Will MHT give me breast cancer?

The honest answer is in numbers, not adjectives. The most quoted figure is from the WHI 2002 combined arm: combined oestrogen + progestogen MHT used for 5-10 years adds roughly 8 extra cases of breast cancer per 1000 women using it — that is in addition to the background rate every woman carries, and the risk attenuates after stopping. Oestrogen-only MHT in women without a uterus shows a smaller and more debated signal. Modern micronised progesterone may carry a lower breast signal than the medroxyprogesterone used in the original WHI cohort, though that evidence is observational rather than randomised. Whatever your starting point, the conversation is individual — your family history, your breast density, your other risks (alcohol, weight, physical activity) all matter, and your prescriber will work through it with you.

Why are patches preferred over tablets?

Oestrogen taken as a tablet is absorbed through the gut and processed by the liver before it reaches the rest of the body. That first-pass liver activity drives a higher clot, stroke and gallbladder signal, and changes liver-made proteins (triglycerides, CRP, sex-hormone-binding globulin). Oestrogen delivered through the skin — patch or gel — bypasses that first pass. Observational data and the ELITE trial show no measurable increase in clot risk at standard transdermal doses. AMS 2023 acknowledges transdermal as the route the conversation usually starts with for that reason. Oral oestrogen is still a reasonable choice when transdermal is not tolerated or strongly not preferred — the prescriber weighs your clot-risk profile first.

Do I need progesterone if I have had a hysterectomy?

Usually no. The reason progesterone is added to systemic oestrogen is to protect the lining of the uterus — unopposed oestrogen drives endometrial hyperplasia and endometrial cancer. If the uterus is gone, that protection is not needed, and oestrogen-only MHT is generally appropriate. One exception: women who had a hysterectomy for endometriosis with residual disease may still be advised to take a progestogen to suppress any oestrogen-responsive tissue left behind. Your prescriber will know whether that applies to you.

I am past 60 — am I too late?

Not automatically, but the conversation changes. The 'window' evidence (ELITE, KEEPS-Cog, the WHI age-stratified re-analysis) shows a more favourable safety signal when MHT is started within roughly 10 years of the final menstrual period or before age 60. Starting later than that, the WHI 2002 harm signal applies — particularly for cardiovascular events and, in the WHIMS study, for dementia in women over 65. That does not mean MHT is forbidden after 60; it means the candidacy conversation tightens, transdermal is strongly preferred, the lowest effective dose is the starting point, and the symptom benefit needs to be substantial enough to outweigh the shifted risk profile. Vaginal-only MHT for genitourinary symptoms is a completely separate question and does not carry the same age-window considerations.

Can MHT prevent dementia or heart disease?

This is the most contested question in the field, and the honest answer is that the timing-hypothesis evidence is evolving rather than settled. ELITE 2016, KEEPS-Cog 2015 and the WHI 2017 age-stratified re-analysis showed a more favourable cardiovascular and cognitive signal when MHT was started inside the window — but those findings are not the same as evidence that MHT prevents heart attacks, strokes, or dementia. MHT is NOT TGA-approved for cardiovascular or dementia prevention. AMS 2023 sits more conservatively on this question than some international bodies (NAMS 2022, IMS, NICE NG23) — and this page names that gap rather than collapsing it. If symptom control is the reason for MHT and the candidacy is otherwise sound, the timing evidence may inform when to start. It does not, on current AU primary-tier evidence, justify starting MHT to prevent these conditions.

I had breast cancer years ago — can I use vaginal oestrogen for dryness and recurrent UTIs?

Often yes, and it is a question worth bringing to your oncologist and prescriber together. Vaginal estradiol (Vagifem) and estriol (Ovestin) at the standard doses deliver very small amounts of oestrogen and most of that stays local — systemic absorption is minimal. For breast-cancer survivors with refractory genitourinary symptoms that non-hormonal treatments have not controlled (vaginal moisturisers, lubricants, pelvic-floor physiotherapy), vaginal oestrogen is often considered acceptable after an oncology conversation. Women on aromatase inhibitors are a more careful case — the conversation is more cautious because aromatase inhibitors aim to keep oestrogen as low as possible. This is exactly the kind of decision that benefits from oncologist, gynaecologist and GP being on the same page.

Is testosterone cream the right treatment if I am exhausted and brain-foggy?

No — and this is one of the most-misframed conversations in current menopause media. Testosterone cream (Androfeme) is TGA-approved in Australia (2024) for one specific indication: hypoactive sexual desire disorder in postmenopausal women — that is, distressing loss of libido. It is supported by RANZCOG, the Endocrine Society of Australia and the international sexual-medicine society ISSWSH for that use. It is NOT approved or supported for energy, mood, wellbeing, cognition or muscle mass. If exhaustion, brain fog or low mood are the main story, the conversation is somewhere else — thyroid, iron, B12, sleep architecture, vasomotor disruption, mood disorder, sleep apnoea, the perimenopause hormonal transition itself — and the prescriber will work through that picture rather than reaching for testosterone.

Menopausal hormone therapy (MHT/HRT)

Menopausal hormone therapy (MHT / HRT) — patient guide

By Dr HB Lo, FACRRM Reviewed 25 May 2026 22 min read

Prescribed for: Moderate-to-severe vasomotor symptoms (hot flushes, night sweats) in peri- or postmenopause · Genitourinary syndrome of menopause (vaginal dryness, painful sex, recurrent urinary tract infections, vulvovaginal atrophy) · Prevention of postmenopausal osteoporosis in selected women — usually as an alternative or adjunct to a bisphosphonate or denosumab when there are also vasomotor symptoms or another reason MHT is appropriate · Premature ovarian insufficiency (POI) and surgical menopause before the natural-menopause age — replacement until approximately age 51 (standard of care) · Postmenopausal hypoactive sexual desire disorder (HSDD) — testosterone cream (Androfeme), TGA-approved in Australia from 2024

Menopausal hormone therapy (MHT — modern name for HRT) is prescribed for moderate-to-severe hot flushes and night sweats, for genitourinary symptoms (vaginal dryness, painful sex, recurrent UTIs), and for bone protection in selected women. It is NOT TGA-approved as primary prevention for heart disease or dementia.

Most women starting MHT begin with a transdermal product (patch or gel) rather than a tablet — the clot and stroke signal is much lower when oestrogen bypasses the liver. If you have a uterus, a progestogen is added — micronised progesterone (Prometrium / Utrogestan) is the modern preference. Vaginal-only symptoms — vaginal-only oestrogen, minimal systemic exposure.

The "window" framing (within ~10 years of the final period or before 60) shows a more favourable safety signal than later initiation. Risk numbers are real and route-dependent; your prescriber walks through them in absolute terms.

This page covers the whole menopausal hormone therapy family — patches, gels, tablets, vaginal-only, the progestogens, tibolone, the testosterone cream — and the conversation that sits underneath all of them.

Before the science

You have been told your bloods are normal. You have been told to try sleeping more, drinking less, exercising more. You have been to general practice three times in the last six months and the conversation never quite reached MHT — not because the GP was hostile, but because in a fifteen-minute appointment it is the conversation that gets deferred. Meanwhile the hot flushes are bending your sleep, the joints ache differently, the brain feels half-speed, and something is going out that you do not have a word for.

The word, when it lands, is usually relief — even when the word is not pleasant. Perimenopause. Menopause. The transition. The body is doing exactly what bodies do at this stage; it is not a defect. And modern menopausal hormone therapy is one tool that exists for the women whose symptoms are bad enough that the trade-off makes sense.

What follows is plain English on what is in the medicine cabinet, how the choices are made, where the evidence is settled and where it genuinely is not. It is not a recommendation to take MHT, and it is not a recommendation to avoid MHT. It is the conversation in writing, so you can come into the consult already knowing the questions.

Find your medicine

Group	Generic	Common brand	Route	Frequency
Oestrogen — transdermal patch	Estradiol	Estradot, Climara	Skin	1-2x weekly
Oestrogen — transdermal gel	Estradiol	Sandrena, Estrogel	Skin	Once daily
Oestrogen — oral	Estradiol	Estrofem, Progynova	Tablet	Once daily
Oestrogen — vaginal tablet	Estradiol 10 mcg	Vagifem	Vaginal	2x weekly
Oestrogen — vaginal cream/pessary	Estriol	Ovestin	Vaginal	1-2x weekly
Oestrogen — vaginal ring	Estradiol	Estring	Vaginal	Every 3 months
Progestogen	Micronised progesterone	Prometrium, Utrogestan	Tablet (nightly)	Daily or 12-14 days/month
Progestogen	Medroxyprogesterone	Provera	Tablet	Daily or 12-14 days/month
Progestogen	Dydrogesterone	Duphaston	Tablet	Daily or 12-14 days/month
Single-tablet (postmenopausal)	Tibolone	Livial	Tablet	Once daily
Testosterone (HSDD only)	Testosterone 1% cream	Androfeme	Skin	Once daily
Combined sequential	Estradiol + dydrogesterone	Femoston	Tablet	Once daily
Combined continuous	Estradiol + dydrogesterone	Femoston Conti	Tablet	Once daily
Combined continuous	Estradiol + norethisterone	Activelle, Kliogest	Tablet	Once daily
Combined patch	Estradiol + norethisterone	Estalis	Skin	2x weekly

A note on the names. “HRT” — hormone replacement therapy — was the old name. Modern usage is MHT — menopausal hormone therapy — because the goal is symptom control and selected risk reduction, not literal replacement of a premenopausal state. Most pharmacies and clinicians still use both terms interchangeably.

What MHT is for

The TGA-approved indications are specific. MHT is approved in Australia for:

Moderate-to-severe hot flushes and night sweats in peri- or postmenopause.
Genitourinary syndrome of menopause — vaginal dryness, painful sex, recurrent urinary tract infections, vulvovaginal atrophy.
Prevention of postmenopausal osteoporosis in selected women. Usually as an alternative or adjunct to a bisphosphonate or denosumab. Used when there are also vasomotor symptoms or another reason MHT is appropriate.
Replacement in premature ovarian insufficiency (POI) and surgical menopause before the natural-menopause age — until about age 51. This is mainstream standard of care.

MHT is NOT TGA-approved for primary cardiovascular prevention. It is not approved for dementia or Alzheimer’s. Not for sarcopenia. Not for “anti-ageing”. Not to “reverse menopause”. The timing-hypothesis trials (ELITE 2016, KEEPS-Cog 2015, the WHI 2017 age-stratified re-analysis) are covered later on this page. They do not change what MHT is approved for. The integrative-GP position is simple. Name the evidence honestly. Do not promote MHT for uses outside its label or outside AMS 2023 endorsement.

The basics

Choose the route first, then the dose. Transdermal (patch or gel) usually starts the conversation in 2026. Oral is reasonable when transdermal is not tolerated. Vaginal-only is a separate pathway with its own rules — see the section below.
If you have a uterus, you also take a progestogen. Mandatory. Unopposed oestrogen drives endometrial cancer.
ED for sudden one-sided leg swelling, calf pain, sudden shortness of breath, chest pain, sudden facial droop, slurred speech, or sudden severe headache. Clot and stroke are rare but real, especially with oral oestrogen.
Do not stop abruptly without prescriber advice. Vasomotor symptoms rebound; bone protection drops off.

Everything else is below.

Which route

The single biggest safety lever in the choice is the route the oestrogen takes.

Transdermal patches (Estradot, Climara) and gels (Sandrena, Estrogel) deliver oestrogen through the skin, bypassing the liver. The clot signal is much lower than with oral — at standard transdermal doses, observational data and the ELITE trial show no measurable increase. Stroke risk is also lower. Triglycerides, CRP and sex-hormone-binding globulin are essentially unchanged. AMS 2023 acknowledges this and treats transdermal as the route the conversation usually starts with when clot risk is a consideration. Practical issues: skin reactions at the patch site, patch fall-off in heat or pools, and the gel needing to dry before contact with others (particularly small children and pre-pubertal household members — skin transfer to others is documented).
Oral estradiol (Estrofem, Progynova) is processed by the liver before reaching the rest of the body. That first-pass activity drives an oral-specific signal: clot risk roughly 1.5-2x baseline, a stroke signal in the WHI cohort using oral conjugated equine oestrogen, and roughly 50% higher gallstone disease and cholecystectomy. It is a reasonable choice when transdermal is not tolerated or strongly not preferred — the prescriber weighs the clot-risk profile first.
Vaginal oestrogen (Vagifem 10 mcg, Ovestin, Estring) is local. Systemic absorption at these doses is minimal. This is a completely separate pathway — see below.

The conversation about route is not about which is “best” — it is about which fits your specific risk picture (smoking status, BMI, family history of clot or stroke, migraine pattern, gallbladder history, skin sensitivity, preference for a tablet versus a skin product).

If you have a uterus

Systemic oestrogen plus an intact uterus equals a progestogen. This is not optional. Unopposed oestrogen drives endometrial hyperplasia and endometrial cancer, and the progestogen exists to keep the lining of the uterus from over-thickening.

Three progestogens are commonly used in Australia.

Micronised progesterone (Prometrium, Utrogestan) is bioidentical to the progesterone your body made. The lipid profile is more favourable than older synthetic progestogens, and the breast-cancer signal in the E3N observational cohort appears lower. Current AMS guidance leans toward micronised progesterone as the preferred progestogen when one is needed. Mild sedation is the reason it is dosed at night — a useful side benefit for many women whose sleep is already disrupted.
Medroxyprogesterone (Provera) is the older synthetic progestogen — and the one used in the WHI 2002 combined arm. Less favourable lipid profile, higher breast-cancer signal in long-term data. Still used in AU but increasingly displaced.
Dydrogesterone (Duphaston) sits between the two — closer to natural progesterone than medroxyprogesterone, possibly lower breast signal in the E3N cohort. Paired with estradiol in the Femoston combined product.

The dose and rhythm depend on whether you are perimenopausal (still having occasional bleeds — usually a sequential regimen, 12-14 nights per month, with a predictable monthly bleed) or postmenopausal (≥12 months past the final period — usually a continuous combined regimen with no scheduled bleed). The prescriber matches the regimen to where you are.

Vaginal-only MHT

This is the part of the conversation many women never hear, even from clinicians who are comfortable with systemic MHT.

If your symptoms are confined to genitourinary syndrome of menopause — vaginal dryness, painful sex, recurrent urinary tract infections, the urgency-without-infection that turns up in midlife — vaginal oestrogen is a separate pathway with its own safety profile.

Vagifem (estradiol 10 mcg vaginal tablet) twice weekly maintenance after loading.
Ovestin (estriol vaginal cream or pessary) 1-2 times weekly maintenance after loading.
Estring (estradiol vaginal ring) replaced every 3 months — AU supply has been intermittent.

Systemic absorption at these doses is minimal. The drug treats the tissue that is in front of it, not the whole body. There is no breast-cancer or clot signal at population level. It can be used long-term. For breast-cancer survivors with refractory urogenital symptoms that non-hormonal options (vaginal moisturisers, lubricants, pelvic-floor physiotherapy) have not controlled, vaginal oestrogen is often considered acceptable after an oncology conversation — women on aromatase inhibitors are a more careful case but not an absolute contraindication.

Vaginal-only MHT does not cover hot flushes and does not give bone protection. It is doing one specific job. If that is the job that needs doing, the conversation may not need to go further than this.

Testosterone for HSDD — what it is and what it is not

In 2024, Androfeme (testosterone 1% cream) became TGA-approved in Australia for hypoactive sexual desire disorder (HSDD) in postmenopausal women — distressing loss of libido that is not attributable to relationship, mood, sleep, medication, or other identifiable cause. Australia is one of the few countries with on-label female testosterone for this indication. RANZCOG, the Endocrine Society of Australia and the international sexual-medicine society ISSWSH support it for HSDD.

It is NOT approved or supported for energy, mood, wellbeing, cognition, “vitality” or muscle mass. The evidence base does not support those uses, and promoting it for them sits outside the label and outside mainstream guidelines.

How it is used in practice:

A small fingertip of 1% cream, applied to the lower abdomen or thigh, rotated.
Baseline total testosterone before starting, then 3-6 monthly.
Target the upper half of the female reference range; if the level drifts into the male range, dose-reduce or stop.
Skin transfer to partners and children is documented — wash hands, cover the application site, let it dry.
Side-effects worth knowing: acne, increased facial or body hair, oily skin. Voice deepening and clitoral enlargement are rare at appropriately monitored doses but can be permanent — which is why monitoring matters.

Androfeme is not PBS-listed (private prescription, around $130-$160 per 50 g tube at 2026 pricing — confirm with your pharmacist).

The timing question

This is the conversation that has shifted most in the last decade, and the one most likely to be misframed.

In 2002, the WHI study (Rossouw et al., JAMA) showed harm with combined conjugated equine oestrogen plus medroxyprogesterone in a cohort whose average age was 63 — that is, on average, well past the natural age of menopause. Combined MHT use for 5-10 years added roughly 8 extra breast cancer cases per 1000 users; cardiovascular harm signals emerged. The result reset a generation of prescribing.

Over the following 15 years, three later analyses re-shaped the picture.

ELITE 2016 (Hodis et al., NEJM) showed that transdermal estradiol started within 6 years of the final menstrual period slowed carotid intima-media thickness progression, while the same therapy started 10 or more years past the final period did not.
KEEPS-Cog 2015 (Gleason et al., PLoS Med) showed neither benefit nor harm to cognition over 4 years in recently postmenopausal women on transdermal estradiol plus oral micronised progesterone.
Manson 2017 (JAMA) re-analysed the WHI cohort by age band. Initiation between 50 and 59 carried a more favourable mortality signal than initiation at 70 or older.

The pattern is real and is what the field calls the “timing hypothesis” or “window of opportunity” — initiation within roughly 10 years of the final menstrual period or before age 60 looks better than initiation later.

What that means for this page, in plain English:

The timing evidence informs the conversation about WHEN to consider MHT if symptom control is the reason for considering it.
It does NOT justify starting MHT to prevent heart disease, stroke or dementia. Those uses sit outside TGA approval and outside AMS 2023 endorsement.
AMS 2023 is noticeably more conservative on the cardiovascular and cognitive framing than NAMS 2022, IMS or NICE NG23. This page names that gap rather than collapsing it. AMS is not wrong and international is not right — the evidence is genuinely evolving, and the AU primary tier waits longer for the dust to settle.

The honest position is: hold both. The timing evidence is real. The prevention claim is not yet supported at AU primary-tier level. The conversation about whether MHT is appropriate for you is about symptom control and individual risk-benefit, not about prevention.

The numbers honestly

Risk in absolute terms is more useful than risk in percentages.

Breast cancer. Combined oestrogen + progestogen MHT used for 5-10 years adds roughly 8 extra cases of breast cancer per 1000 women using it, on top of the baseline rate every woman carries. Oestrogen-only MHT in women without a uterus shows a smaller and more debated signal. The risk attenuates after stopping. Family history, breast density, alcohol, weight, and physical activity all modify your baseline.
Clot in the leg or lung (VTE/PE). Oral oestrogen approximately 1.5-2x baseline. Transdermal oestrogen — no measurable increase at standard doses in observational data and in ELITE. Risk is highest in the first year. The clot signal is the biggest argument for transdermal-first.
Stroke. Oral oestrogen showed an increased signal in the WHI (oral conjugated equine oestrogen). Transdermal carries a lower risk.
Gallbladder disease. Oral oestrogen approximately 50% higher rate of gallstones and cholecystectomy; transdermal much lower.
Endometrial cancer. Driven by unopposed oestrogen in a woman with a uterus. Prevented by mandatory progestogen co-prescription.
Migraine with aura. A relative contraindication to oral oestrogen because of additive ischaemic stroke risk. Transdermal at the lowest effective dose is often acceptable after a careful conversation. Migraine without aura is not a contraindication.
Ovarian cancer. A modest signal with longer-term (typically >5 years) MHT use in some observational analyses; absolute risk small.

Compounded bioidentical hormones and oestrogen pellets

This is a separate pathway that deserves a plain answer rather than a shrug.

Mainstream guidelines (AMS 2023, NAMS 2022, the International Menopause Society, RANZCOG) do not endorse compounded bioidentical hormones or oestrogen pellets for routine use. The central concerns:

The actual amount of hormone in a compounded preparation can drift batch to batch — variable dosing is the documented problem.
These preparations are not TGA-evaluated for safety, efficacy or quality.
Reliable endometrial protection requires a matched progestogen at a known dose for a known number of days — the same protection mainstream regimens build in deliberately. Pellet regimens often do not include this.
There is no good evidence that compounded preparations are safer or more “natural” than TGA-registered MHT — and TGA-registered estradiol and estriol are themselves bioidentical hormones at known doses.

Women already on this pathway are welcome to bring that conversation to a prescriber without judgement. But if you are starting the conversation from zero, the TGA-registered products are where the evidence sits.

Integrative levers

Most women considering MHT also want to know what else moves the dial. This section is the longer version of that conversation.

Strong evidence

Resistance training plus weight-bearing exercise. Independent of MHT, this is the single biggest non-hormonal lever for bone density, sarcopenia prevention, glucose control, mood and sleep in the menopause transition. Two or three resistance sessions plus weight-bearing aerobic activity per week is the evidence-based minimum.
Pelvic-floor physiotherapy. Strong evidence for urinary urgency, stress incontinence, prolapse-related symptoms, and painful sex. Often overlooked, often transformative.
CBT-VMS — cognitive behavioural therapy for vasomotor symptoms. Modest RCT evidence (Hunter et al., MENOS trials) reducing the bother and impact of hot flushes even when frequency does not change much. Useful in women who cannot or do not want to take MHT.
CBT-I — cognitive behavioural therapy for insomnia. Recommended first for chronic insomnia in midlife women. NICE NG23 endorses.
Alcohol reduction. Worsens hot flushes, sleep, mood and bone density; increases breast cancer risk independent of MHT. NHMRC ≤ 10 standard drinks/week and ≤ 4 in any one day; less is better.
Vitamin D adequacy plus calcium adequacy. Mandatory for bone synergy — MHT (or a bisphosphonate) does not work as a bone agent if calcium and vitamin D are deficient. Target 25(OH)D 75-100 nmol/L; calcium 1000-1200 mg/day total from food first.

Moderate evidence

Soy isoflavones, 50-100 mg/day, modest improvement in hot-flush frequency and severity in meta-analyses. Whole-food soy (tofu, tempeh, edamame, soy milk) is preferable to concentrated supplements. Caution if you have a personal history of oestrogen-receptor-positive breast cancer — discuss with oncology before concentrated supplements; whole-food soy is generally considered safe even in this group.
Ashwagandha, 600 mg/day standardised extract, modest RCT signal for hot flushes, sleep and stress in perimenopausal women. Caution in autoimmune thyroid disease (can raise free T4 / suppress TSH).
Sage (Salvia officinalis), 280 mg/day standardised extract, modest vasomotor evidence in small RCTs.
Omega-3 EPA/DHA, 1-2 g/day combined, for cardiovascular health, mood, and the dry-eye disease that often turns up at this stage.
Magnesium, 300-400 mg/day in the evening, modest help for sleep, mild vasomotor symptoms, and bone health.
Mediterranean-style dietary pattern for cardiovascular, mood and cognitive outcomes in midlife.

Limited or emerging evidence

Black cohosh — short-term (up to 6 months) for vasomotor symptoms; rare hepatotoxicity reported. Stop and seek review for unexplained right-upper-quadrant pain, nausea, jaundice or dark urine.
Red clover — modest effect on hot-flush frequency in some RCTs.
Flaxseed — 25-40 g/day ground flaxseed shows modest vasomotor effect in some trials; adequate water to avoid GI bloating.

Specific to being on MHT

St John’s wort induces oestrogen metabolism (CYP3A4) and can reduce MHT effectiveness. Avoid co-use.
Thyroxine dose may need rechecking 6-8 weeks after starting or stopping oral MHT — oral oestrogen raises thyroid-binding globulin. Transdermal effect is smaller.
Anticonvulsants (lamotrigine specifically) — oestrogen lowers lamotrigine levels. Seizure-control review if MHT is started or stopped.
Warfarin INR monitoring is increased after starting or changing oral oestrogen dose.

How long do I stay on MHT?

The older framing was “the lowest effective dose for the shortest possible duration”. The modern framing — AMS 2023, NICE NG23 — is that there is no automatic time limit, and the question is reviewed at least annually with the prescriber. If symptom control and other benefits continue to outweigh the risks for that individual woman, continuation is appropriate. If symptoms have settled and the risk-benefit picture has shifted, stepping down or stopping is appropriate.

Vasomotor symptoms typically settle over 5-7 years for most women, with significant individual variation. Once they ease, stepping down the dose and reassessing is part of the normal conversation — not an automatic discontinuation.

Vaginal-only MHT for genitourinary symptoms has a different long-term safety conversation from systemic MHT. Long-term continuation of vaginal oestrogen is generally fine and is the standard approach for women whose urogenital symptoms otherwise return.

Tap any section below to expand the detail.

Side effects in detail

Common (usually mild and settling)

Breast tenderness, especially in the first 1-3 months.
Light bleeding or spotting in the first 3-6 months on a continuous combined regimen.
Mood fluctuation in the first weeks, usually settling.
Headache in the first weeks, usually settling.
Mild fluid retention or bloating.
Patch site reactions (transdermal).
Sedation at night (micronised progesterone — often a benefit).

Uncommon

Persistent breast tenderness — review the regimen.
New onset migraine — review.
New onset depressed mood that does not settle — review.

Rare but important — ED or urgent contact

Sudden one-sided leg swelling, calf pain, sudden shortness of breath, chest pain, coughing blood — possible clot. Stop the next dose and go to ED.
Sudden facial droop, arm or leg weakness, slurred speech, sudden severe headache, sudden visual loss — stroke signs. Call 000.
Severe right-upper-abdominal pain with jaundice, pale stools or dark urine — possible gallbladder or liver problem. Urgent contact.
Any unscheduled vaginal bleeding beyond 6 months on a continuous combined regimen, or after a long bleed-free interval — gynaecology review.
A new breast lump, asymmetric change, nipple discharge or skin change — urgent review.

Drugs, food and alcohol

Tell the prescriber and pharmacist before combining with:

St John’s wort — induces oestrogen metabolism, reduces MHT effectiveness. Avoid.
Rifampicin, phenytoin, carbamazepine, phenobarbital, primidone, topiramate, modafinil — strong CYP3A4 inducers. Reduce oestrogen levels; specialist input on dose adjustment.
Some antiretrovirals (ritonavir-boosted regimens, efavirenz) — variable effects on oestrogen and progestogen levels; specialist input.
Thyroxine — oral oestrogen raises thyroid-binding globulin and may increase thyroxine requirements. Recheck TSH 6-8 weeks after starting or stopping oral MHT.
Warfarin — oral oestrogen can alter INR; increase monitoring.
Lamotrigine — oestrogen lowers lamotrigine levels; seizure-control review.
Tamoxifen — MHT in women on tamoxifen for breast-cancer treatment is generally not used; vaginal oestrogen for refractory genitourinary symptoms is a separate, oncology-led decision.
Aromatase inhibitors (anastrozole, letrozole, exemestane) — MHT undermines the treatment intent. Contraindicated.

Smoking is not a drug interaction but a major modifier — it increases clot, stroke and heart-attack risk additively with oral oestrogen. Transdermal is strongly preferred in smokers, and smoking cessation is part of the conversation.

Alcohol worsens hot flushes, sleep and mood, increases breast cancer risk independent of MHT, and worsens bone density. NHMRC ≤ 10 standard drinks/week and ≤ 4 in any one day; less is better.

Food. No specific food restrictions. Whole-food soy (tofu, tempeh, edamame) is generally fine alongside MHT and may modestly help vasomotor symptoms in its own right.

Monitoring — what tests and when

Baseline — BP, weight, BMI, breast clinical exam, cervical screening up to date, mammogram up to date per BreastScreen Australia age-band recommendations, lipid profile if indicated. Total testosterone if Androfeme is being considered. TSH if not recent. Vitamin D if not recent.
3 months — symptom review, side-effect review, BP. Adjust regimen if needed.
6-12 months — full review. Any unscheduled bleeding beyond 6 months on continuous combined regimen needs gynaecology investigation.
Annually thereafter — full review, including risk-benefit reassessment. Mammogram per BreastScreen age band. BP. Testosterone level if on Androfeme (3-6 monthly initially, then annually once stable).
Anytime — message the prescriber for unscheduled bleeding, new severe headache, breast change, leg swelling, or any of the red-flag symptoms above.

Sick-day, surgery and pause guidance

Minor illness generally does not need an MHT pause. Carry on.
Do not stop abruptly without prescriber advice. Vasomotor symptoms rebound and bone protection drops off.
Elective surgery — oral MHT is often paused 4-6 weeks before high-clot-risk surgery per anaesthetic and surgical guidance. Transdermal is often continued. Confirm with the prescriber and the surgical team.
Travel — long-haul flights add their own clot risk on top of oral oestrogen; transdermal is the easier conversation for frequent long-haul travellers. Hydration, movement and compression stockings are sensible regardless.

Pregnancy and breastfeeding

MHT is not for pregnancy or breastfeeding. Importantly, MHT is not contraception — perimenopausal women who could still conceive need contraception if pregnancy is not desired, regardless of MHT. The general rule is contraception for one year after the final menstrual period if over 50, two years if under 50.

For premature ovarian insufficiency or surgical menopause before the natural-menopause age, hormone replacement until approximately age 51 is the mainstream standard of care — and the conversation includes contraception until POI has been confirmed.

Cost

Most MHT items are on the PBS. From 1 January 2026, the PBS co-payment is:

General patient: up to $25.00 per script
Concession card holder: up to $7.70 per script

Some MHT items are Authority Required or Streamlined Authority — confirm with your pharmacist. Vaginal oestrogen is generally unrestricted PBS.

Androfeme (testosterone cream) is not PBS-listed and is a private prescription — approximately $130-$160 per 50 g tube at 2026 pricing. Confirm with your pharmacist.

Compounded preparations are not PBS-listed.

Australian context

The Australasian Menopause Society 2023 Position Statement on MHT is the AU primary-tier reference. Jean Hailes for Women’s Health publishes patient-facing resources that align with the AMS position. RANZCOG and the Endocrine Society of Australia contribute to the testosterone-for-HSDD position and the POI standard of care.

This page is consistent with AMS 2023. Where AMS 2023 sits more conservative than NAMS 2022, IMS or NICE NG23 — particularly on the timing-hypothesis framing for cardiovascular and cognitive evidence — this page names the gap rather than collapsing it. The integrative-GP point of differentiation is to give you both positions and let the conversation happen, not to choose for you.

If menopause is overlapping with mood, relationship or sexual-violence history: Lifeline 13 11 14, Beyond Blue 1300 22 4636, 1800RESPECT 1800 737 732 are 24/7 AU support lines.

When to message the prescriber

Vasomotor symptoms not controlled on the current regimen after a fair trial.
Side effects you cannot live with.
Breakthrough bleeding (any unscheduled bleeding beyond 6 months on continuous combined; any new bleeding after a long bleed-free interval).
A new health condition or new medicine that might interact.
Planning elective surgery.
Planning to stop.
Anything from the red-flag list above.

Track these between now and your next visit

Symptom log — hot flushes per day, night sweats, sleep quality, mood, energy. A simple 1-10 scale a couple of times a week is enough.
Any bleeding — when, how heavy, how long.
Any new symptoms — headache pattern change, breast tenderness, mood change, leg discomfort.
Any new medicines or supplements — including over-the-counter and herbal products.

Bring the list to your review appointment.

This is general information, not personal medical advice. Every woman is biochemically and clinically unique. The decisions about MHT — whether, which, what dose, what route, how long — are made with the doctor who prescribes them and, where relevant, with your gynaecologist or oncologist. If anything on this page appears to contradict advice from your treating doctor, follow your doctor; they have context about your situation that this page cannot.
Reading this page does not establish a doctor-patient relationship with Dr Hoebing Lo. If you are not a current patient, please discuss MHT with your own GP, women’s-health specialist or gynaecologist.
About the integrative content. The lifestyle, dietary and complementary recommendations on this page summarise current published research. Effect sizes are approximations from clinical studies; individual response will vary, and real-world results are commonly smaller than trial results. Supplements and herbal products are not interchangeable with prescribed medication and can interact with it. Discuss any new supplement, herbal product or significant dietary change with your prescriber and pharmacist first.
Medico-legal note. MHT sits in a sensitive medico-legal space. This page reflects the current evidence base, the Australasian Menopause Society 2023 Position Statement, NICE NG23 (2024 update), the NAMS 2022 Hormone Therapy Position Statement and the ATA / Endocrine Society position on testosterone in women. Where the AU primary tier sits more conservatively than international bodies — particularly on the timing-hypothesis evidence for cardiovascular and cognitive outcomes — this page names the gap honestly rather than collapsing it. The timing-hypothesis evidence is genuinely evolving rather than settled, and nothing on this page should be read as promoting MHT for cardiovascular prevention, dementia prevention, “anti-ageing”, energy, mood, wellbeing, cognition or muscle. Final formal medico-defence (Avant / MIGA) sign-off on the framing of this page is pending as at the last-reviewed date.
Currency. This page reflects clinical practice as of the last-reviewed date. Medicine evolves; specific details may date between reviews. Pricing shown is indicative; confirm with your pharmacist.
No commercial relationships. Dr Hoebing Lo has no financial or commercial relationship with the manufacturer of any medicine, brand or supplement mentioned on this page.
Emergencies. If you have sudden swelling of one leg, calf pain, sudden shortness of breath, chest pain, coughing blood, sudden facial droop, slurred speech, sudden severe headache, sudden visual loss, or severe abdominal pain with jaundice, call 000 or go to your nearest emergency department. Do not wait, and do not message us first.

Frequently asked questions

Will MHT give me breast cancer?

The honest answer is in numbers, not adjectives. The most quoted figure is from the WHI 2002 combined arm: combined oestrogen + progestogen MHT used for 5-10 years adds roughly 8 extra cases of breast cancer per 1000 women using it — that is in addition to the background rate every woman carries, and the risk attenuates after stopping. Oestrogen-only MHT in women without a uterus shows a smaller and more debated signal. Modern micronised progesterone may carry a lower breast signal than the medroxyprogesterone used in the original WHI cohort, though that evidence is observational rather than randomised. Whatever your starting point, the conversation is individual — your family history, your breast density, your other risks (alcohol, weight, physical activity) all matter, and your prescriber will work through it with you.
Why are patches preferred over tablets?

Oestrogen taken as a tablet is absorbed through the gut and processed by the liver before it reaches the rest of the body. That first-pass liver activity drives a higher clot, stroke and gallbladder signal, and changes liver-made proteins (triglycerides, CRP, sex-hormone-binding globulin). Oestrogen delivered through the skin — patch or gel — bypasses that first pass. Observational data and the ELITE trial show no measurable increase in clot risk at standard transdermal doses. AMS 2023 acknowledges transdermal as the route the conversation usually starts with for that reason. Oral oestrogen is still a reasonable choice when transdermal is not tolerated or strongly not preferred — the prescriber weighs your clot-risk profile first.
Do I need progesterone if I have had a hysterectomy?

Usually no. The reason progesterone is added to systemic oestrogen is to protect the lining of the uterus — unopposed oestrogen drives endometrial hyperplasia and endometrial cancer. If the uterus is gone, that protection is not needed, and oestrogen-only MHT is generally appropriate. One exception: women who had a hysterectomy for endometriosis with residual disease may still be advised to take a progestogen to suppress any oestrogen-responsive tissue left behind. Your prescriber will know whether that applies to you.
What about compounded bioidentical hormones and oestrogen pellets?

Mainstream guidelines (AMS 2023, NAMS 2022, the International Menopause Society, RANZCOG) do not endorse compounded bioidentical hormones or oestrogen pellets for routine use. The central concerns are variable dosing (the actual amount in the preparation can drift batch to batch), lack of TGA evaluation, and difficulty achieving reliable endometrial protection with a matched progestogen — the same protection mainstream regimens build in deliberately. There is also no good evidence they are safer or more 'natural' than TGA-registered MHT, which is itself bioidentical estradiol or estriol delivered at known doses. Patients who are already on a compounded pathway are welcome to bring that conversation to a prescriber without judgement — but if you are starting from zero, the registered products are where the evidence base sits.
I am past 60 — am I too late?

Not automatically, but the conversation changes. The 'window' evidence (ELITE, KEEPS-Cog, the WHI age-stratified re-analysis) shows a more favourable safety signal when MHT is started within roughly 10 years of the final menstrual period or before age 60. Starting later than that, the WHI 2002 harm signal applies — particularly for cardiovascular events and, in the WHIMS study, for dementia in women over 65. That does not mean MHT is forbidden after 60; it means the candidacy conversation tightens, transdermal is strongly preferred, the lowest effective dose is the starting point, and the symptom benefit needs to be substantial enough to outweigh the shifted risk profile. Vaginal-only MHT for genitourinary symptoms is a completely separate question and does not carry the same age-window considerations.
Can MHT prevent dementia or heart disease?

This is the most contested question in the field, and the honest answer is that the timing-hypothesis evidence is evolving rather than settled. ELITE 2016, KEEPS-Cog 2015 and the WHI 2017 age-stratified re-analysis showed a more favourable cardiovascular and cognitive signal when MHT was started inside the window — but those findings are not the same as evidence that MHT prevents heart attacks, strokes, or dementia. MHT is NOT TGA-approved for cardiovascular or dementia prevention. AMS 2023 sits more conservatively on this question than some international bodies (NAMS 2022, IMS, NICE NG23) — and this page names that gap rather than collapsing it. If symptom control is the reason for MHT and the candidacy is otherwise sound, the timing evidence may inform when to start. It does not, on current AU primary-tier evidence, justify starting MHT to prevent these conditions.
I had breast cancer years ago — can I use vaginal oestrogen for dryness and recurrent UTIs?

Often yes, and it is a question worth bringing to your oncologist and prescriber together. Vaginal estradiol (Vagifem) and estriol (Ovestin) at the standard doses deliver very small amounts of oestrogen and most of that stays local — systemic absorption is minimal. For breast-cancer survivors with refractory genitourinary symptoms that non-hormonal treatments have not controlled (vaginal moisturisers, lubricants, pelvic-floor physiotherapy), vaginal oestrogen is often considered acceptable after an oncology conversation. Women on aromatase inhibitors are a more careful case — the conversation is more cautious because aromatase inhibitors aim to keep oestrogen as low as possible. This is exactly the kind of decision that benefits from oncologist, gynaecologist and GP being on the same page.
Is testosterone cream the right treatment if I am exhausted and brain-foggy?

No — and this is one of the most-misframed conversations in current menopause media. Testosterone cream (Androfeme) is TGA-approved in Australia (2024) for one specific indication: hypoactive sexual desire disorder in postmenopausal women — that is, distressing loss of libido. It is supported by RANZCOG, the Endocrine Society of Australia and the international sexual-medicine society ISSWSH for that use. It is NOT approved or supported for energy, mood, wellbeing, cognition or muscle mass. If exhaustion, brain fog or low mood are the main story, the conversation is somewhere else — thyroid, iron, B12, sleep architecture, vasomotor disruption, mood disorder, sleep apnoea, the perimenopause hormonal transition itself — and the prescriber will work through that picture rather than reaching for testosterone.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.