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Mechanism

Estrogens

Female sex hormones (estradiol E2, estrone E1, estriol E3) produced in the ovaries and, in smaller amounts, in adipose tissue. They regulate the menstrual cycle, bone density, lipid profile, cognition, mood, and thermoregulation. Their abrupt drop at menopause causes the climacteric syndrome.
Category
Scientific evidence
Very high
Number of findings
4
Sources
Our own summaries · Cited studies

Effect by goal · level of evidence

Menopause and climacteric syndrome

declines Very high physiology (A)
Basis of the climacteric

Their fall causes hot flashes, night sweats, vaginal dryness, sleep disturbance, mood changes, and accelerated bone loss. Hormone therapy (MHT) is the most effective treatment for moderate-to-severe symptoms if there is no contraindication.

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Bone density

protects Very high physiology (A)
Anti-osteoporosis

Stimulates osteoblasts and inhibits osteoclasts. Its postmenopausal decline causes accelerated bone loss. Together with vitamin D, calcium, and weight-bearing exercise it is the best prevention.

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Lipid and cardiovascular profile

protects Moderate cohorts (AA)
Window of opportunity

Before menopause it protects against cardiovascular events. After menopause that advantage disappears rapidly. MHT started within the 'window of opportunity' (10 years after menopause) maintains protection.

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Cognition and mood

modulates Moderate cohorts + RCTs (AA)
Perimenopausal depression pathway

Estradiol modulates mood and cognition via receptors in the hippocampus, prefrontal cortex, and hypothalamus. Its fluctuation in perimenopause is associated with a higher risk of depression.

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Information, not medical advice. Scientific evidence reflects the quality of the studies.

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