HRT (Hormone Replacement Therapy) and Its Role in Longevity and Health Optimisation: Friend or Foe?

Most of us know that HRT helps with hot flashes and other unpleasant symptoms of the perimenopausal and menopausal years. It also assists in keeping our skin looking younger and bone strong.

But what about its other health impacts, questions many frequently ask. Is it good or detrimental to our brain health, Alzheimer’s and breast cancer risk? What about the purported increased incidence of strokes? True or false? Is HRT an actual friend, or a foe?

Let’s look at what the evidence has to say.

DISCLAIMER: This blog post is for informational purposes only and is not a substitute for individualised medical advice. All HRT prescribing decisions should be made by a qualified clinician following individual risk assessment.

The risk of doing nothing is underreported. The risk of the wrong formulation is real. This brief tells you what the evidence actually says.

1. The Background: Why HRT became controversial

HRT used to be standard care for menopausal symptoms and chronic disease prevention. That changed with the 2002 Women’s Health Initiative (WHI) trial, which reported increased risks of heart attack, stroke, and breast cancer in postmenopausal women taking oral conjugated equine estrogens (CEE) combined with medroxyprogesterone acetate (MPA), a synthetic progestin.

Reference: Women’s Health Initiative trial (2002); Risks, Benefits, and Treatment Modalities of Menopausal Hormone Therapy, PMC8034540 (2021)

What followed was mass cessation of HRT prescriptions. But subsequent analyses revealed a critical flaw in that narrative: the WHI predominantly enrolled older women (average age 63) — more than 10 years past menopause. The elevated cardiovascular risks applied almost exclusively to women who started HRT after age 60 or a decade post-menopause. For women under 60 or within 10 years of menopause onset, the benefit-risk ratio is demonstrably favourable.

Reference: The 2017 Hormone Therapy Position Statement of The North American Menopause Society (NAMS), Menopause Journal (2017)

The WHI also used an outdated, synthetic regimen. Most of its elevated risks are attributable specifically to the combination of oral CEE (estrogen derived from mares) and MPA (a synthetic type of progesterone) — not to dermal estrogen and bioidentical (or body identical as often called in the UK) progesterone. 

Reference: Risks, Benefits, and Treatment Modalities of Menopausal Hormone Therapy: Current Concepts, PMC8034540 (2021)

2. The Hormone Landscape

Not all hormones are equivalent. The biological effects, safety profiles, and clinical outcomes differ significantly based on the formulation chosen.

Estrogens

Conjugated equine estrogens (CEE), derived from the urine of pregnant mares, are the oldest and most studied preparation. Oral estradiol (E2) is converted to estrone (E1) during first-pass liver metabolism, meaning that oral delivery elevates estrone — a pro-inflammatory estrogen associated with increased adipocyte cytokine expression (=inflammatory molecules) and faster ER+ breast cancer growth in obese postmenopausal women.

Reference: The Major Pre- and Postmenopausal Estrogens Play Opposing Roles in Obesity-Driven Mammary Inflammation and Breast Cancer Development, Cell Metabolism (2020)

Transdermal estradiol bypasses first-pass liver metabolism. This avoids increases in clotting factors, inflammatory markers, hypertriglyceridemia, and venous thromboembolism (VTE) risk — all sequelae of oral estrogen’s liver passage. Hence the oral version of estrogen is best avoided. (You’d be surprised to know how many of my clients coming into my practise are on oral estrogens, prescribed by fancy hormone clinics! – Well, at least I am surprised!)

Reference: Risks, Benefits, and Treatment Modalities of Menopausal Hormone Therapy: Current Concepts, PMC8034540 (2021)

Progestogens: The Critical Distinction

This is where the evidence diverges most sharply — and where prescribing decisions have the greatest impact on long-term outcomes.

Medroxyprogesterone acetate (MPA) is a synthetic progestin resembling testosterone. Its use alongside CEE in the WHI is responsible for the majority of the trial’s negative findings. In contrast, bioidentical progesterone (P4) — specifically oral micronized progesterone (OMP, such as found in the UK/ on NHS readily available Utrogestan) — has a fundamentally different and demonstrably safer profile.

Reference: Bioidentical Hormone Replacement — Guiding Principles for Practice, Natural Medicine Journal (2010); Progesterone vs. Synthetic Progestins and the Risk of Breast Cancer: A Systematic Review and Meta-Analysis, PMC4960754 (2016)

Comparison Table: Bioidentical Progesterone vs. Synthetic Progestins

References: PEPI Trial; Natural Medicine Journal (2010); Progesterone vs. Synthetic Progestins Meta-Analysis PMC4960754 (2016); Progesterone and the Risk of Breast Cancer E3N Cohort; Impact of Micronized Progesterone on Cardiovascular Events, AJEC (2022)

3. Progesterone for Endometrial Protection: Getting the Dose and Route Right

Any woman with an intact uterus using systemic estrogen requires progestogen to prevent endometrial hyperplasia and cancer. Unopposed estrogen over time causes endometrial proliferation — this was the primary driver of early HRT risks before combination therapy became standard.

The evidence for oral micronized progesterone (OMP) providing adequate endometrial protection is robust:

• Sequential oral OMP at 200 mg/day for 12–14 days per month protects the endometrium for up to 5 years.
• Continuous oral OMP at 100 mg/day also provides endometrial protection.
• Vaginal OMP at 4% (45 mg/day) or 100 mg every other day may provide protection for 3–5 years (off-label use).
• Transdermal progesterone does NOT provide adequate endometrial protection and should not be relied upon for this purpose.

Reference: The Impact of Micronized Progesterone on the Endometrium — A Systematic Review, Climacteric (2016); Micronized Progesterone Regulation of the Endometrium, Int J Gynecol Pathol (2001)

The REPLENISH Phase 3 trial — the first adequately powered study of combined oral E2/P4 — found zero cases of endometrial hyperplasia or cancer after 12 months across all dose groups, with meaningful reductions in vasomotor symptom frequency from week 3 onward.

Reference: REPLENISH Trial, Climacteric (2018); DOI: 10.1080/13697137.2018.1455657

Vaginal progesterone gel exploits a uterine first-pass effect: despite lower serum progesterone levels than intramuscular delivery, endometrial tissue concentrations are higher, allowing effective local protection with minimal systemic exposure.

Reference: First-Pass Effect of Vaginal Progesterone Gel, Gynecological Endocrinology (2004); DOI: 10.1080/09513590410001692519

4. Cardiovascular Risk: The Timing Hypothesis

Cardiovascular disease kills 1 in 3.2 women in the US — more than any other condition. Women fare worse than men: 64% of women (vs. 50% of men) who die suddenly of coronary heart disease had no prior symptoms. Within 5 years of a first heart attack, 47% of women die compared to 36% of men.

Reference: Menopausal Hormone Replacement Therapy and Reduction of All-Cause Mortality and CVD, PMC9178928 (2023)

The timing hypothesis — now supported by multiple randomised controlled trials, imaging studies, and meta-analyses — holds that the cardiovascular effects of HRT are entirely dependent on when it is initiated relative to menopause. The biological basis is the ‘healthy endothelium hypothesis’: estrogen protects healthy vasculature but cannot reverse established atherosclerotic disease – Hence the earlier commenced, the better! 

Reference: PMC9178928 (2023); ELITE Trial, NEJM (2015), DOI: 10.1056/nejmoa1505241

The ELITE trial — a randomised, double-blind, placebo-controlled imaging study — demonstrated that estradiol therapy initiated within 6 years of menopause significantly slowed carotid artery intima-media thickness (CIMT) progression compared to placebo. CIMT acts as a screening tool for early-stage atherosclerosis, helping to predict risk for stroke and coronary artery disease. In women 10+ years post-menopause, there was no significant difference. Timing determines outcome.

Reference: ELITE Trial, NEJM (2015)

The Danish Osteoporosis Prevention Study (DOPS) — the only RCT to closely replicate the populations seen in observational studies — found that 10 years of HRT reduced cardiovascular disease by 52% and all-cause mortality by 43% compared to no HRT in early postmenopausal women. This is huge! (R)

Reference: PMC9178928 (2023) — DOPS data

Meta-analyses confirm: HRT initiated in women under 60 and/or within 10 years of menopause reduces all-cause mortality by 30% and coronary heart disease by 48%. Notably, statins — the first-line recommendation for primary cardiovascular prevention in women — do not statistically significantly reduce CHD or all-cause mortality in women when used for primary prevention. HRT does.

Note: The null effect of statin therapy on primary CVD prevention in women contrasts with that of men. With careful separation of women from men and primary from secondary prevention trials, the first sex-specific meta-analysis to analyze primary CVD prevention trials showed that statin therapy reduced CHD in men but not in women. All-cause mortality was neither reduced in men nor women in primary CVD prevention RCTs (R). 

Reference: PMC9178928 (2023); Cochrane Group meta-analysis confirming 30% mortality reduction; sex-specific statin meta-analyses

Reference: PMC9178928 (2023); JUPITER trial; Metabolic Syndrome after Menopause, Menopause Journal (2020)

5. Venous Thromboembolism (VTE) and Stroke: Route of Delivery Is Everything

The risk of venous thromboembolism (VTE) and ischaemic stroke with HRT appears to almost entirely be a function of the route of estrogen delivery — not the use of HRT itself.

Oral estrogen increases VTE risk through liver metabolism, stimulating production of clotting factors. Transdermal estrogen bypasses this pathway.

Reference: Hormone Therapy and Recurrence of Venous Thromboembolism, Menopause Journal (2011)

• Oral estrogen is associated with significantly increased VTE risk.
• Transdermal estrogen does not increase VTE risk — multiple observational studies and the ESTHER study confirm this.
• For ischaemic stroke: transdermal estrogens are the safest option; oral estrogen, particularly CEE, increases stroke risk.
• Among progestogens: norpregnane derivatives (e.g. norgestrel) appear thrombogenic. Micronized progesterone (=bioidentical progesterone) and pregnane derivatives appear safe with respect to VTE.

Reference: ESTHER Study, Stroke (2016), DOI: 10.1161/STROKEAHA.116.013052; Oral vs. Transdermal Estrogens and VTE, Menopause Journal (2011); Impact of Micronized Progesterone on Cardiovascular Events, AJEC (2022)

A UK nested case-control study found that compared to oral CEE + MPA (synthetic progesterone), oral estradiol (bioidentical estrogen) combined with dydrogesterone reduced VTE risk by 44%, and transdermal preparations showed no increased VTE risk whatsoever.

Reference: PMC8034540 (2021) — UK nested case-control study

6. Breast Cancer: The Most Misunderstood Risk

Breast cancer risk in the context of HRT is nuanced, frequently misrepresented, and critically dependent on the type of progestogen used, the type of estrogen, duration, and whether the woman has had a hysterectomy.

Estrogen alone — potentially protective

In the WHI trial, CEE-alone in women post-hysterectomy significantly reduced breast cancer incidence. A 2024 meta-analysis of 10 randomised trials confirmed that estrogen-alone use is associated with a 23% reduction in breast cancer incidence. This finding has been consistent across 20 years of follow-up. 

Reference: Randomized Trials of Estrogen-Alone and Breast Cancer Incidence: A Meta-Analysis, 2024, PMID 38653905; 

Estrogen Therapy and Breast Cancer in Randomized Clinical Trials, 2022, PMID 35969882  

Synthetic progestins — increased risk

The E3N European cohort study (54,548 women) found increased breast cancer risk with estrogen plus synthetic progestogens, but no statistically significant increased risk with estrogen plus bioidentical progesterone. 

However, the most recent E3N analysis did find an increased risk with estrogen + P4 (=bioidentical progesterone)/dydrogesterone (a synthetic progesterone) used for more than 5 years — an important nuance that warrants monitoring in long-term users.

Reference: E3N Cohort and E3N-EPIC Cohort studies; Breast Cancer Risk and Progestagens, PLOS ONE (2013), DOI: 10.1371/journal.pone.0078016

A 2016 systematic review and meta-analysis found bioidentical progesterone to be associated with a 33% lower breast cancer risk compared to synthetic progestins when each is combined with estrogen. 

Reference: Progesterone vs. Synthetic Progestins and the Risk of Breast Cancer, PMC4960754 (2016) 

At the tissue level, bioidentical progesterone actually decreases breast cell proliferation, while estradiol increases it. Combined bioidentical estrogen + progesterone resulted in proliferation comparable to progesterone alone or placebo. CEE/MPA (horse estrogen + synthetic progestin) significantly increased breast cell proliferation from baseline; Bioidentical estrogen + progesterone did not.

Reference: Breast cell proliferation studies referenced in Climacteric (2018), DOI: 10.1080/13697137.2018.1455657

Reference: E3N Cohort; PMC4960754 (2016); PLOS ONE (2013); WHI CEE-alone trial; Use of Menopausal Hormone Therapy Beyond Age 65, PMC11465799 (2024)

7. Bone Health: A Clear and Consistent Benefit

HRT reduces the risk of fractures across all skeletal sites. A systematic review and meta-analysis of 28 studies found HRT reduced total fracture risk by 26%, hip fracture risk by 28%, and vertebral fracture risk by 37%.

Reference: Effect of Hormone Therapy on the Risk of Bone Fractures: A Systematic Review and Meta-Analysis of RCTs, PubMed 26529613 (2015) 

The protective effect is strongest when HRT is initiated before age 60 and with bioidentical estradiol vs. CEE (estrogen derived from horse urine). The protection attenuates after discontinuation, supporting long-term use in appropriate candidates.

Minimal effective estradiol levels for preventing postmenopausal bone loss have been identified: circulating E2 levels of 60 pg/ml (approximately 220 pmol/L) — corresponding to early cycle phase levels — produce significant reductions in bone resorption markers. Higher levels provide no additional skeletal benefit.

Reference: Minimal Levels of Serum Estradiol Prevent Postmenopausal Bone Loss, 1992, PMID 1458336 

8. Cognition, Sleep, and Metabolic Health

Brain and Cognition

Progesterone exerts neuroprotective effects by shielding brain cells against glutamate toxicity. Synthetic progesterone not only appears to fail to replicate this protection — it actively decreases the neuroprotective effects of estrogen. When HRT is initiated early (perimenopausal or early postmenopausal), it appears to have a neutral or protective effect on cognition. When initiated late (>10 years post-menopause), it may increase risk of Alzheimer’s disease — consistent with the timing hypothesis.

Reference: Bioidentical Hormone Replacement — Guiding Principles for Practice, Natural Medicine Journal (2010); PMC8034540 (2021)

Sleep

Progesterone is converted to allopregnanolone in the brain, a neuroactive steroid that exerts GABAergic effects, promoting sleep. Polysomnography studies confirm that estrogen + bioidentical progesterone — but not estrogen + synthetic progesterone — significantly improves sleep efficiency and reduces time spent awake after sleep onset. 

Reference: Sleep data from REPLENISH trial; Polysomnography studies referenced in Climacteric (2018)

Another study showed that Progesterone had no effect on undisturbed sleep but restored normal sleep (including increasing deep sleep, growth hormone secretion and thyroid hormone regulation) when sleep was disturbed (while currently available hypnotics tend to inhibit deep sleep), acting as a “physiologic” regulator rather than as a hypnotic drug. Use of progesterone might provide novel therapeutic strategies for the treatment of sleep disturbances, in particular in aging where sleep is fragmented and of lower quality (R).

Metabolic Health and Diabetes

Menopause is a metabolic inflection point. Hormonal changes increase insulin resistance, reduce glucose tolerance, and raise new-onset diabetes risk. HRT improves insulin sensitivity, lowers fasting glucose and HbA1c, and reduces new-onset type 2 diabetes by 20–30%. Women with diabetes face a 5.1-fold greater coronary heart disease risk compared to women without diabetes — more than double the relative risk seen in men. Preventing diabetes through timely HRT initiation might therefore be a direct cardiovascular prevention strategy.

Reference: What Drives Metabolic Syndrome After Menopause, Menopause Journal (2020); PMC9178928 (2023); JUPITER trial diabetes data

9. Testosterone in Women: The Overlooked Hormone

Women produce three times as much testosterone as oestrogen before menopause. Testosterone levels often decline with age (and unhealthy lifestyle choices) and abruptly following surgical removal of the ovaries. Low testosterone states are associated with: dysphoric mood, unexplained fatigue, reduced libido, impaired cognition, vasomotor symptoms, bone loss, and decreased muscle strength.

Reference: Should We Be Prescribing Testosterone to Perimenopausal and Menopausal Women? BJGP, PMC7098532 (2020) 

A systematic review and meta-analysis of testosterone treatment in women found that supplementation significantly improved sexual desire, arousal, orgasm, pleasure, and self-image in postmenopausal women. Clinical benefits extend to bone density, cognitive performance, mood, motivation, energy, and urogenital symptoms.

Reference: PMC7098532 (2020); International Menopause Society Global Position Statement on testosterone for women

Transdermal testosterone at physiological doses appears to bring no adverse effects on blood pressure, lipid profile, renal function, liver function, or blood indices. There appears to be no increased breast cancer risk in the short term.

Reference: PMC7098532 (2020); International Menopause Society Global Position Statement

There are currently no licensed testosterone preparations for women in the UK. Male-licensed preparations (Testogel, Tostran) are prescribed off-label at approximately 1/10th of the male dose. NICE guidelines and the British Menopause Society (BMS) support testosterone use for menopausal women with low libido where HRT alone is insufficient, with BMS extending this to include fatigue and low wellbeing.

Reference: NICE guidelines; BMS 2016 recommendations; PMC7098532 (2020)

10. Longevity and All-Cause Mortality: The Biological Ageing Data

HRT initiated at the right time, in the right formulation, might not merely be for symptom management. It can be a systemic anti-ageing intervention with measurable effects on biological age and all-cause mortality.

A 2024 study found that postmenopausal women with a history of HRT use were biologically younger than non-users — and that this biological age gap mediated the association between HRT and reduced mortality. 

Reference: Hormone Therapy and Biological Aging in Postmenopausal Women, PMID 39207753 (2024) 

The Leisure World Cohort Study found that long-term estrogen therapy was associated with significantly lower all-cause mortality in older women.

Reference: Increased Longevity in Older Users of Postmenopausal Estrogen Therapy: The Leisure World Cohort Study, PMC7219089 (2018) 

A large 2024 real-world study of HRT use beyond age 65 found that estrogen therapy was associated with a 19% reduction in all-cause mortality, fewer cancers (breast, lung, colorectal), reduced congestive heart failure, VTE, atrial fibrillation, acute heart attack, and dementia. The greatest benefits were observed with low-dose, vaginal or transdermal preparations, and estradiol (bioidentical) over CEE (derived from horse urine).

Reference: Use of Menopausal Hormone Therapy Beyond Age 65 Years and Its Effects on Women’s Health Outcomes, PMC11465799 (2024)

Compared to other primary prevention strategies, HRT stands alone: lipid-lowering therapy, aspirin, and ACE inhibitors all fail in studies to reduce all-cause mortality in women for primary cardiovascular prevention. HRT, when timed correctly, might be able to do all three: it appears to reduce cardiovascular disease, all-cause mortality, and new-onset diabetes while improving quality-adjusted life years and reducing the economic burden of chronic disease.

Reference: PMC9178928 (2023) 

11. Practical: Suggested Best Use

Estrogen — Preferred Routes

• Transdermal estradiol patch or Estradiol gel 

Reference: PMC8034540 (2021); Harvard Health

Progesterone — Preferred: Oral Micronized Progesterone (OMP)

• Sequential regimen (perimenopausal / within 12 months of last period): 200 mg/night for 12 consecutive days per month (Utrogestan — 2 x 100 mg capsules).
• Continuous regimen (>1 year post-menopause): 100 mg/night every evening (Utrogestan — 1 x 100 mg capsule).
• Vaginal OMP (45 mg/day or 100 mg every other day) provides endometrial protection for 3–5 years with minimal systemic exposure.

Reference: Climacteric (2016); Liverpool Women’s NHS — Utrogestan Patient Information Leaflet; REPLENISH trial

Testosterone — Off-Label in Women

• Testogel 1%: start at 1/10 sachet (5 mg/day), each sachet lasts 10 days.
• Tostran 2%: 1 metered pump (0.5–10 mg) on alternate days.
• AndroFeme 1% cream: 0.5 ml/day (5 mg/day), each 50 ml tube lasts 100 days (private prescription only).
• Target: FAI <5%; reassess at 6 months.

Reference: BMS Testosterone Guidance; PMC7098532 (2020) 

12. Post-Hysterectomy: Does Bioidentical Progesterone Still Have a Role?

Conventionally, progestogen is prescribed solely to protect the endometrium. Remove the uterus, and the textbook says progesterone is no longer necessary. The evidence, however, tells a more nuanced story — one that requires weighing real systemic benefits against a small and incompletely characterised breast cancer signal.

The Case For: Systemic Benefits Are Real

As mentioned earlier, progesterone has benefits that go beyond the uterus. It has beneficial effects on the brain, sleep, and mood.

The Caution: Breast Cancer Signal Cannot Be Ignored

The cleaner option for breast cancer risk in a post-hysterectomy woman likely is estrogen alone. The randomised trial evidence consistently shows estrogen alone reduces breast cancer incidence by approximately 23% relative to placebo. Adding progesterone — even bioidentical — changes that equation.

The 2024 real-world population study (R) found estrogen + progesterone was associated with a slight increase in breast cancer risk. It is substantially lower than the increase seen with synthetic progestins, but it is not zero. The E3N cohort data also showed a risk signal emerging with E2 + P4 beyond 5 years of continuous use — a finding that should inform duration decisions.

Reference: Use of Menopausal Hormone Therapy Beyond Age 65, PMC11465799 (2024); E3N Cohort most recent analysis; Randomized Trials of Estrogen-Alone and Breast Cancer Incidence, PMID 38653905 (2024)

The absolute risk increase — where detected — remains small in the context of short-to-medium duration use in younger postmenopausal women, and is substantially lower than the risk associated with synthetic progestins across all available evidence.

The Framework: Shared Decision-Making

For women with a uterus, adding a progesterone is a must, and benefits likely outweigh any downsides on long term health optimisation and prevention overall. However, in post-hysterectomy women, the decision to add bioidentical progesterone should not be automatic — but nor should it be reflexively dismissed. The relevant questions might be:

• Are sleep disturbance, mood dysregulation, anxiety, or cognitive symptoms present and inadequately controlled on estrogen alone? If yes, bioidentical progesterone has a legitimate evidence base.
• What is the individual’s baseline breast cancer risk? Personal or strong family history of hormone receptor-positive breast cancer warrants greater caution and specialist input.
• What is the anticipated duration of use? The breast cancer signal in observational data appears most relevant beyond 5 years. Shorter-term use for targeted symptom management carries a more favourable risk profile.
• What dose is appropriate? Lower doses of OMP (100 mg/night rather than 200 mg) may provide CNS benefits with reduced systemic exposure — though dose-specific breast data in this population are limited.

Reference: PMC11465799 (2024); E3N Cohort; PMID 38653905 (2024); Climacteric (2018); Natural Medicine Journal (2010)

13. Contraindications and Caution Zones

HRT is not appropriate for all women. Established contraindications include unexplained vaginal bleeding, active liver disease, personal history of oestrogen-dependent cancers (unless specialist-supervised), and known thrombophilic disorders (where transdermal routes may still be considered under specialist review).

Women who initiate HRT more than 10–20 years from menopause onset, or aged 60 or older, face a less favourable benefit-risk ratio for cardiovascular and dementia outcomes. For these women, shared decision-making and periodic re-evaluation are essential.

Reference: NAMS 2017 Position Statement; PMC8034540 (2021)

Conclusion: The Evidence-Based Framework

HRT is neither friend or foe — it should be used as a precision tool. The evidence base, when read in its entirety rather than through the distorted lens of the 2002 WHI headlines, is compelling:

• Timed correctly (within 10 years of menopause, before age 60), HRT reduces all-cause mortality by 30–50%, cardiovascular disease by 48–52%, fractures by 26–37%, and new-onset diabetes by 20–30%.
• Bioidentical progesterone in most studies does not appear to be associated with a statistically significant increase in breast cancer risk (unlike synthetic progestins) (R), though long-term use beyond 5 years warrants monitoring and may be associated with a slight increase in risk.
• Bioidentical progesterone does not appear to increase cardiovascular or thrombotic risk.
• However, it should not be described as entirely risk-free in all contexts: some observational datasets report a modest increase in breast cancer risk with combined estrogen + progesterone use, particularly with longer duration (R), while others found no increase in risk (R). Further research is needed on this topic. 
• Transdermal estradiol eliminates the VTE and stroke risks associated with oral formulations.
• Testosterone supplementation appears to be safe, effective, and underutilised in perimenopausal and menopausal women.
• Early initiation exploits the ‘window of opportunity’ — once significant atherosclerosis or cognitive decline is established, HRT cannot reverse it.
• Biological age data confirm HRT is associated with younger epigenetic clocks and reduced mortality — not merely symptom management.

DISCLAIMER: This blog post is for informational purposes only and is not a substitute for individualised medical advice. All HRT prescribing decisions should be made by a qualified clinician following individual risk assessment.