Sexual dysfunction and sexual health in women

• Female sexual dysfunction (FSD) is any persistent problem of desire, arousal, orgasm or pain that causes personal distress. Prevalence estimates put it at 40% to 50% of women when problems of any kind are asked about. ^[2]
• The current working classification is the ISSWSH classification (also used by the Fourth International Consultation on Sexual Medicine): hypoactive sexual desire disorder (HSDD), female sexual arousal disorder, female orgasm disorder and genitopelvic pain and penetration disorder. ^[2]
• Arousal disorders are split into a cognitive (mental) component and a genital (lubrication/engorgement) component, because a woman can feel aroused mentally without the expected genital response, or the other way round. ^[2]
• Genito-pelvic pain disorders split into entry pain (often driven by pelvic floor muscle over-activity) and deep pain (often linked to pelvic pathology or deeper penetration). ^[1]
• A thorough sexual history and a focused pelvic examination are the diagnostic core. Screening questionnaires such as the Female Sexual Function Index and the Female Sexual Distress Scale-Revised can support the diagnosis but do not replace a conversation. ^[2]
• Treatment matches the cause: cognitive behaviour therapy (CBT) is the first-line treatment for desire and arousal disorders, pelvic floor physical therapy is the first-line treatment for genito-pelvic pain disorders, and vaginal moisturizers and topical vaginal estrogen are recommended for genitourinary syndrome of menopause. ^[2]

By the end of this page you should be able to:

1. Define female sexual dysfunction and explain why the distress criterion separates a normal variation from a disorder. ^[1]
2. Tell the ISSWSH/ICSM disorders apart by their defining symptoms and how they present. ^[2]
3. Take and structure a sexual history and perform a focused examination without causing shame or pain. ^[2]
4. Distinguish lifelong from acquired problems, and generalised from situational ones. ^[1]
5. Choose first-line treatment for each category: psychosexual therapy, cognitive behaviour therapy, pelvic floor physical therapy, and medical treatment where appropriate. ^[2]
6. Recognise and manage genitourinary syndrome of menopause, including after breast cancer treatment. ^[3][4]
7. Counsel a woman on the place (and limits) of testosterone, flibanserin and other off-label medicines. ^[5][2]

A woman's sexual response is better modelled as a circle than a straight line. Motivation and desire do not always come first; sexual arousal can come first and desire can follow. This is why the older model (desire, then arousal, then orgasm) missed women whose arousal arrived before their desire. ^[1]

The ISSWSH and Fourth ICSM grouping separates four categories. ^[2]

1. Hypoactive sexual desire disorder (HSDD): reduced or absent spontaneous or responsive desire for sexual activity, with loss of interest in initiating or continuing sex, and clear personal distress. The problem can be lifelong or acquired, generalised or situational. ^[1][5]
2. Female sexual arousal disorder: distressing difficulty or inability to become or stay aroused. It has two subtypes that can occur alone or together. ^[2]
   • Female genital arousal disorder: difficulty attaining or maintaining genital response (lubrication and engorgement).
   • Female cognitive arousal disorder: difficulty feeling mentally engaged or "turned on".
3. Female orgasm disorder: distressing compromise of orgasm frequency, intensity, timing or pleasure. ^[1]
4. Genito-pelvic pain and penetration disorder: difficulty with penetration, pain during or after penetration, fear or anxiety about pain, or tightening of the pelvic floor muscles that makes penetration difficult or impossible. ^[1][2]

Genitourinary syndrome of menopause (GSM) is not a dysfunction diagnosis in this sense, but its symptoms (dryness, dyspareunia, urinary symptoms) are the most common cause of acquired sexual pain in midlife and beyond. It is covered separately below. ^[3][4]

Problems with sexual function of some kind are reported by an estimated 40% to 50% of women. ^[2] When the stricter criterion of distress is applied, prevalence falls: in one cohort, self-reported decreased sexual desire with distress was present in about 12% of women aged 45 to 64 years in the United States, about 14% of women aged 65 to 79 years in Australia, and about 32% of women aged 40 to 64 years in Australia. In a European community survey, low desire rose from 11% in women aged 20 to 29 years to 53% in women aged 60 to 70 years, while distress fell, so the prevalence of HSDD stayed relatively stable at 6% to 13% across ages. ^[5] In an Asian population survey of more than 3,000 women aged 40 to 80 years, lack of interest in sex was self-reported by about 27% (range 17% to 50% by country). ^[5]

Genitourinary syndrome of menopause affects an estimated 50% to 70% of postmenopausal women to some degree, although it is consistently underdiagnosed and undertreated. ^[3]

Many women never volunteer the problem unless it is asked about directly. ^[1] Screening therefore starts with routine, permission-giving questions, not with a questionnaire. ^[2]

Sexual function is shaped by biology, psychology, the relationship and the culture the woman lives in. These domains interact, and a problem in one can create problems in another.

Biological contributors include menopause and the fall in estrogen and androgen, pregnancy and the postpartum, breastfeeding, chronic illness (diabetes, cardiovascular disease, multiple sclerosis, cancer), neurological or vascular disease, pelvic organ prolapse and incontinence, and genital skin disease. ^[1][4] Medications are a common and often missed cause: selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors, antihypertensives, anticonvulsants, lithium, antipsychotics, opioids and benzodiazepines, estrogens and the combined contraceptive, and treatments used after breast cancer. ^[1]

Psychological contributors include depression and anxiety (which may be cause or consequence), body image concerns (after surgery, weight change, skin disease, scarring), past sexual abuse or trauma, grief, and poor sexual knowledge or unrealistic expectations. ^[1][2] Relationship contributors include poor communication, a partner with a sexual dysfunction, discrepant desire, conflict, domestic violence and shame. ^[2]

A useful frame: if the problem is mainly entry pain, think pelvic floor muscle over-activity and local pathology; if it is mainly low desire, think hormones, mental health, medications and the relationship; if it is mainly arousal without desire, think both.

Desire is generated in the brain, not the genitals. Dopaminergic pathways signal reward and motivation, while serotonergic and prolactinergic tone tends to inhibit them. Estrogen modulates vaginal epithelium and vascular response; testosterone has independent effects on desire in the central nervous system, as described below. ^[1][5]

Arousal has two parts that can fail separately.

• Genital arousal is increased blood flow to the clitoris, labia and vagina, with lubrication produced partly by mucin and partly by vascular transudation. Nitric oxide and adrenergic signalling drive the haemodynamics; estrogen and androgen maintain the epithelium and smooth muscle. ^[5]
• Cognitive arousal is the mental experience of being "engaged" or "turned on". It can be preserved while the genitals fail to respond, or impaired while the genitals respond normally. ^[2]

Orgasm is a spinal reflex driven by sensory input from the clitoris and other genital structures, modulated by central reward circuits. It depends on adequate arousal, on the absence of pain, and on the ability to stay present during stimulation. ^[1]

Dyspareunia ("difficult or painful intercourse") and vaginismus (involuntary tightening of the pelvic floor that prevents or impedes penetration) are the commonest symptom labels, and both sit within genito-pelvic pain and penetration disorder. ^[1][2] Pain is divided into:

• Superficial or entry pain: usually caused by vulval disease (lichen sclerosus, dermatitis, infection, vestibulodynia), scarring, atrophic epithelium in menopause, or involuntary pelvic floor tightening.
• Deep pain: linked to pelvic pathology such as endometriosis, pelvic inflammatory disease, ovarian mass or tumour, prolapse or bladder/rectal disease.

A sexual history should be part of routine care, taken without making assumptions. Open-ended questions such as "Are you sexually active?", "Is sex comfortable?" and "Do you have any concerns about your sexual function?" are supported by consensus and patient preference. ^[2]

Structure the history into four layers. ^[2]

1. Current function: desire, arousal, orgasm and pain. What happens, and what bothers her?
2. Chronology: lifelong or acquired; one, several or all partners; one situation or all; better or worse than before.
3. Context: pregnancy, postpartum, breastfeeding, contraception, menopause, medical illness, medications, stressors, relationship.
4. Distress: how it affects her and, if she wishes, her partner; what she hopes to gain.

Pain histories should record exactly when pain occurs (before touch, with penetration, at deep penetration, after sex) and where. ^[2]

Examination is tailored to the complaint and is not always required. ^[2] When it is done, it should be unhurried, with consent at each step, and with the same basic approach whether the problem is desire, arousal, pain or any combination.

• General: blood pressure; signs of thyroid disease; systemic androgen excess (acne, hirsutism, clitoromegaly) if virilization is suspected; screen for depression.
• Abdomen and pelvis: for masses, tenderness or distension.
• External genitalia: inspect skin (lichen sclerosus, dermatitis, atrophy, fissures, scarring); check the vestibule for focal tenderness ("Q-tip test" for provoked vestibulodynia).
• Pelvic floor assessment: resting tone and the ability to contract and relax.
• Speculum and bimanual examination: only when indicated, and adapted for pain. A woman with severe pain may need an examination under anaesthesia or deferred.
• Neurological screening: when sensory or motor symptoms suggest a nerve lesion.

When GSM is suspected, the findings are classic: pale, thin, dry epithelium, loss of rugae, introital stenosis, clitoral atrophy and, in some women, fusion of the labia minora. ^[3][4]

The differential is in two parts: other causes of the symptoms (anxiety, depression, relationship conflict, endocrine disease), and other causes of a presenting complaint (bleeding, pain, mass).

The diagnosis is clinical. Laboratory tests are used to find a contributor, not to confirm the diagnosis. ^[1][2]

• Validated questionnaires: the Female Sexual Function Index and the Female Sexual Distress Scale-Revised may help quantify the problem and track change. ^[2]
• Blood tests, if indicated: thyroid function; prolactin; total testosterone and sex-hormone-binding globulin when androgen status is relevant or testosterone therapy is being considered; estradiol in a younger woman when premature ovarian insufficiency is suspected. ^[4][5]
• Glucose, lipids and cardiovascular risk assessment: when vascular disease is plausible. ^[1]
• Pelvic imaging or examination under anaesthesia: for deep dyspareunia or a suspected pelvic mass.
• Swabs and biopsy: for suspected infection, lichen sclerosus or vulval intraepithelial neoplasia.
• Sexually transmitted infection screen: when risk factors are present.

There is no testosterone level that diagnoses HSDD, and no serum concentration that is a treatment target. Testosterone is measured to exclude mid-range or high levels that would argue against androgen deficiency as the cause, and to monitor therapy if it is prescribed. ^[5]

• Do not treat sex as a performance. The therapeutic goal is a comfortable, satisfying sexual life on her terms, not a frequency target. ^[2]
• Avoid pain-first. Continuing to have painful intercourse perpetuates the fear-pain cycle. If penetration hurts, stop penetration and work on comfort first. ^[1]
• Educate. Many problems resolve once the couple understands anatomy, arousal physiology and that desire often follows arousal. ^[2]
• Treat the partner when appropriate. A partner with erectile dysfunction or low desire is part of the problem. ^[2]
• Consider trauma-informed care. A history of sexual violence changes the pace and the content of treatment; refer or work within that framework. ^[2]

Psychosexual therapy (sex therapy, relationship therapy, education and permission-giving) has been the traditional treatment and remains central. ^[2]

• Cognitive behaviour therapy (CBT) is the first-line treatment for disorders of sexual desire and arousal, including mindfulness-based and group formats. ^[2]
• Mindfulness-based therapy improves sexual desire and arousal in women with desire or arousal disorder. ^[2]
• CBT is also first-line for vaginismus, and CBT for chronic pain improves sexual function when pain is a feature. ^[2]
• Pelvic floor physical therapy (PFPT) is the first-line treatment for genito-pelvic pain disorders: it trains the pelvic floor to relax, improves awareness and control, and addresses muscle guarding. ^[2]
• Couple therapy addresses communication and discrepant expectations.

There is no drug licensed in the UK specifically for FSD. Treatment therefore relies on treating contributors, psychosexual therapy and, where appropriate, off-label use with full counselling. ^[2]

• Testosterone: NICE advises considering added testosterone when menopausal hypoactive desire persists despite HRT given alone. ^[4] The ISSWSH clinical practice guideline supports systemic transdermal testosterone (about 300 mcg/day, roughly one-tenth of a standard male 1% gel dose) for HSDD, titrated to keep total testosterone within the premenopausal physiological range. ^[5] It is monitoring-based, not a dose-for-all. ^[5]
  • Total testosterone and sex-hormone-binding globulin are measured before starting, and total testosterone is monitored during treatment. There is no testosterone level that diagnoses HSDD and no level that is a treatment target. ^[5]
  • Compounded testosterone, pellets, intramuscular injections and oral formulations are not recommended; transdermal preparations have the best data. ^[5]
  • In a meta-analysis of 36 trials, testosterone increased acne (relative risk 1.46) and hair growth (relative risk 1.69). Longer safety data beyond two years are limited. ^[5]
  • Licensed transdermal female patches are not widely available; male formulations used off-label require careful dosing. ^[5]
• Flibanserin: approved in the United States for premenopausal HSDD. Meta-analyses show modest increases in satisfying sexual events and desire, and it is expensive. It must not be combined with alcohol or potent CYP3A4 inhibitors. ^[2]
• Bremelanotide: an on-demand injectable approved in the United States for premenopausal HSDD. Not generally available in the UK. ^[2]
• Bupropion (150 mg twice daily): may help antidepressant-induced sexual dysfunction; evidence is limited. ^[2]
• Nitric-oxide enhancers (sildenafil, tadalafil): not FDA or EMA-approved for women; ACOG guidance cautions against use for arousal or interest disorders outside clinical trials. ^[2]
• Dehydroepiandrosterone (DHEA) and tibolone: may help libido in some menopausal women. ^[4][2]
• Non-medical measures: combine with psychosexual therapy; HRT (especially transdermal) and adequate treatment of genitourinary symptoms often improve desire. ^[4]

Management follows the same ladder: education, CBT, and treatment of the contributing cause. For drug-induced arousal problems, consider reducing or switching the offending medication if safe. For genital arousal failure with adequate desire, address estrogen deficiency, vascular risk and medication. ^[1][5]

CBT and sex therapy are the treatments, including training (directed masturbation programmes, sensate focus) and devices. Adequate arousal and the absence of pain are prerequisites. Medication-induced orgasm delay (especially with SSRIs) can be addressed by switching or adding bupropion. ^[2]

• Pelvic floor PT is first-line for most genito-pelvic pain disorders. ^[2]
• Treat the local cause: lichen sclerosus with potent topical steroid, infection with antimicrobial, dermatitis by avoiding irritants.
• Provoked vestibulodynia: topical lidocaine, PFPT, sometimes botulinum toxin or surgery (vestibulectomy) in refractory cases, in specialist hands. ^[2]
• Vaginismus: a stepped programme of education, relaxation, gradual desensitisation, progressive dilator use and CBT, with the partner involved. ^[2]

GSM is the accepted term for the vulval, vaginal and urinary symptoms and signs caused by the fall in estrogen (and androgen) in the genitourinary tract during and after the menopause, or earlier if ovarian function is lost surgically or medically. ^[3] It is extremely common and very treatable once it is recognised.

Symptoms include vaginal dryness, burning and irritation, pain on intercourse, postcoital spotting, urinary urgency, frequency and dysuria, and recurrent urinary tract infection. Signs include pale thin epithelium, loss of rugae, introital narrowing, clitoral atrophy and, in some women, fusion of the labia minora. ^[3][4]

Screen by taking a symptom history and performing a genitourinary examination, and actively exclude coexisting conditions such as overactive bladder, incontinence, prolapse, lichen sclerosus and infection. ^[3]

The AUA/SUFU/AUGS 2025 guideline, the NICE menopause guideline (NG23, last updated 15 April 2026) and the menopause literature agree on the following hierarchy. ^[3][4]

• Offer local low-dose vaginal estrogen to improve discomfort/irritation, dryness and dyspareunia. It can be used on its own or with systemic HRT, and continued long-term. Absorption is largely local; systemic absorption is minimal compared with oral HRT. ^[3][4]
• Vaginal dehydroepiandrosterone (prasterone) and ospemifene (oral) are options when vaginal estrogen is not suitable or is ineffective. ^[3][4]
• Vaginal moisturizers and lubricants are offered, alone or with hormonal treatment, and are first-line if hormonal treatment is contraindicated. ^[3][4]
• Pelvic floor physical therapy helps associated pelvic floor over-activity. ^[2][3]
• Local estrogen, intravaginal DHEA and ospemifene do not increase endometrial cancer risk, and local low-dose vaginal estrogen shows no link to the development of breast cancer; no endometrial surveillance is needed on account of their use alone. ^[3]
• In recurrent urinary tract infection, low-dose vaginal estrogen reduces the risk of future infection. ^[3]
• Laser, radiofrequency and energy-based devices are not supported by evidence and should not be offered except in trials. ^[3]
• Women with a personal history of breast cancer should try non-hormonal options first; low-dose vaginal estrogen may then be considered with the oncology team, including during aromatase inhibitor therapy. ^[3][4]
• Unregulated "bioidentical" preparations and vaginal laser therapy should not be offered. ^[4]

Sexual interest and function commonly change in pregnancy, often falling in the first and third trimesters. Pain in pregnancy requires exclusion of obstetric causes. Postpartum dyspareunia is common, especially after perineal trauma; it should be asked about at postnatal follow-up and managed with local measures and, where appropriate, oestrogen. ^[4]

Sexual dysfunction in an adolescent is uncommon and usually psychosocial. Consider trauma, abuse, body image, sexuality, and medication effects. Experienced counsellors or adolescent gynaecology services are often more appropriate than medical treatment. ^[2]

Breast cancer and its treatment produce HSDD and GSM through loss of ovarian function, endocrine therapy and body image change. Management combines psychosexual care, non-hormonal measures first, and, if needed, vaginal estrogen with breast cancer specialists. ^[3][4]

Lifelong (primary) dysfunction often has psychological or relational roots; the same treatment ladder applies, paced more slowly and with trauma-informed care. ^[1][2]

• Deterioration of relationship quality and mental health if the problem is left unsaid.
• Worsening of pelvic pain cycles when painful sex continues.
• Bone, cardiovascular and sexual consequences of undertreated menopause if GSM is not recognised.
• Adverse effects of off-label medicines if used without monitoring. ^[5]

With assessment, information and the right match of treatment, most women improve. Problems that have been present for years, or that involve trauma, usually take longer. Many need maintenance rather than one-off treatment. ^[2]

• Ask. Because most women will not volunteer the problem, a routine, permission-giving question at key consultations (postpartum, contraception, menopause, before starting medications with sexual side effects) is the single most effective preventive step. ^[2]
• Review medications before prescribing those likely to affect sexual function, and discuss alternatives. ^[1]
• Treat genitourinary symptoms early in the menopause, before atrophy becomes established and the pain cycle sets in. ^[3][4]
• Maintain pelvic floor health during pregnancy and postpartum with education and physical therapy when indicated. ^[2]

• Female sexual dysfunction is a persistent problem of desire, arousal, orgasm or pain that causes personal distress; prevalence estimates for any problem are 40% to 50% of women. ^[2]
• The ISSWSH/ICSM classification groups it as HSDD, female sexual arousal disorder (cognitive and/or genital), female orgasm disorder, and genito-pelvic pain and penetration disorder. ^[1][2]
• Mental engagement and genital response can fail independently. ^[2]
• Assessment rests on a structured sexual history and a focused, consented examination; validated questionnaires support but do not replace it. ^[2]
• CBT is first-line treatment for desire and arousal disorders and for vaginismus; pelvic floor physical therapy is first-line for genito-pelvic pain disorders. ^[2]
• Genitourinary syndrome of menopause is common, underdiagnosed and very treatable with low-dose vaginal estrogen, prasterone or ospemifene, plus moisturizers and lubricants; laser is not supported by evidence. ^[3][4]
• Testosterone is considered only for menopausal or postmenopausal HSDD that has not improved with HRT, at about 300 mcg/day transdermally, monitored by total testosterone, with limited long-term safety data. ^[4][5]
• Flibanserin, bremelanotide and nitric-oxide enhancers are niche, restricted or not approved options; bupropion can help antidepressant-induced dysfunction. ^[2]
• Medications, mood disorders and relationship factors are common, correctable contributors: always ask before diagnosing a "psychological" problem. ^[1][2]
• Most women with sexual concerns will not volunteer them unless clinicians ask permission-giving questions. ^[1][2]

Desire, arousal and orgasm are part of the wider picture of women's health: menopause and hormone replacement therapy; urinary incontinence and pelvic organ prolapse; chronic pelvic pain; vulvar disorders; candidiasis and other causes of vaginitis; endometriosis and adenomyosis; depression and anxiety disorders; migraine and sexual side effects of medicines; and postpartum care and breastfeeding. Plain-text cross-references are preferred for sites not yet verified, so links have not been embedded here.

References are listed in the front matter and are cited above as ^[1] American College of Obstetricians and Gynecologists 2019, reaffirmed 2025; ^[2] American Family Physician 2025; ^[3] AUA/SUFU/AUGS 2025; ^[4] NICE NG23 (updated 15 April 2026); ^[5] ISSWSH testosterone guideline (Parish et al., 2021).