Hormone Therapy During Menopause — Evidence-based. Individualized. And for many women, one of the most effective medical options

Note: A shorter version of this article appeared in Nina Ruge’s newsletter at www.stayoung.de. Below you will find the detailed medical classification with a scientific basis.

Between the mid-40s and early 50s, many women notice significant changes in their physical regulation. Sleep becomes more fragmented. Nighttime temperature control functions less steadily. Mood fluctuates more quickly. Concentration declines. Joints become more sensitive. Body fat increasingly redistributes abdominally. These changes often begin during perimenopause – years before menstruation ceases completely.

The cause is not “aging” in an unspecific sense, but the progressive decline of estradiol and increasing hormonal instability. Estrogen does not act only on the menstrual cycle. It influences vascular function, bone metabolism, neuronal activity, glucose metabolism, connective tissue, and mucous membranes. As this regulatory influence declines, both acute symptoms and long-term changes in disease risk emerge.

This is where menopausal hormone therapy (MHT) comes in.

Hot flashes are the most well-known symptom of menopause, but they are neither the only nor always the most burdensome. The decline in estradiol affects central regulatory systems throughout the entire organism. In the brain, estrogen acts on serotonin, dopamine, and GABA systems, influences vascular tone and temperature regulation, stabilizes mucous membranes, modulates inflammatory processes, supports collagen synthesis, and regulates glucose metabolism. Accordingly, the symptoms that occur during peri- and postmenopause are diverse.

MHT is the most effective therapy for vasomotor symptoms and significantly reduces the frequency and intensity of hot flashes. Studies also show improvements in sleep quality, particularly in combination with micronized progesterone, which has a calming effect via GABA receptors. Mood swings, irritability, and reduced cognitive performance in early menopause may also stabilize under therapy. Joint and muscle pain, often associated with estrogen decline, decrease. The genitourinary syndrome of menopause – including vaginal dryness, dyspareunia, and recurrent urinary symptoms – responds well to both systemic and local estrogen therapy. Changes in skin and mucous membranes may also improve. In cases of hormonally related loss of libido, stabilizing estrogen levels may indirectly contribute to improvement; in selected cases, testosterone may also be considered.

The therapeutic effect is systemic and biologically plausible. Estrogen modulates neurotransmitters, stabilizes vascular reactions, has anti-inflammatory effects, and influences mitochondrial energy production. Accordingly, many women report not only fewer hot flashes, but an overall more stable physical and mental regulation (1, 2, 3, 4, 5).

With the transition into postmenopause, not only subjective well-being changes, but also the long-term risk profile. The decline in estradiol contributes to accelerated bone loss, increased visceral fat accumulation, reduced insulin sensitivity, and changes in lipid profile.

MHT has been shown to reduce bone density loss and significantly lower the risk of osteoporotic fractures. It improves insulin sensitivity and may delay the manifestation of type 2 diabetes. When initiated early – before the age of 60 or within ten years after menopause – it does not increase the risk of myocardial infarction or stroke; rather, data suggest favorable cardiovascular effects within this time window. There is also evidence that early initiation of therapy may be associated with a lower risk of Alzheimer’s disease.

Finally, observational data suggest that women who begin individualized hormone therapy early may have lower overall mortality than comparable women without therapy. MHT is therefore not only symptom-oriented treatment but – in the appropriate context – also a preventive intervention (3, 6, 7, 8, 9).

Modern MHT uses bioidentical estradiol, structurally identical to the body’s own hormone. The goal is physiological substitution in individually adjusted dosages.

Estradiol can be administered transdermally (gel, patch, spray), orally (tablet), or locally vaginally. The route of administration influences metabolism and the vascular system differently. Transdermal estradiol is often preferred because it bypasses hepatic first-pass metabolism and does not cause relevant activation of procoagulant factors. Large analyses show that transdermal preparations do not increase the risk of venous thrombosis. Metabolically, this form is also more neutral than oral estrogens. Oral preparations undergo first-pass metabolism in the liver and have a stronger influence on coagulation and lipid metabolism. In cases of elevated cardiometabolic risk, transdermal administration is therefore usually recommended.

If a uterus is present, estradiol must be combined with a progestogen to protect the endometrium. Micronized progesterone is preferred, as it is considered metabolically more favorable and additionally shows positive effects on sleep.

For isolated urogenital symptoms, local vaginal estrogens are highly effective and have minimal systemic relevance.

The choice of preparations is part of the individualization process. There is no standard model – but rather a therapy that must fit the individual risk situation (1, 2, 10).

Concern about breast cancer is, for many women, the central factor in deciding against hormone therapy. This uncertainty largely stems from the WHI study published in 2002. At that time, results were widely communicated without sufficient differentiation between participants’ age, type of hormones used, and individual risk profiles.

Today, the data are more differentiated. Estrogen alone – in women without a uterus – does not increase breast cancer risk. With combined therapy of estrogen and progestogen, the risk of developing breast cancer may increase slightly with longer duration of use. This risk depends, among other factors, on the type of progestogen and duration of therapy. Combinations with micronized progesterone are considered more favorable than older synthetic progestogens.

It is important to distinguish between incidence and mortality. Current data do not show that women receiving modern hormone therapy die more frequently from breast cancer. A possible slight increase in incidence declines after discontinuation of therapy and approaches the general population risk.

Equally important: Hormone therapy does not cause breast cancer. However, if undetected tumor cells are already present, it may accelerate their growth. Therefore, accompanying preventive care is essential. Regular mammography and medical supervision are not optional additions but integral components of responsible therapy.

For context: The additional risk associated with several years of combined hormone therapy is in a similar range to other modifiable factors, such as significant overweight or regular alcohol consumption. Risks must be evaluated relatively and within the overall context – not in isolation (1, 3).

For a long time, it was recommended to discontinue hormone therapy after five years as a general rule. This blanket “5-year rule” no longer reflects current knowledge.

The duration of MHT depends on symptoms, individual risk profile, and personal benefit. If symptoms persist, therapy is well tolerated, and regular medical check-ups are performed, it may be continued beyond several years. What matters is not calendar duration, but repeated medical reassessment.

MHT is also not a static therapy. Hormone levels, tissue sensitivity, and individual needs change throughout peri- and postmenopause. Therefore, therapy usually begins with a low dose, which is adjusted as needed – depending on symptom control, side effects, and life phase.

Important in this context: Routine hormone testing is generally not required in women over 45 with typical symptoms. Many patients request blood values for reassurance “on paper.” However, during perimenopause, estradiol and FSH levels fluctuate considerably; single measurements are therefore often difficult to interpret and do not provide a reliable basis for decision-making. Diagnosis is primarily clinical – based on age, cycle changes, and symptoms, not on an isolated laboratory value.

If a uterus is present, the endometrium must be protected under combined therapy and evaluated in case of abnormal bleeding (2). Regular mammography remains mandatory. The therapy is effective – but it requires supervision.

Ideally, over time, the patient develops a good understanding of her own hormonal regulation. She observes which dose provides stability, recognizes changes early, and discusses adjustments in a structured manner with her physician. Individualization here means informed fine-tuning – not self-medication (1, 3).

As effective as MHT can be, it is not suitable for every woman. There are clear medical contraindications. These include active or recently treated breast cancer, active endometrial carcinoma, current thrombosis, or a recent myocardial infarction or stroke. In these situations, systemic hormone therapy is generally not indicated.

The situation is more complex in women with treated and currently tumor-free breast cancer. Increasingly differentiated data are emerging, particularly for patients who have entered pronounced menopause abruptly due to anti-hormonal therapies. Systemic MHT may be discussed in selected cases – but exclusively under oncological supervision in specialized centers. This is not a standard recommendation, but an individual risk assessment.

Family history is also often overestimated. A precise medical history is crucial. Multiple first-degree relatives with breast cancer at a young age may indicate genetic predisposition; in such cases, genetic counseling with testing for BRCA or other risk genes may be appropriate.

By contrast, a single grandmother with breast cancer at an advanced age does not represent an independent risk factor for MHT. The background risk for breast cancer increases with age in general – regardless of hormone therapy.

The decision for or against MHT should therefore not be based on generalized fear, but on a structured, individualized risk assessment in consultation with a physician (1, 3).

Modern menopausal hormone therapy is among the best-studied interventions in women’s health today. It is the most effective treatment for vasomotor symptoms, improves sleep and urogenital symptoms, protects against accelerated bone loss, and has favorable effects on metabolic and cardiovascular risk factors when initiated early.

It is not a universal anti-aging concept and does not replace lifestyle measures. But it addresses a central biological mechanism of menopause – the decline in estradiol – and can thereby positively influence both symptoms and certain long-term risks.

In practice, a different problem is often observed: Many women have received a prescription or even already have hormones at home – yet do not begin therapy. This hesitation usually stems from uncertainty, particularly regarding breast cancer risk. This uncertainty is understandable, but often based on outdated or oversimplified information.

An informed decision does not mean ignoring risks. It means placing benefits and risks into realistic perspective – absolutely, relatively, and within the personal context. For many healthy women within the appropriate time window, the benefits clearly outweigh the potential risks.

Prerequisites are individually adjusted dosing, often with transdermal estradiol, and regular medical monitoring. The decision should be made neither out of fear nor ideology, but based on current data and personal risk factors.

For many women, MHT is not an obligation, but a very good option – provided it is understood, supervised, and regularly reviewed (1, 3, 6, 7, 8).

If you are unsure which steps make sense for you, we can review this together. Feel free to schedule a consultation appointment.

(1) The North American Menopause Society (NAMS). The 2022 Hormone Therapy Position Statement. Menopause. 2022.

(2) Nolan BJ, et al. Micronized Progesterone for Sleep: A Systematic Review and Meta-analysis. JCEM. 2021.

(3) Davis SR, et al. Treating menopause — MHT and beyond. Nat Rev Endocrinol. 2022.

(4) NAMS 2020 Genitourinary Syndrome of Menopause Position Statement.

(5) Weidlinger S, et al. Die Menopause und ihre Auswirkungen auf Haut und Haare. 2023.

(6) Wells G, et al. HRT and osteoporosis prevention. Endocr Rev. 2002.

(7) Mauvais-Jarvis F, et al. MHT and Type 2 Diabetes Prevention. Endocr Rev. 2017.

(8) Manson JE, Kaunitz AM. Menopause Management. NEJM. 2016.

(9) Song Q, et al. MHT and Alzheimer risk. 2025.

(10) Vinogradova Y, et al. HRT and venous thromboembolism risk. BMJ. 2019.