Menopause Treatment: MHT & Non-hormonal Options
Written 21st April 2020 - Last Update 27th August 2026
Menopause Treatment: MHT & Non-hormonal Options
MHT regimens and non-hormonal options. See Overview for definitions/physiology, Symptoms, Diagnosis & Assessment for diagnosis, and Premature ovarian insufficiency for how POI dosing/timing differs.
MHT — the headline
MHT is the most effective treatment for the vasomotor symptoms of menopause (hot flushes and night sweats) for women of all ages. None of the alternative therapies, e.g. black cohosh, have been proven to give any benefit. MHT should not be used for primary prevention of cardiovascular disease.
The “window of opportunity”
Current guidance frames MHT risk around age and time since menopause, not just the older WHI headline figures (much of the WHI cohort started MHT well after menopause, skewing early risk perception).
Within 10 years of menopause, MHT does not increase coronary heart disease risk. A 2015 Cochrane review: starting oral MHT in this window (or age <60) lowers all-cause mortality (RR 0.70) and halves CHD risk (RR 0.52), with no stroke-risk increase — though VTE risk stays elevated (RR 1.74). Starting later raises VTE further (RR 1.96), adds a stroke-risk increase, and the mortality/CHD benefit disappears. Starting after age 60 (or >10 years post-menopause) is generally not recommended. Transdermal routes at standard doses do not appear to raise VTE/stroke risk the way oral does — prefer it for women with those risk factors, obesity, or abnormal LFTs.
Premature (<40) and early (40–44) menopause carry materially higher lifetime CVD risk — the rationale for MHT until the average age of natural menopause in this group, not just symptom control. Frequent or persistent vasomotor symptoms are themselves an independent CVD risk marker — a prompt for broader cardiovascular risk assessment.
Contraindications
Absolute: oestrogen-dependent cancers (breast, endometrial), undiagnosed vaginal bleeding, personal history of VTE — for oral MHT specifically; transdermal has better VTE-risk data in low-risk women.
Relative (individualise, transdermal often preferred): established CVD, uncontrolled hypertension, active liver disease, active SLE, migraine (not a contraindication, but low-dose transdermal is preferable).
Risk–benefit (WHI-derived, per 10,000 woman-years)
Combined oestrogen + progestogen (women with a uterus)
Effect Extra/fewer events Fractures (all types) 46 fewer Hip fractures 6 fewer Invasive breast cancer 8 more Stroke 9 more DVT 12 more Pulmonary embolism 9 more Gallbladder disease 20 more Dementia 22 more Urinary incontinence (self-reported) 872 more Oestrogen-only (post-hysterectomy) — a more favourable profile than combined therapy
Effect Extra/fewer events Invasive breast cancer 8 fewer Fractures (all types) 56 fewer Hip fractures 6 fewer Stroke 11 more DVT 7 more Gallbladder disease 33 more Urinary incontinence (self-reported) 872 more
Unopposed oestrogen has a more favourable profile than combined HRT — progestogen drives most of the added breast cancer risk; oestrogen-only actually reduces it below baseline.
Starting MHT
MHT — starting regimens
Situation Regimen Uterus intact, <12 months since LMP Cyclical combined: oestrogen + progestogen 10–14 days/month Uterus intact, >12 months since LMP Continuous combined: oestrogen + progestogen daily Post-hysterectomy Oestrogen-only, e.g. oestradiol patch 25–100mcg transdermal once or twice weekly, or oestradiol 1–4mg PO daily Vaginal symptoms only Local vaginal oestrogen — no progestogen needed Premature (<40) or early (<45) menopause MHT at least until age 50 unless contraindicated
Cyclical is useful while still having spontaneous menses, or under 2 years post-menopause, since breakthrough bleeding is more common on a continuous regimen. Continuous therapy produces amenorrhoea in about 90% by 12 months, but breakthrough spotting is common in the first 3–4 months. A levonorgestrel IUD can be used for the progestogen component and is especially useful for troublesome peri-menopausal bleeding.
Vaginal symptoms only: short-term (1–2 year) local oestrogen use appears safe, but long-term safety data are lacking — consider intermittent withdrawal to reassess ongoing need. Used as monotherapy beyond 6 months, add progesterone for 12 days to check for a withdrawal bleed.
Review: at 6 months, then regularly — general health check, breast check, 2-yearly mammogram, bone density if indicated, and investigate any unexpected bleeding beyond 6 months. No fixed maximum duration — continuation is an individualised benefit–risk decision, with annual review once past 4–5 years since breast cancer risk rises with duration. Stopping: tapering is no better than stopping abruptly for symptom recurrence — about 50% get resurgent symptoms either way.
New bleeding on MHT: exclude unexplained postmenopausal bleeding, abnormal exam findings, or an overdue CST before starting. Manage breakthrough bleeding expectantly or by changing the progestogen dose unless it is heavy, persistent or unresponsive to a change in therapy, which needs investigation. On continuous MHT, bleeding beyond the first 6 months needs a pelvic exam, cervical co-test and transvaginal ultrasound — refer promptly if endometrial thickness is >4mm, or for any further bleeding. On cyclical MHT, bleeding outside the scheduled withdrawal bleed needs the same work-up, threshold ≥5mm.
Other hormonal options
- Tibolone 2.5mg daily: oestrogenic/progestogenic/weak androgenic steroid, an alternative to combined MHT though less effective. Only use more than 12 months post-menopause — increases breast cancer recurrence and stroke risk in women over 65 — avoid after breast cancer.
- Testosterone: may benefit HSDD after full assessment — not a routine addition to MHT for general symptoms. Australian product: AndroFeme 1.
- Bioidentical/compounded hormones: not recommended — unregulated, no efficacy/safety data.
Non-hormonal options for vasomotor symptoms
Non-hormonal options are modest compared with MHT. Choice depends on concurrent symptoms, comorbidities and preference — start low, increase according to response.
Non-hormonal drug options — hot flushes
Drug class Example regimen Flush reduction SNRI Venlafaxine 37.5mg mane, increasing to 75mg ~60% SNRI Desvenlafaxine 50mg mane, increasing to 150mg ~64% SSRI Escitalopram 5mg mane, increasing to 20mg 50–60% SSRI Citalopram 10mg mane, increasing to 20mg 43–50% Gabapentinoid Gabapentin 100–300mg nocte, increasing to tds 50–80% Gabapentinoid Pregabalin 75mg bd 65–71% Antihypertensive Clonidine 25microg bd, increasing to 75microg bd ~40% (only PBS-listed non-hormonal option) Antispasmodic Oxybutynin 2.5–5mg bd 50–60% NK3 antagonist Fezolinetant 45mg daily ~60–70%
Avoid fluoxetine/paroxetine with tamoxifen — both inhibit CYP2D6 and reduce its active metabolite; use an SNRI or an alternative SSRI instead.
Fezolinetant reduces flushes within the first week, via KNDy-neuron NK3 blockade. Check LFTs regularly — around 2% develop transaminase elevation, usually reversible on stopping. Contraindicated with oestrogens/progestogens. Not yet PBS-listed.
CBT and a 5-session hypnotherapy course both reduce flushes and improve sleep/mood. Weight loss (if overweight) also helps; acupuncture, yoga, exercise and relaxation therapy show no benefit. Complementary medicines (vitamin E, soy, red clover, magnesium, black cohosh) are not currently recommended — evidence is inconsistent to absent, and black cohosh has documented liver toxicity.
Vaginal dryness / genitourinary syndrome of menopause (GSM)
GSM affects roughly half of postmenopausal women aged 50–60, rising to 70% by age 70, but remains under-diagnosed — ask proactively.
First-line: genital skin care (breathable cotton underwear, fragrance-free cleansing), plus lubricants and moisturisers — silicone-based products generally outperform water-based, used daily (moisturiser) or as needed (lubricant). If ineffective, or if other GSM symptoms are present: local vaginal oestrogen — the most effective option for isolated genitourinary symptoms, and does not require a progestogen even with an intact uterus. Maximal absorption occurs in the first 2 weeks of nightly use; full effect can take up to 8 weeks, then transition to maintenance dosing of 2–3 applications/week.
Exclude mimics if symptoms persist: candida, bacterial vaginosis, trichomoniasis, cystitis, vulval dermatoses, pelvic floor dysfunction.
Vaginal oestrogen regimens
Product Regimen Estriol 1mg/g cream One applicatorful (0.5mg) nightly for 2–3 weeks, then twice weekly Estriol pessary 500microg Nightly for 2–3 weeks, then once or twice weekly Estradiol pessary 10microg Nightly for 2 weeks, then twice weekly
Vaginal oestrogen reduces recurrent UTI frequency and is not associated with increased cardiovascular disease, VTE or breast cancer risk.
Vaginal DHEA (prasterone) — a 6.5mg nightly insert, converted locally to oestrogens/androgens without affecting the endometrium — is an alternative for symptoms not responding to first-line measures.
GSM affects up to 70% of breast cancer survivors and often drives poor treatment adherence — vaginal oestrogen has not been shown to increase recurrence/mortality risk, and can be considered after oncologist consultation; estriol is often preferred for its more limited systemic conversion.
Vaginal laser therapy is not currently recommended outside clinical trials — RCTs show no clear advantage over vaginal oestrogen and long-term safety data are lacking.
Troubleshooting MHT
Review within 6–12 weeks of starting (earlier for severe mood disturbance, or a history of adverse reactions to hormonal contraception) — full therapeutic effect can take up to 3 months.
| Problem | Management |
|---|---|
| Mastalgia | Reduce oestrogen dose first; if it persists, switch progestogen (drospirenone/tibolone: lower rates). |
| Headache / migraine | Transdermal is preferable, mandatory in migraine with aura. Start low, titrate up. |
| Fluid retention | Switch to a progestogen with anti-mineralocorticoid effect (drospirenone), or reduce oestrogen dose. |
| Mood disturbance | A recognised progestogen effect. Micronised progesterone is probably least likely to trigger it; an oestrogen-only trial can clarify the cause. |
| Poor symptom control | Stepwise oestrogen (and matched progestogen) increase. Check transdermal technique first — moisturisers/soap can block absorption. |
| GLP-1 agonists (semaglutide, tirzepatide) | Can reduce oral MHT absorption via delayed gastric emptying. Double the oral progestogen dose for 4 weeks after any GLP-1 dose increase. |
MHT after cancer
Requires multidisciplinary, individualised care with the treating oncology team.
| Cancer | MHT | Notes |
|---|---|---|
| Breast | Avoid (avoid tibolone too) | Vaginal oestrogen: no consensus, consult breast team |
| Cervical SCC/adenocarcinoma | Acceptable | Not hormonally responsive |
| Endometrial (Stage I–II) | May be considered | Limited data, no additional harm shown |
| Endometrial (Stage III–IV) | Not recommended | No safety data |
| Uterine sarcoma | Not recommended | Some are ER/PR-positive |
| Ovarian — high-grade serous/clear cell/mucinous | Acceptable | Limited data suggests no harm |
| Ovarian — low-grade serous/endometrioid | Not recommended | |
| Vulval/vaginal | Acceptable | Not hormonally responsive |
| Colorectal, haematological | Acceptable |
Referral
Consider referral: a hard-to-assess benefit–harm balance (complex comorbidity, age ≥60, high VTE/familial breast cancer risk, endometriosis); premature/early menopause; persistent symptoms despite therapy; or persistent MHT adverse effects.