A note from Bex
Perimenopause shouldn't be a mystery. But for most of us, it is.
I spent years feeling like my body was changing in ways nobody could properly explain. The hot flushes, the brain fog, the anxiety that seemed to appear out of nowhere, the sleep that stopped working — I kept being told it was "just hormones" or "part of getting older."
That answer wasn't good enough for me. So I went looking for real answers — not clickbait. I spoke to OB/GYNs, nutritionists, and wellness experts. I read everything I could find on what neuroscientists, pelvic health physiotherapists, and psychologists had to say. And what I found was that the real information does exist — it's just locked away in academic journals and clinical certifications, or buried beneath the noise of social media.
That's why I built this course. Not to give you a list of tips, but to give you the actual science — explained in plain language, the way a knowledgeable friend would explain it if she happened to have spent countless hours learning what not to do. Because when you understand what is genuinely happening in your body, everything changes. The symptoms make sense. The choices become clearer. And you stop feeling like your body is working against you.
Every woman deserves to understand her own biology. Start here.
— Bex
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Read the full module and complete the knowledge check at no cost. If you'd like to continue to Modules 2–10, enrol for full access.
About This Module
- What you'll learn: How the female hormonal system works — the key hormones, the structures that produce them, and why they affect organs well beyond the reproductive system.
- Why it matters: This foundational knowledge makes every subsequent module click into place. When you understand what estrogen actually does, the symptoms of perimenopause start to make profound sense.
- Knowledge check: 5 questions at the end — 70% pass mark required to unlock Module 2.
To understand perimenopause, we first need to understand how the female hormonal system works when it is in full operation. Most women were never taught this in detail — and yet this knowledge is foundational to everything that follows. When you understand what estrogen actually does, why progesterone matters, and how the communication loop between your brain and your ovaries keeps the whole system running, the symptoms of perimenopause start to make profound sense.
This module covers the key hormones involved in female reproductive and overall health, the structures that produce them, how they communicate through the body, and why they affect organs well beyond the reproductive system. This is not a medical textbook — but it is the level of understanding that will make every subsequent module click into place.
The Ovaries: Far More Than Reproductive Organs
The ovaries are two almond-sized organs sitting either side of the uterus. For most of a woman's reproductive life, each ovary contains thousands of follicles — fluid-filled sacs each housing an immature egg. Each month, a surge of hormones from the brain stimulates a follicle to mature, release its egg (ovulation), and then transform into a temporary gland called the corpus luteum. This cycle, which most women experience from puberty to perimenopause, is a remarkably sophisticated hormonal choreography.
But the ovaries do far more than manage reproduction. They are your primary source of three critical hormones — estrogen, progesterone, and testosterone — whose influence extends to the brain, bones, heart, skin, gut, urinary tract, and muscles. When ovarian function begins to change in perimenopause, the effects are felt throughout the entire body.
The Three Estrogens
'Estrogen' is not a single hormone. It is a family of related hormones. The three most important are:
- Estradiol (E2) — the most potent form and the dominant estrogen during reproductive years. Produced primarily by the ovarian follicles, it has receptors in almost every tissue in the body — including the brain, bones, heart, bladder, skin, and gut. Estradiol is the form that declines most significantly at menopause.
- Estrone (E1) — becomes the dominant estrogen after menopause. Produced in adipose (fat) tissue by the conversion of androgens (including DHEA). Significantly less potent than estradiol. This is why body composition and the estrobolome (gut bacteria that metabolise estrogens) become more important after menopause.
- Estriol (E3) — produced in large quantities during pregnancy, primarily by the placenta. The weakest of the three. Used in some forms of localised vaginal therapy.
Because estradiol has receptors in the brain, bones, heart, bladder, skin, and gut — a decline in estradiol in perimenopause affects all of these systems. Hot flushes, brain fog, joint pain, dry skin, and urinary changes are not random or unrelated. They are all expressions of reduced estradiol signalling in different tissues.
Progesterone: The Overlooked Hormone
Progesterone is produced primarily by the corpus luteum — the temporary gland that forms after ovulation each menstrual cycle. It dominates the second half (luteal phase) of the cycle. Progesterone has multiple critical roles: it prepares the uterine lining for implantation, maintains pregnancy in its early stages, and — crucially — has significant effects on the brain and nervous system.
Progesterone (specifically its metabolite allopregnanolone) acts as a positive modulator of GABA-A receptors in the brain — producing calming, anti-anxiety, and sleep-promoting effects. This is why many women feel calmer and sleep better in the luteal phase of their cycle, and why declining progesterone in perimenopause can trigger anxiety, irritability, and insomnia — often before hot flushes begin. Progesterone is frequently the first hormone to decline in perimenopause, as cycles become increasingly anovulatory (no ovulation, therefore no corpus luteum, therefore no progesterone).
Testosterone in Women
Testosterone is not only a male hormone. Women produce approximately one-tenth of the testosterone that men produce, primarily in the ovaries and adrenal glands. Testosterone in women plays an important role in libido and sexual response, energy and motivation, muscle mass and bone density, cognitive function, and mood. Testosterone declines gradually from the mid-20s, and the ovarian contribution decreases further in perimenopause and menopause. This is why many women notice reduced libido, lower energy, and difficulty maintaining muscle — often before they recognise other menopausal symptoms.
DHEA and the Adrenal Hormones
DHEA (dehydroepiandrosterone) is an androgen (male-type hormone) produced by the adrenal glands. It serves as a precursor to both testosterone and estrogen. DHEA declines steadily from the mid-20s. After menopause, when ovarian estrogen production ceases, peripheral conversion of DHEA and other adrenal androgens becomes an increasingly important source of estrogen (particularly estrone). This is one reason why adrenal health, stress management, and body composition matter increasingly in perimenopause and beyond.
FSH and LH: The Pituitary Messengers
Follicle-Stimulating Hormone (FSH) and Luteinising Hormone (LH) are produced by the pituitary gland — a pea-sized structure at the base of the brain. FSH stimulates the ovarian follicles to grow and produce estrogen. LH triggers ovulation — the release of the egg. In a healthy reproductive cycle, these hormones rise and fall in a precise rhythm. As ovarian reserve declines in perimenopause, the ovaries become less responsive to FSH, and the pituitary responds by producing increasingly higher levels. Rising FSH is often the first measurable laboratory sign that perimenopause has begun, and elevated FSH levels (along with symptoms) are commonly used in diagnosis.
The HPO Axis: How Your Brain and Ovaries Talk to Each Other
The Hypothalamic-Pituitary-Ovarian (HPO) axis is the hormonal communication loop that regulates the entire reproductive and hormonal system. The hypothalamus (an area at the base of the brain) releases Gonadotropin-Releasing Hormone (GnRH) in pulses, which signals the pituitary gland to release FSH and LH. These hormones travel through the bloodstream to the ovaries, which respond by producing estrogen and progesterone. Rising estrogen then feeds back to the hypothalamus and pituitary to reduce GnRH, FSH, and LH release — a classic negative feedback loop that keeps hormone levels balanced.
In perimenopause, as ovarian follicle reserves decline and estrogen production becomes erratic, this feedback loop becomes dysregulated. The pituitary releases more and more FSH in an attempt to stimulate the increasingly unresponsive ovaries. This dysregulation is what causes the dramatic hormonal fluctuations — and the wide variety of symptoms — that characterise the perimenopause transition.
The HPO Axis — Your Hormonal Communication Loop
In Perimenopause
Follicle reserves deplete → ovaries produce less consistent estrogen → feedback signal weakens → pituitary pumps out more and more FSH trying to compensate → estrogen fluctuates erratically → symptoms begin.
Hormone Receptors Are Everywhere
One of the most important concepts in understanding perimenopause is that estrogen receptors are distributed throughout virtually every organ system in the body. Estrogen receptors are present in the brain (including the hippocampus, hypothalamus, and prefrontal cortex), the heart and blood vessels, bones, skin and collagen, the urinary tract and bladder, the gut, and the muscles. This is why the loss of estrogen at menopause is not simply a reproductive event. It is a whole-body physiological transition with implications for cardiovascular health, bone density, cognitive function, skin integrity, urinary health, metabolic function, and mood.
Estradiol (E2) — Receptor Sites Across Every Body System
Declining estradiol affects all eight systems simultaneously — which is why perimenopause symptoms vary so widely between women.
Dr. Sara Gottfried — Optimising Female Hormone Health (Huberman Lab)
The Female Hormonal Cycle Explained — Estrogen, Progesterone & More
Dr. Natalie Crawford — Female Hormone Health, Fertility & Vitality (Huberman Lab)
- Prior JC (2018). Progesterone is important for transgender women's therapy — applying evidence for the benefits of progesterone in ciswomen. J Clin Endocrinol Metab 104(4):1181–1186. — View Source
- Brinton RD et al. (2015). Perimenopause as a neurological transition state. Nat Rev Endocrinol 11(7):393–405. — View Source
- Santoro N & Randolph JF Jr (2011). Reproductive hormones and the menopause transition. Obstet Gynecol Clin North Am 38(3):455–466. — View Source
- Harlow SD et al. (2012). STRAW+10: Addressing the Unfinished Agenda of Staging Reproductive Aging. Menopause 19(4):387–395. — View Source
Module Summary
- The HPO (Hypothalamic-Pituitary-Ovarian) axis governs reproductive hormone production through a negative feedback loop. As ovarian reserve declines, this regulation becomes erratic — causing the unpredictable hormone fluctuations that define perimenopause.
- Estrogen exists in three main forms: estradiol (E2, most biologically potent), estrone (E1, produced post-menopause), and estriol (E3). E2 acts on receptors in virtually every organ system — brain, heart, bone, skin, gut, bladder and blood vessels.
- Perimenopause is defined not by age but by menstrual irregularity and hormonal fluctuation. It typically begins in the mid-to-late 40s but can start in the late 30s, and is confirmed retrospectively after 12 consecutive months without a period.
- The STRAW+10 staging system provides a standardised clinical framework for classifying menopausal transition stages based on menstrual pattern and hormone levels. A single FSH or E2 blood test is rarely diagnostically definitive in perimenopause.
- Understanding the HPO axis and hormone receptor biology provides the scientific foundation for every module that follows — vasomotor symptoms, mood, cognition, bone health, sleep and metabolic changes all trace back to estrogen's withdrawal from these systems.
- Harlow SD et al. (2012). Executive summary of the Stages of Reproductive Aging Workshop +10. Menopause, 19(4), 387–395.
- Prior JC. (2019). Progesterone as a bone-trophic hormone. CeMCOR / Endocrine Reviews, 11(2), 386–398.
- Burger HG et al. (2007). Hormonal changes in the menopause transition. Recent Progress in Hormone Research, 57, 257–275.
- Hall JE. (2015). Endocrinology of the menopause. Endocrinology and Metabolism Clinics of North America, 44(3), 485–496.
- Speroff L & Fritz MA. (2011). Clinical Gynecologic Endocrinology and Infertility (8th ed.). Lippincott Williams & Wilkins.
Includes diagrams, key takeaways & full references — formatted for print or screen.
Module 1 — Knowledge Check
Answer all 5 questions. You need 70% (4 out of 5) to pass and unlock Module 2. Unlimited retries — this is a reflection exercise, not an examination.