Dryness, burning, irritation, discomfort with penetration, and changes in sexual function can begin during perimenopause—even while periods are still occurring. Research shows that genital dryness becomes more common across the menopausal transition, while human vulvar and vaginal tissues contain both estrogen- and androgen-responsive biological systems.[1–5]

In brief

• Genital symptoms can begin before menopause. In the 2025 Australian Women’s Midlife Years study, vaginal dryness was about 2.5 times as prevalent in late perimenopause as in premenopause.[1]

• Dryness becomes more common across the menopausal transition. Longitudinal SWAN data show increasing vaginal dryness with advancing menopausal stage.[2]

• The vulvar vestibule is hormone-responsive. Human vestibular tissue expresses estrogen, progesterone, and androgen receptors.[4]

• Genital hormone biology is not exclusively estrogenic. Human vaginal tissue contains androgen receptors and enzymes capable of converting DHEA into active androgens.[5]

• DHEA has human clinical evidence, but primarily by the intravaginal route. Randomized trials of intravaginal prasterone in postmenopausal women demonstrated improvement in dyspareunia and vaginal tissue measures.[7]

• Direct external vulvar DHEA remains an evidence gap. Existing intravaginal studies cannot establish the pharmacokinetics or clinical effects of a directly applied external vulvar formulation.

Can vulvar symptoms begin before menopause?

Yes. Genital dryness and sexual discomfort can emerge during the menopausal transition, before the final menstrual period.[1–3]

Menopause itself is defined retrospectively: it is reached after 12 consecutive months without a menstrual period. The hormonal transition begins years earlier.

This distinction matters because women are often taught to expect genital changes only after menopause, when estrogen has fallen into a consistently postmenopausal range.

The evidence shows a more gradual process.

In the 2025 Australian Women’s Midlife Years study, researchers examined symptoms across reproductive stages in women aged 40–69. Among the sexual symptoms evaluated, vaginal dryness was particularly associated with late perimenopause: its prevalence was approximately 2.54 times that seen in premenopausal women after adjustment for relevant factors.[1]

Longitudinal findings from the Study of Women’s Health Across the Nation, or SWAN, tell a similar story. In 2,435 women followed for up to 17 years, vaginal dryness was reported by 19.4% at baseline and 34.0% at the thirteenth study visit. Advancing menopausal stage was independently associated with developing dryness.[2]

Sexual function also changes across the transition. SWAN investigators have documented changes in desire, arousal, lubrication, and sexual pain as women move through midlife and menopause.[3]

The important point is straightforward:

A woman can still be having periods and already be experiencing meaningful genital and sexual changes.

What these epidemiologic studies generally do not tell us is precisely which genital tissue is responsible for the symptom.

That distinction matters.

Are “vaginal dryness” and vulvar dryness the same thing?

Not necessarily. “Vaginal dryness” is often used as a broad symptom description rather than a precise anatomical diagnosis.

Women may use the phrase to describe:

• dryness inside the vaginal canal;

• dryness or friction at the vaginal opening;

• burning or irritation of the vestibule;

• discomfort of the labia minora;

• tenderness at the posterior opening during penetration;

• reduced lubrication during sexual arousal.

These experiences can involve different tissues.

The vagina is the internal muscular canal.

The vulva is the external genital anatomy, including the labia and clitoral structures.

The vestibule lies inside the labia minora and surrounds the urethral and vaginal openings.

These structures are contiguous, but they are not anatomically identical.

That means a woman who says:

“My vagina feels dry”

may actually be describing discomfort centered at the vestibule or external vulvar tissue.

Much of the epidemiologic literature uses women's self-reported symptom language and therefore cannot reliably determine whether a complaint labeled “vaginal dryness” originates from the vagina, vestibule, vulva, or a combination of these areas.[1,2]

This is one reason greater anatomical precision matters in both research and clinical care.

Does the vulva respond to hormones?

Yes. Human vulvar vestibular tissue contains multiple sex-steroid receptors, including androgen and estrogen receptors.[4]

Hormone responsiveness is not something that suddenly appears when periods stop.

Johannesson and colleagues examined biopsies of vestibular mucosa from healthy reproductive-age women and demonstrated expression of estrogen receptors, progesterone receptors, glucocorticoid receptors, and androgen receptors.[4]

Receptor expression also varied with hormonal environment. For example, some receptor patterns differed according to menstrual-cycle phase and oral-contraceptive use.[4]

This establishes an important biological point:

The vestibule is a steroid-responsive tissue during reproductive life.

The vaginal literature provides further evidence that genital hormone biology involves more than estrogen alone.

Is genital tissue biology only about estrogen?

No. Estrogen is critically important, but female genital tissue also contains androgen receptors and local steroid-metabolizing machinery.[4,5]

Estrogen influences epithelial maturation, blood flow, tissue hydration, vaginal pH, connective tissue, and the vaginal microbial environment. Local vaginal estrogen is an established treatment for genitourinary syndrome of menopause in appropriate patients.[6]

None of that is controversial.

But estrogen is not the only steroid signal present in genital tissue.

Human vaginal tissue also expresses androgen receptors.[5]

More importantly, research by Cellai and colleagues demonstrated expression of steroidogenic enzymes capable of converting DHEA into downstream androgens including testosterone and dihydrotestosterone, or DHT, within human vaginal tissue.[5]

In cultured human vaginal smooth-muscle cells, exposure to DHEA resulted in production of androstenedione, testosterone, and DHT and activated androgen-responsive cellular signaling. Blocking the androgen receptor blocked those effects.[5]

This is evidence of local intracrine androgen metabolism.

Intracrinology refers to the ability of peripheral tissues to convert precursor hormones such as DHEA into active hormones locally, depending on the enzymes present in that tissue.

This does not mean every woman with genital symptoms has an androgen deficiency.

It also does not mean that every woman needs DHEA or testosterone.

It means something more specific:

Describing female genital tissue as exclusively estrogen-dependent is biologically incomplete.

One limitation is important. The vaginal tissue examined in the Cellai study came from postmenopausal women, and the authors specifically noted that additional work is needed to characterize these pathways in premenopausal women.[5]

We should therefore not assume that steroid metabolism is identical at every reproductive stage.

What does the evidence for DHEA actually show?

The strongest human clinical evidence is for intravaginal prasterone in postmenopausal women—not for direct external vulvar DHEA.

Prasterone is pharmaceutical DHEA.

A 6.5-mg intravaginal prasterone insert has been studied in randomized controlled trials in postmenopausal women with moderate-to-severe dyspareunia associated with vulvovaginal atrophy/genitourinary syndrome of menopause.[7]

Those trials demonstrated changes including:

• improvement in vaginal epithelial maturation;

• reduction in vaginal pH;

• improvement in moderate-to-severe dyspareunia compared with placebo.[7]

This establishes clinical activity for intravaginal DHEA in postmenopausal women.

It does not automatically establish the same result for:

• perimenopausal women;

• direct external vulvar application;

• another dose;

• another formulation;

• another delivery system.

Those are separate research questions.

Does vaginal DHEA affect tissue at the vaginal opening?

Possibly. Preliminary human evidence suggests that intravaginal prasterone can be associated with measurable changes in vestibular tissue.[8]

In a 2023 prospective pilot study, Goldstein and colleagues followed 11 menopausal women using 6.5 mg intravaginal prasterone daily for 20 weeks.[8]

Investigators reported improvements in measures of vestibular tissue appearance and vestibular pain in addition to vaginal changes.[8]

This finding is scientifically interesting because the vestibule lies outside the vaginal canal and contains hormone-responsive tissue.

But the study had important limitations.

It was:

• small;

• open-label;

• uncontrolled;

• conducted in menopausal women;

• and used intravaginal, rather than direct external vulvar, DHEA.[8]

It therefore cannot answer the separate question:

What happens when DHEA is applied directly to external vulvar tissue?

That question remains insufficiently studied.

Are the vulva and vagina the same treatment target?

No. They are neighboring hormone-responsive tissues, but anatomical proximity does not prove identical drug exposure or identical clinical response.

An intravaginal treatment may influence nearby structures. The vestibular findings following intravaginal prasterone suggest that this can occur.[8]

But that does not establish:

intravaginal exposure = direct external vulvar exposure

or:

vaginal response = equivalent response throughout the external vulva.

Route of administration matters in pharmacology.

A treatment placed inside the vaginal canal and a treatment placed directly on external vulvar tissue begin in different anatomical environments.

Whether those routes produce different local concentrations, tissue distribution, systemic exposure, or clinical effects must be determined directly.

This is an important evidence gap in vulvar medicine.

Why should vulvar care begin before menopause?

Because care does not need to mean waiting until symptoms are severe enough to meet the definition of a postmenopausal syndrome.

Earlier vulvar care can simply mean:

• learning where symptoms are actually occurring;

• recognizing changes in dryness, friction, or sensitivity;

• avoiding products that irritate increasingly sensitive tissue;

• using appropriate moisturizers or lubricants when helpful;

• addressing repeated friction or painful penetration;

• discussing persistent symptoms with a qualified clinician;

• and recognizing the external vulva as a distinct anatomical site rather than treating all genital symptoms as “vaginal.”

The conceptual shift is simple:

Menopause should not be the first time a woman is taught to pay attention to her vulvar tissue.

What if I already use systemic HRT or vaginal estrogen?

Persistent external symptoms deserve evaluation rather than the assumption that one treatment should necessarily address every genital tissue.

Systemic menopausal hormone therapy acts throughout the body.

Local vaginal estrogen delivers estrogen principally to the genitourinary tract.

Both can be appropriate and effective therapies.

But neither fact automatically tells us what is happening in every area of the external vulva.

If symptoms persist, a more useful question may be:

Where exactly is the symptom, which tissue is involved, and what else could be causing it?

Persistent burning, itching, fissuring, bleeding, skin changes, urinary symptoms, or pain can also arise from conditions including infection, inflammatory or dermatologic disease, vulvodynia, pelvic-floor dysfunction, and other causes.

These symptoms should be evaluated rather than assumed to be hormonal.

Does this mean women should use DHEA during perimenopause?

No. The current evidence does not establish that every perimenopausal woman should use externally applied DHEA.

The scientific rationale and the clinical evidence are not the same thing.

We know that:

• genital dryness and sexual symptoms can emerge during the menopausal transition;[1–3]

• the vulvar vestibule contains multiple sex-steroid receptors, including androgen receptors;[4]

• human vaginal tissue contains androgen receptors and enzymes capable of converting DHEA into active androgens;[5]

• intravaginal DHEA has demonstrated clinical activity in postmenopausal women;[7]

• and intravaginal prasterone has produced preliminary measured changes in vestibular tissue.[8]

What we do not yet know is whether a defined dose and formulation of DHEA applied directly to external vulvar tissue produces clinically meaningful benefit in perimenopausal women.

That requires direct study.

What does the evidence establish — and what does it not?

Established

Genital dryness and sexual symptoms can emerge before the final menstrual period.[1–3]

Vaginal dryness becomes more common with advancing menopausal stage.[1,2]

Human vulvar vestibular tissue contains sex-steroid receptors, including androgen receptors.[4]

Human vaginal tissue contains androgen receptors and enzymes capable of converting DHEA into downstream androgens.[5]

Intravaginal prasterone has randomized clinical-trial evidence in postmenopausal women with dyspareunia associated with vulvovaginal atrophy/GSM.[7]

Supported, but still limited

Intravaginal prasterone may affect vestibular as well as vaginal tissue. This has been demonstrated in a small, uncontrolled pilot study.[8]

Not established

That every perimenopausal genital symptom is hormonal.

That every woman with external vulvar symptoms has inadequate androgen signaling.

That serum DHEA or testosterone reliably reflects local hormone activity within vulvar tissue.

That treating the vagina necessarily provides equivalent exposure to every external vulvar structure.

That evidence from intravaginal DHEA automatically applies to externally applied DHEA.

That direct external vulvar DHEA has been shown in controlled trials to prevent or treat perimenopausal vulvar symptoms.

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Frequently asked questions

Can vulvar dryness start during perimenopause?

Yes. Genital dryness becomes more common across the menopausal transition, although most epidemiologic studies use the broad symptom term “vaginal dryness” and do not precisely localize the complaint to vaginal versus external vulvar tissue.[1,2]

Is the vulva affected by hormones?

Yes. Human vestibular tissue expresses multiple sex-steroid receptors, including androgen and estrogen receptors.[4]

Is vaginal estrogen the same as treating the external vulva?

No. They are different anatomical sites and routes of administration. Vaginal treatment can potentially influence nearby tissue, but equivalent exposure or effect throughout the external vulva cannot simply be assumed.

Does DHEA have evidence for genital symptoms?

Yes—but the strongest clinical evidence is for intravaginal prasterone in postmenopausal women.[7] Direct external vulvar DHEA has not yet been established by comparable controlled clinical trials.

Does every woman in perimenopause need DHEA?

No. Hormone-responsive tissue biology does not establish that every symptom is caused by androgen deficiency or that every woman will benefit from DHEA.

The central idea

For decades, genital care has largely entered the medical conversation after menopause, after symptoms become established and after medicine has a name for the syndrome.

But the biology does not suddenly begin at the final menstrual period.

These tissues were hormone-responsive before menopause.

And increasingly, the epidemiology shows that genital symptoms can begin before it too.[1–4]

The appropriate conclusion is not that every woman in perimenopause requires hormonal treatment.

It is simpler:

Vulvar health belongs in the perimenopause conversation.

Women should know what the vulva is, recognize when it changes, understand that the vulva and vagina are not interchangeable treatment targets, and have new symptoms taken seriously before menopause rather than only after it.

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Prime is in development

The Vulva Company is developing Prime, an external vulvar-care formulation intended for the perimenopausal stage.

Join the early-access list for research updates and first availability.

The Vulva Company is also developing a research program to directly investigate external vulvar DHEA delivery. Existing evidence supporting the biological rationale should not be interpreted as product-specific proof of clinical efficacy.

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Educational note: This article is provided for educational purposes and is not intended to diagnose, treat, cure, or prevent any medical condition. New, persistent, recurrent, or worsening vulvar, vaginal, sexual, or urinary symptoms should be evaluated by an appropriately qualified healthcare professional.

By Laura Kelly, DAOM, L.Ac., Dipl. OM is a Primary care provider in California specializing in women’s health and aging, and a nationally board-certified provider by NCCAOM. Research Scholar, Ronin Institute. ORCID 0000-0001-6586-7308. More about Dr. Kelly.

Published August 2026 · Last scientifically reviewed August 2026

References

1. Islam RM, Bond M, Ghalebeigi A, Wang Y, Walker-Bone K, Davis SR. Prevalence and severity of symptoms across the menopause transition: cross-sectional findings from the Australian Women’s Midlife Years (AMY) Study. Lancet Diabetes Endocrinol. 2025;13:765–776. doi:10.1016/S2213-8587(25)00138-X.

2. Waetjen LE, Crawford SL, Chang P-Y, Reed BD, Hess R, Avis NE, et al. Factors associated with developing vaginal dryness symptoms in women transitioning through menopause: a longitudinal study. Menopause. 2018;25(10):1094–1104. doi:10.1097/GME.0000000000001130.

3. Avis NE, Colvin A, Karlamangla AS, Crawford S, Hess R, Waetjen LE, et al. Change in sexual functioning over the menopausal transition: results from the Study of Women’s Health Across the Nation. Menopause. 2017;24(4):379–390. doi:10.1097/GME.0000000000000770.

4. 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. doi:10.1016/j.contraception.2007.06.014.

5. Cellai I, Di Stasi V, Comeglio P, Maseroli E, Todisco T, Corno C, et al. Androgen production within the human vagina. Endocrinology. 2021;162(2):bqaa219. doi:10.1210/endocr/bqaa219.

6. The NAMS 2020 Genitourinary Syndrome of Menopause Position Statement Editorial Panel. The 2020 genitourinary syndrome of menopause position statement of The North American Menopause Society. Menopause. 2020;27(9):976–992. doi:10.1097/GME.0000000000001609.

7. Labrie F, Archer DF, Koltun W, Vachon A, Young D, Frenette L, et al. 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. PMID: 26731686.

8. 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.