painful sex?

In several carefully examined estrogen-deficient and postmenopausal cohorts, provoked genital tenderness was concentrated predominantly at the vestibule. In one study, 91% of women had significant vestibular tenderness while only 2% had significant lateral vaginal-wall tenderness.[3]

This does not mean all painful sex originates there, but it identifies the vestibule as an important tissue to examine when penetration becomes painful.

Does DHEA help the vestibule?

A small prospective study found significant improvement in vestibular tissue measures and vestibular pain during 20 weeks of intravaginal prasterone treatment.[9]

Because the study was small and uncontrolled, it should be considered preliminary evidence.

Has DHEA been adequately studied when applied directly to the external vulva?

Not yet. The strongest clinical evidence concerns intravaginal prasterone. Comparable controlled trials designed specifically around direct external vulvar or vestibular DHEA delivery remain an important evidence gap.

Why can't we compare 6.5 mg vaginal prasterone directly with the dose in a vulvar cream?

Because the number of milligrams applied is not the same as the number of milligrams absorbed.

Different anatomical sites have different epithelial barriers, exposed surface areas and local environments. Formulation also affects delivery.

A dose comparison across routes therefore requires pharmacokinetic measurements rather than simple milligram arithmetic.

Does locally administered DHEA enter the bloodstream?

Some can. FDA pharmacology data demonstrate additional systemic steroid exposure following vaginal prasterone administration.[12]

The degree of systemic exposure from an external vulvar formulation must be measured separately, because vaginal and vulvar administration are not equivalent routes.

Is DHEA non-hormonal?

No. DHEA is an endogenous steroid precursor and participates in hormone biology. It is not estrogen or testosterone, but tissues can convert it into active estrogens and androgens.

A Note on the Evidence

Throughout this page, we deliberately distinguish among:

established human mechanistic evidence;

randomized clinical evidence;

preliminary clinical observations;

internal exploratory data;

and

questions that remain unanswered.

Evidence from prescription intravaginal prasterone should not be interpreted as proof of efficacy or safety for a different externally applied formulation.

Likewise, The Vulva Co's preliminary internal exposure observations are not presented as clinical proof.

The purpose of this review is simpler:

to show where the evidence currently leads, where it stops, and why direct vulvar research is the logical next step.

Educational note: For educational purposes only; not intended to diagnose, treat, cure or prevent any medical condition. Persistent or new symptoms should be evaluated by a qualified healthcare provider.

By Laura Kelly, DAOM, L.Ac., Dipl. O.M. A California-licensed primary care provider and nationally board-certified clinician with a clinical focus on women’s health and healthy aging. Research Scholar, Ronin Institute. ORCID: 0000-0001-6586-7308. More about Dr. Kelly

References

1. Cellai I, Di Stasi V, Comeglio P, et al. Insight on the intracrinology of menopause: androgen production within the human vagina. Endocrinology. 2021;162(2):bqaa219. doi:10.1210/endocr/bqaa219. PMID: 33247714.

2. Labrie F, Archer DF, Koltun W, et al.; VVA Prasterone Research Group. Efficacy of intravaginal dehydroepiandrosterone (DHEA) on moderate to severe dyspareunia and vaginal dryness, symptoms of vulvovaginal atrophy, and of the genitourinary syndrome of menopause. Menopause. 2016;23(3):243-256. doi:10.1097/GME.0000000000000571. PMID: 26731686. Republished in Menopause. 2018;25(11):1339-1353.

3. Goetsch MF, Garg B, Lillemon J, Clark AL. Where does postmenopausal dyspareunia hurt? A cross-sectional report. Menopause. 2022;29(6):646-653. doi:10.1097/GME.0000000000001956. PMID: 35231008.

4. Goetsch MF, Lim JY, Caughey AB. Locating pain in breast cancer survivors experiencing dyspareunia: a randomized controlled trial. Obstet Gynecol. 2014;123(6):1231-1236. doi:10.1097/AOG.0000000000000283.

5. Sargeant P, Moate R, Harris JE, Morrison GD. Ultrastructural study of the epithelium of the normal human vulva. J Submicrosc Cytol Pathol. 1996;28(2):161-170. PMID: 8964040.

6. Johannesson U, Sahlin L, Masironi B, Rylander E, Bohm-Starke N. Steroid receptor expression in the vulvar vestibular mucosa—effects of oral contraceptives and menstrual cycle. Contraception. 2007;76(4):319-325. PMID: 17900445.

7. Johannesson U, Blomgren B, Hilliges M, Rylander E, Bohm-Starke N. The vulval vestibular mucosa—morphological effects of oral contraceptives and menstrual cycle. Br J Dermatol. 2007;157(3):487-493. doi:10.1111/j.1365-2133.2007.08066.x. PMID: 17627793.

8. Goetsch MF, Lim JY, Caughey AB. A practical solution for dyspareunia in breast cancer survivors: a randomized controlled trial. J Clin Oncol. 2015;33(30):3394-3400. doi:10.1200/JCO.2014.60.7366. PMID: 26215946.

9. Goldstein SW, Goldstein I, Kim NN. Vestibular tissue changes following administration of intravaginal prasterone: a vulvoscopic open-label pilot study in menopausal women with dyspareunia. Sex Med. 2023;11(3):qfad028. doi:10.1093/sexmed/qfad028.

10. Goetsch MF, Garg B, Lillemon J, Clark AL. Treating where it hurts—a randomized comparative trial of vestibule estradiol for postmenopausal dyspareunia. Menopause. 2023;30(5):467-475. PMID: 36787525.

11. van der Bijl P, van Eyk AD. Comparative in vitro permeability of human vaginal, small intestinal and colonic mucosa. Int J Pharm. 2003;261(1-2):147-152. PMID: 12878403.

12. U.S. Food and Drug Administration, Center for Drug Evaluation and Research. NDA 208470: INTRAROSA (prasterone) vaginal insert. Clinical Pharmacology and Cross-Discipline Reviews. 2016.

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DHEA for the Vulva: What the Evidence Actually Shows