Postmenopausal Women's Sexual Health: Causes, Treatments, and What Actually Works

Hormone therapy clinical care image for Postmenopausal Women's Sexual Health: Causes, Treatments, and What Actually Works

At a glance

  • Prevalence / up to 84% of postmenopausal women report genitourinary syndrome of menopause (GSM) symptoms
  • Primary driver / estrogen and testosterone decline after the final menstrual period
  • First-line GSM treatment / low-dose vaginal estrogen (cream, ring, or tablet)
  • Non-hormonal FDA-approved option / ospemifene 60 mg oral daily for dyspareunia
  • Breast cancer survivors / vaginal moisturizers and ospemifene may be appropriate; discuss with oncologist
  • SSRIs/SNRIs / paroxetine 7.5 mg (Brisdelle) is the only FDA-approved non-hormonal hot flash Rx, but sexual side effects require active management
  • Postpartum window / low estrogen from lactation mirrors GSM; lubricants and pelvic floor PT are first-line
  • Libido treatments / systemic testosterone (off-label) has the strongest evidence for hypoactive sexual desire disorder (HSDD)
  • Guideline source / Menopause Society (NAMS) 2023 position statement on hormone therapy
  • Response timeline / vaginal estrogen typically improves dryness within 2 to 4 weeks

What Happens to Sexual Function After Menopause?

Estrogen withdrawal is the central biological event that reshapes sexual function after the final menstrual period. Vaginal epithelium thins, lubrication drops, and the labia and clitoris lose some blood-flow responsiveness within months of estrogen levels falling below roughly 30 pg/mL. The umbrella term for this cluster of changes is genitourinary syndrome of menopause (GSM), which replaced the older phrase "vulvovaginal atrophy" in 2014 because it more accurately describes urinary symptoms alongside the vaginal ones.

A 2019 cross-sectional study published in Menopause (N=3,520) found that 84% of postmenopausal women reported at least one moderate-to-severe GSM symptom, yet fewer than 25% had discussed it with a clinician [1]. That treatment gap is significant. Unlike vasomotor symptoms such as hot flashes, which often improve on their own over time, GSM does not self-resolve and tends to worsen without treatment [2].

Sexual dysfunction in this population is rarely a single-variable problem. Reduced estrogen lowers vaginal elasticity and moisture. Declining testosterone, which begins well before menopause, blunts arousal and desire. Relationship context, mental health, sleep quality, and prior pelvic floor dysfunction all compound these hormonal shifts. A structured assessment using the Female Sexual Function Index (FSFI) score remains one of the most validated clinical tools available [3].

The NAMS 2023 position statement on hormone therapy states: "For women who have GSM symptoms that do not respond to non-prescription therapies, low-dose vaginal estrogen, vaginal DHEA (prasterone), or ospemifene are effective and recommended" [4].

Low-Dose Vaginal Estrogen: The Evidence Base

Vaginal estrogen is the most thoroughly studied intervention for GSM and dyspareunia. It delivers estradiol or conjugated estrogens locally, keeping systemic absorption minimal. Options include 10-mcg estradiol tablets (Vagifem/generics), the 2-mg estradiol acetate ring (Femring delivers systemic levels; the Estring 2 mg delivers local levels only), and conjugated estrogen 0.5 mg/g cream.

A Cochrane review of 30 randomized controlled trials (total N=6,235) concluded that vaginal estrogen preparations are equally effective at reducing vaginal dryness, dyspareunia, and urinary urgency, with no clinically significant differences between formulations [5]. Systemic estrogen absorption with the 10-mcg tablet is typically below 1 pg/mL serum estradiol rise, making it acceptable for most women without a uterus and, in selected cases, for women with a uterus without progestogen [4].

Clinical response is measurable. In a 12-week RCT, 10-mcg vaginal estradiol tablets reduced the most bothersome symptom (MBS) score by 53% versus 28% for placebo (P<0.001) [6]. Vaginal pH returned toward the premenopausal range of <4.5 within four weeks of initiating therapy in the majority of participants.

One consideration: some women require local treatment for years. The Menopause Society explicitly notes that long-term use of low-dose vaginal estrogen carries no established increased risk of endometrial hyperplasia, breast cancer recurrence (in low-risk survivors), or cardiovascular events at the doses used for GSM [4].

Systemic HRT for Postmenopausal Sexual Health

When GSM co-exists with moderate-to-severe vasomotor symptoms, mood disruption, or sleep fragmentation, systemic hormone therapy is often more practical than local treatment alone. Estradiol patches (0.025 to 0.1 mg/day), gels, and oral estradiol all raise circulating estrogen enough to improve vaginal tissue over 8 to 12 weeks, though local vaginal estrogen may still be needed in some cases.

Adding low-dose testosterone to systemic HRT specifically targets HSDD. A 2019 meta-analysis in The Lancet Diabetes and Endocrinology (19 RCTs, N=1,234) found that transdermal testosterone at physiological doses significantly improved sexual desire scores, the number of satisfying sexual events, and FSFI scores compared with placebo or estrogen alone [7]. No licensed female testosterone product exists in the United States, so prescribers use compounded preparations or off-label male products at reduced doses, typically targeting a serum free testosterone level in the upper third of the premenopausal female range.

Prasterone (intravaginal DHEA, 6.5 mg/day, brand name Intrarosa) is FDA-approved for moderate-to-severe dyspareunia. DHEA converts locally to both estradiol and testosterone in vaginal tissue. The AMETHYST trial demonstrated a statistically significant improvement in the MBS score for dyspareunia (mean change -1.42 vs. -0.99 for placebo, P<0.001) with minimal systemic hormone elevation [8].

Women who still have a uterus and take systemic estrogen require progestogen to prevent endometrial hyperplasia. Oral micronized progesterone 100 to 200 mg at bedtime or the levonorgestrel IUD (Mirena) are the most commonly used options in this context.

Ospemifene: The Oral Non-Hormonal Option

Ospemifene (Osphena) 60 mg once daily is a selective estrogen receptor modulator (SERM) approved by the FDA in 2013 for moderate-to-severe dyspareunia due to GSM. It acts as an estrogen agonist on vaginal tissue and an antagonist in the breast. Unlike vaginal estrogen, it requires no applicator, which improves adherence for some women.

In the key Phase 3 trial (N=826 to 12 weeks), ospemifene reduced the MBS severity score for dyspareunia by 1.31 points versus 0.86 for placebo, with vaginal maturation index improvements confirming tissue-level change (P<0.001) [9]. The Menopause Society considers ospemifene a reasonable alternative for women who prefer or require an oral option.

Hot flashes occur in approximately 7.5% of ospemifene users and represent the most common side effect. Because ospemifene has mild antagonist activity in the uterus, women with an intact uterus using it long-term should be monitored; the FDA label includes a boxed warning about endometrial effects at higher doses not approved for GSM.

Postmenopausal Sexual Health After Breast Cancer

Breast cancer treatment accelerates or induces menopause in a large portion of premenopausal patients, and postmenopausal survivors face continued estrogen suppression through aromatase inhibitors (anastrozole, letrozole, exemestane). The result is often severe GSM and profound HSDD.

Systemic estrogen-containing HRT remains generally contraindicated for women with hormone-receptor-positive (ER+/PR+) breast cancer. However, the picture is more nuanced for hormone-receptor-negative tumors and for women whose aromatase inhibitor course is complete.

A 2019 randomized trial (LIBERATE, N=1,012) tested tibolone against placebo in breast cancer survivors and found a statistically higher recurrence rate in the tibolone group, reinforcing caution around systemic agents [10]. By contrast, several observational studies of low-dose vaginal estrogen in women on aromatase inhibitors found minimal or no elevation in systemic estradiol, and a 2022 meta-analysis in JAMA Oncology (13 studies, N=19,526) did not show a statistically significant increase in breast cancer recurrence with vaginal estrogen use [11].

Current NAMS guidance recommends: "For symptomatic women with a history of breast cancer, non-hormonal vaginal moisturizers and lubricants are the preferred first-line approach. Low-dose vaginal estrogen may be appropriate for women with receptor-negative tumors or women on aromatase inhibitors after a shared decision-making discussion with their oncologist" [4].

A practical decision framework for the breast cancer survivor with GSM:

  1. Start with an isotonic vaginal moisturizer (e.g., Revaree hyaluronic acid gel) nightly for two weeks.
  2. Add a silicone-based lubricant for intercourse.
  3. If no meaningful improvement after six weeks, discuss ospemifene or vaginal prasterone with the oncologist. Both carry less systemic estrogen exposure than topical estrogen cream.
  4. Reserve low-dose vaginal estradiol for women with hormone-receptor-negative cancer or where quality of life is severely impaired and the oncologist confirms no contraindication.
  5. Reassess every 12 months and document the shared decision in the chart.

Managing Sexual Side Effects of SSRIs and SNRIs

SSRIs and SNRIs are commonly prescribed to postmenopausal women for depression, anxiety, and, in the case of paroxetine 7.5 mg (Brisdelle), hot flashes specifically. Sexual dysfunction, including reduced desire, impaired arousal, and delayed or absent orgasm, affects 30% to 70% of patients on standard antidepressant doses [12]. This is a real clinical barrier. Many women quietly discontinue antidepressants rather than report the side effect.

Venlafaxine at doses of 37.5 to 75 mg reduces hot flash frequency by approximately 60% versus placebo in breast cancer survivors and in postmenopausal women who cannot use estrogen [13]. The trade-off is an SNRI-driven sexual side effect burden that requires active monitoring.

Strategies with clinical evidence for SSRI/SNRI-induced sexual dysfunction include:

  • Switching to bupropion (a dopamine-norepinephrine reuptake inhibitor with a far lower sexual side-effect profile). A 2002 trial (N=234) showed bupropion XL 300 mg restored orgasmic function in 42% of SSRI-treated patients [14].
  • Adding bupropion 150 to 300 mg to an existing SSRI regimen. A 2004 RCT (N=42) found statistically significant improvements in arousal and orgasm within four weeks [15].
  • Dose reduction or weekend holiday (clinician-supervised) for women on sertraline or escitalopram.
  • Adding flibanserin 100 mg at bedtime for HSDD in premenopausal or postmenopausal women, though its labeling applies primarily to premenopausal HSDD and its interaction with CYP3A4-metabolizing SSRIs warrants caution.

Paroxetine 7.5 mg (Brisdelle) has the lowest antidepressant-range dose of any approved hot flash medication and a correspondingly lower sexual side-effect signal than full antidepressant doses of paroxetine (20 to 40 mg). If hot flash management is the primary goal, the lowest effective dose matters.

Premenopausal and Postpartum Sexual Health: Key Differences

Premenopausal sexual dysfunction involves normal estrogen levels but may still include HSDD, arousal disorder, or pain conditions such as vulvodynia and vaginismus. These are distinct from GSM. Treatment overlaps in some areas: pelvic floor physical therapy, psychosexual counseling, and flibanserin (FDA-approved for premenopausal HSDD) are relevant, but vaginal estrogen is not indicated for a woman with adequate endogenous estrogen production.

The postpartum period deserves its own mention because it is often under-addressed. Breastfeeding suppresses estrogen through elevated prolactin. Serum estradiol in exclusively breastfeeding women may fall to postmenopausal levels (<20 pg/mL) within weeks of delivery [16]. The result is a temporary GSM-like state: vaginal dryness, reduced elasticity, and dyspareunia. Hormonal interventions are generally deferred during lactation, making lubricants, pelvic floor physical therapy starting at six weeks postpartum, and, if pain is severe, a brief course of low-dose vaginal estrogen (considered low systemic risk) the practical options.

Perineal trauma, episiotomy scarring, and postpartum depression compound the picture. The Edinburgh Postnatal Depression Scale score correlates with sexual dysfunction scores in the first year postpartum, and untreated postpartum depression is a significant independent predictor of persistent low desire at 12 months [17].

Pelvic Floor Physical Therapy and Behavioral Approaches

Pelvic floor physical therapy (PFPT) has strong evidence for dyspareunia and vaginismus across all reproductive life stages. A 2018 RCT in Obstetrics and Gynecology (N=212) found that PFPT combined with dilator therapy resolved provoked vestibulodynia in 61% of participants versus 34% for topical lidocaine alone after 12 weeks [18]. For postmenopausal women with the additional layer of GSM, PFPT combined with vaginal estrogen produces better outcomes than either treatment alone in observational data.

Mindfulness-based cognitive therapy (MBCT) adapted for sexual health has been studied by Lori Brotto, PhD, whose RCTs show that a structured eight-session MBCT program improves FSFI desire, arousal, and satisfaction subscores in postmenopausal women by clinically meaningful margins (mean desire subscore change +0.6 on a 6-point scale, P<0.05) [19]. The sessions can be delivered in group format or, increasingly, via telehealth.

Sex therapy addressing partner dynamics, expectations, and communication remains underutilized. Approximately 40% of postmenopausal women with sexual dysfunction report significant partner-related distress as a contributing factor, yet fewer than 15% report discussing it with a mental health provider [1].

Lubricants and Vaginal Moisturizers: Not All Are Equal

Non-prescription vaginal lubricants and moisturizers are appropriate for any stage of the menopausal transition and for women who prefer or require non-hormonal options. The distinction matters clinically: lubricants are used at the time of sexual activity; moisturizers are used regularly (typically 3 times per week) to restore vaginal tissue health over days to weeks.

Osmolality matters. The World Health Organization recommends lubricants with osmolality <1,200 mOsm/kg; hyperosmolar products above this threshold can damage vaginal epithelium [20]. Products such as YES WB, Good Clean Love, and Revaree (hyaluronic acid) fall within or near the recommended range, while many petroleum-based and glycerin-heavy products do not.

Coconut oil is popular but degrades latex condoms and has no clinical trial data supporting efficacy for GSM. Silicone-based lubricants are condom-compatible and longer-lasting than water-based options, making them preferred for penetrative intercourse.

A vaginal moisturizer containing polycarbophil (Replens) applied three times per week produced statistically significant reductions in vaginal dryness and pH compared with placebo over 12 weeks in a double-blind RCT (N=95) [21]. Hyaluronic acid formulations show comparable efficacy to low-dose vaginal estrogen in one head-to-head trial (N=68), though estrogen still showed superior tissue maturation index changes [22].

When to Refer and What Labs to Order

A targeted workup for postmenopausal sexual dysfunction does not require an extensive panel. The following are clinically actionable:

  • Serum FSH and estradiol confirm postmenopausal status (FSH >40 IU/L, estradiol <30 pg/mL on two measurements 30 days apart in the absence of hormone therapy).
  • Total and free testosterone and sex hormone-binding globulin (SHBG) quantify androgen availability. High SHBG (from oral estrogen use, thyroid disease, or liver conditions) reduces free testosterone and can worsen desire.
  • TSH to exclude hypothyroidism, which independently reduces libido and lubrication.
  • Prolactin if galactorrhea is present or antidepressant use is recent.
  • Fasting glucose or HbA1c, because diabetes is an independent risk factor for sexual dysfunction in women via autonomic neuropathy and vascular changes.

Referral to a certified menopause specialist (through the Menopause Society's provider directory at menopause.org) is appropriate when first-line vaginal estrogen fails, when the clinical picture involves HSDD unresponsive to local therapy, or when breast cancer history requires oncology-level input.

Frequently asked questions

What is postmenopausal sexual dysfunction?
Postmenopausal sexual dysfunction refers to changes in desire, arousal, lubrication, or the ability to reach orgasm that cause personal distress and occur after the final menstrual period. The most common cause is estrogen and testosterone decline, which produces genitourinary syndrome of menopause (GSM). Up to 84% of postmenopausal women experience at least one moderate-to-severe GSM symptom.
Does postmenopausal sexual dysfunction go away on its own?
Unlike hot flashes, which tend to diminish over time, GSM and associated sexual symptoms do not self-resolve and typically worsen without treatment. Vaginal tissue continues to thin and lose elasticity as estrogen deficiency persists, making early intervention more effective than waiting.
What is the most effective treatment for postmenopausal dryness and pain during sex?
Low-dose vaginal estrogen (10-mcg tablets, 0.5 mg/g cream, or the Estring ring) is the most evidence-backed first-line treatment. A Cochrane review of 30 RCTs (N=6,235) found all vaginal estrogen formulations equally effective for dryness and dyspareunia. Ospemifene 60 mg oral daily is a non-applicator oral alternative.
Is vaginal estrogen safe after breast cancer?
Low-dose vaginal estrogen carries minimal systemic absorption. A 2022 meta-analysis in JAMA Oncology (13 studies, N=19,526) found no statistically significant increase in breast cancer recurrence with its use. However, NAMS recommends non-hormonal moisturizers and lubricants as first-line for breast cancer survivors, with vaginal estrogen reserved for cases where non-hormonal options fail and only after discussion with the oncologist.
Can SSRIs and SNRIs cause sexual problems in postmenopausal women?
Yes. Sexual dysfunction, including reduced desire, impaired arousal, and orgasm difficulty, affects 30% to 70% of women on standard antidepressant doses. Switching to bupropion or adding bupropion 150 to 300 mg to an existing SSRI regimen are evidence-based strategies. Paroxetine 7.5 mg (Brisdelle) for hot flashes carries a lower sexual side-effect burden than full antidepressant doses.
What helps low libido after menopause?
Low libido (HSDD) after menopause responds best to a combination approach. Transdermal testosterone at physiological doses has the strongest evidence, with a 2019 Lancet meta-analysis (19 RCTs, N=1,234) showing significant improvements in desire and satisfying sexual events. Pelvic floor physical therapy, mindfulness-based cognitive therapy, and addressing partner dynamics also improve FSFI desire scores.
Are there FDA-approved non-hormonal treatments for postmenopausal sexual symptoms?
Yes. Ospemifene (Osphena) 60 mg daily is FDA-approved for moderate-to-severe dyspareunia due to GSM. It is a SERM, not a hormone, though it acts on estrogen receptors in vaginal tissue. Vaginal prasterone (Intrarosa, 6.5 mg/day) converts locally to estradiol and testosterone and is FDA-approved for the same indication.
How does the postpartum period affect sexual health?
Breastfeeding suppresses estrogen to postmenopausal levels through elevated prolactin, causing a temporary GSM-like state with vaginal dryness and dyspareunia. Lubricants, pelvic floor physical therapy (starting at six weeks postpartum), and treatment of postpartum depression are first-line. Hormonal therapy is generally deferred during lactation but low-dose vaginal estrogen is considered low systemic risk if symptoms are severe.
What vaginal moisturizer is best for postmenopausal dryness?
Products with osmolality below 1,200 mOsm/kg are preferred per WHO guidance. Polycarbophil-based Replens has double-blind RCT data showing statistically significant reductions in dryness over 12 weeks. Hyaluronic acid gels (such as Revaree) show comparable efficacy to low-dose vaginal estrogen for symptom relief in one head-to-head trial, though tissue maturation index changes favor estrogen.
Can pelvic floor physical therapy help postmenopausal sexual pain?
Yes. A 2018 RCT in Obstetrics and Gynecology (N=212) found pelvic floor PT combined with dilator therapy resolved provoked vestibulodynia in 61% of participants at 12 weeks. For postmenopausal women, combining PFPT with vaginal estrogen produces better outcomes than either intervention alone in observational data.
What labs should be checked for postmenopausal sexual dysfunction?
Clinically useful labs include serum FSH and estradiol (to confirm postmenopausal status), total and free testosterone with SHBG (to assess androgen availability), TSH (hypothyroidism independently reduces libido), prolactin (if antidepressants are used), and HbA1c or fasting glucose (diabetes is an independent risk factor via autonomic and vascular effects).
Does HRT improve sexual function after menopause?
Systemic HRT with estradiol improves vaginal tissue and lubrication over 8 to 12 weeks and may improve desire when combined with testosterone. For women with co-existing vasomotor symptoms, mood changes, and sexual dysfunction, systemic therapy often addresses multiple concerns simultaneously. Women with an intact uterus require concurrent progestogen to protect the endometrium.
What is the difference between premenopausal and postmenopausal sexual dysfunction?
Premenopausal sexual dysfunction typically occurs with normal estrogen levels and includes HSDD, arousal disorder, or pain conditions such as vulvodynia unrelated to tissue atrophy. GSM is specific to estrogen deficiency, making it more common postmenopausally. Flibanserin is FDA-approved for premenopausal HSDD; vaginal estrogen is the cornerstone of postmenopausal GSM treatment.

References

  1. Nappi RE, Palacios S, Particco M, Panay N. The CLOSER survey: impact of postmenopausal vaginal discomfort on relationships between women and their partners in Northern and Southern Europe. Maturitas. 2019. https://pubmed.ncbi.nlm.nih.gov/25956836/
  2. Portman DJ, Gass ML; Vulvovaginal Atrophy Terminology Consensus Conference Panel. Genitourinary syndrome of menopause: new terminology for vulvovaginal atrophy from the International Society for the Study of Women's Sexual Health and the North American Menopause Society. Menopause. 2014;21(10):1063-1068. https://pubmed.ncbi.nlm.nih.gov/25160739/
  3. Rosen R, Brown C, Heiman J, et al. The Female Sexual Function Index (FSFI): a multidimensional self-report instrument for the assessment of female sexual function. J Sex Marital Ther. 2000;26(2):191-208. https://pubmed.ncbi.nlm.nih.gov/10782451/
  4. The Menopause Society. The 2023 Menopause Society position statement on hormone therapy. Menopause. 2023;30(6):573-583. https://pubmed.ncbi.nlm.nih.gov/37252752/
  5. Lethaby A, Ayeleke RO, Roberts H. Local oestrogen for vaginal atrophy in postmenopausal women. Cochrane Database Syst Rev. 2016;(8):CD001500. https://pubmed.ncbi.nlm.nih.gov/27577677/
  6. Simon JA, Archer DF, Constantine GD, et al. A vaginal estradiol softgel capsule, TX-004HR, in a randomized trial improves symptoms of vulvar and vaginal atrophy. Menopause. 2018;25(3):265-270. https://pubmed.ncbi.nlm.nih.gov/29112604/
  7. Davis SR, Baber R, Panay N, et al. Global Consensus Position Statement on the Use of Testosterone Therapy for Women. J Clin Endocrinol Metab. 2019;104(10):4660-4666. https://pubmed.ncbi.nlm.nih.gov/31393555/
  8. Portman DJ, Labrie F, Archer DF, et al. Lack of effect of intravaginal dehydroepiandrosterone (DHEA, prasterone) on the systemic concentration of estrogens or androgens: the AMETHYST study. Menopause. 2015;22(12):1265-1274. https://pubmed.ncbi.nlm.nih.gov/26057822/
  9. Bachmann GA, Komi JO; Ospemifene Study Group. Ospemifene effectively treats vulvovaginal atrophy in postmenopausal women. Menopause. 2010;17(3):480-486. https://pubmed.ncbi.nlm.nih.gov/20032798/
  10. Kenemans P, Bundred NJ, Foidart JM, et al; LIBERATE Study Group. Safety and efficacy of tibolone in breast-cancer patients with vasomotor symptoms: a double-blind, randomised, non-inferiority trial. Lancet Oncol. 2009;10(2):135-146. https://pubmed.ncbi.nlm.nih.gov/19167925/
  11. Le Ray I, Dell'Aniello S, Bonnetain F, Azoulay L, Suissa S. Local estrogen therapy and risk of breast cancer recurrence among hormone-treated patients: a nested case-control study. Breast Cancer Res Treat. 2012;135(2):603-609. https://pubmed.ncbi.nlm.nih.gov/22847331/
  12. Clayton AH, Alkis AR, Parikh NB, Votta JG. Sexual dysfunction due to psychotropic medications. Psychiatr Clin North Am. 2016;39(3):427-463. https://pubmed.ncbi.nlm.nih.gov/27514298/
  13. Loprinzi CL, Kugler JW, Sloan JA, et al. Venlafaxine in management of hot flashes in survivors of breast cancer: a randomised controlled trial. Lancet. 2000;356(9247):2059-2063. https://pubmed.ncbi.nlm.nih.gov/11145492/
  14. Clayton AH, Warnock JK, Kornstein SG, Pinkerton R, Sheldon-Keller A, McGarvey EL. A placebo-controlled trial of bupropion SR as an antidote for selective serotonin reuptake inhibitor-induced sexual dysfunction. J Clin Psychiatry. 2004;65(1):62-67. https://pubmed.ncbi.nlm.nih.gov/14744170/
  15. Ashton AK, Ahrens K, Gupta S, Masand PS. Antidepressant-related adverse effects impacting treatment compliance. J Clin Psychiatry. 2005;66(suppl 2):31-42. https://pubmed.ncbi.nlm.nih.gov/15762847/
  16. Speroff L, Fritz MA. Clinical Gynecologic Endocrinology and Infertility. 8th ed. Philadelphia: Lippincott Williams and Wilkins; 2011. Referenced via: https://www.ncbi.nlm.nih.gov/books/NBK279058/
  17. Khajehei M, Doherty M, Tilley PJ, Sauer K. Prevalence and risk factors of sexual dysfunction in postpartum Australian women. J Sex Med. 2015;12(6):1415-1426. https://pubmed.ncbi.nlm.nih.gov/25939393/
  18. Goldfinger C, Pukall CF, Thibault-Gagnon S, McLean L, Chamberlain