What's Happening to My Hormones?
We often talk about hormones as though they were a group of unruly chemicals that suddenly begin causing trouble in midlife.
Usually, oestrogen receives most of the blame. Progesterone, cortisol, testosterone and FSH are then added to the list, until almost any change in how a woman feels can be described as a “hormonal imbalance.”
The biology is more precise than that.
Hormones do not work independently, and they are not all changing for the same reason. Some come from the ovaries; others from the brain, thyroid, adrenal glands or pancreas. Some drive the menstrual cycle, while others respond to ovarian activity.
Understanding who they are, and the conversation taking place between them, makes the menopause transition considerably less mysterious.
Hormones are a communication system
A hormone is a chemical messenger. It travels through the bloodstream and delivers information to cells with the correct receptor (signal receiver).
The menstrual cycle is regulated through the hypothalamic–pituitary–ovarian, or HPO Axis. This is not a physical structure. It is a feedback system connecting the hypothalamus and pituitary gland in the brain with the ovaries.
No single hormone controls it. Each signal affects the next, while information from the ovaries returns to the brain and adjusts what happens afterwards.
The message that begins in the brain
The hypothalamus releases gonadotrophin-releasing hormone, or GnRH, in pulses. GnRH instructs the pituitary gland to release two hormones: follicle-stimulating hormone (FSH) and luteinising hormone (LH).
FSH encourages ovarian follicles (the egg sacs) to develop. They contain immature eggs, and their surrounding cells produce oestradiol and inhibin B. LH (Luteinising hormone) supports hormone production within the follicle and helps trigger ovulation.
After ovulation, the emptied follicle becomes the corpus luteum. This temporary structure produces progesterone and some oestradiol during the second half of the cycle.
Oestradiol, progesterone and inhibin B then send feedback to the hypothalamus and pituitary. The brain is not simply issuing instructions; it is continually listening to the ovarian response.
The first hormonal signs of ovarian ageing
Perimenopause begins because the number of remaining ovarian follicles is falling—not because the brain suddenly stops communicating.
As the follicle group becomes smaller, production of inhibin B declines. Inhibin B normally helps restrain FSH, so the pituitary releases more FSH in an attempt to stimulate the ovaries.
Anti-Müllerian hormone, or AMH, also falls as the number of small growing follicles (egg sacs) diminishes. AMH is useful in some fertility settings as an indicator of ovarian reserve, but it cannot reliably predict the precise timing of an individual woman’s menopause.
FSH and AMH tell us something about follicle supply and ovarian response. They do not explain, by themselves, how a woman feels.
Oestradiol does not simply fall
Oestradiol is the main and most biologically active form of oestrogen during the reproductive years. It helps build the womb lining and supports ovulation, but its receptors are also present in the brain, bones, blood vessels, skin and genitourinary tissues.
During early perimenopause, rising FSH can sometimes stimulate a remaining follicle strongly. Oestradiol may then become unusually high. In another cycle the ovarian response may be weak and the level much lower.
This is why describing perimenopause as “oestrogen deficiency” misses much of the experience. The more important feature is often variability.
After menopause, the large fluctuations gradually diminish and oestradiol settles at a much lower level. Symptoms associated with fluctuation may ease, while sustained lower oestrogen has different implications for bone and genitourinary health.
You can read more about that distinction in What is Perimenopause? and What is Postmenopause?
Progesterone depends on ovulation
Progesterone does not simply decline alongside oestrogen. Its production depends largely on ovulation.
As ovulation becomes less consistent during perimenopause, the corpus luteum is not formed every month. Progesterone exposure therefore becomes shorter, lower or absent in some cycles. This can contribute to changing bleeding patterns and removes the familiar monthly rise in progesterone and its neuroactive metabolites.
After the final menstrual period, ovulation ends and the cyclical rise in progesterone ceases.
FSH and LH: messengers, not villains
FSH and LH are sometimes blamed for menopause symptoms because their levels become high. Their principal role, however, is to regulate ovarian activity.
They rise because the pituitary is receiving less inhibin B and, later, less oestradiol feedback. High FSH is therefore mainly evidence that the feedback system has changed. Possible effects outside the ovaries are being researched, but FSH and LH are not established as the direct cause of most familiar menopause symptoms.
Their levels also vary during perimenopause. A single normal FSH result cannot rule the transition out, and a high result does not show the full hormonal pattern. This is why NICE advises that women over 45 with typical symptoms and menstrual changes are usually identified clinically rather than through routine hormone testing.
What happens to testosterone?
Testosterone is not exclusively a male hormone. In women, androgens are produced by the ovaries and adrenal glands and contribute to sexual function, bone and muscle biology.
Unlike oestradiol, testosterone does not usually collapse at the final menstrual period. Its pattern is influenced substantially by ageing and varies between women. Libido, energy and confidence are also affected by health, medication, sleep, relationships, stress and discomfort during sex; they cannot be read from one testosterone result.
What about cortisol, insulin, thyroid hormones and melatonin?
These hormones matter, but they do not belong to the HPO axis.
Cortisol helps coordinate the stress response. Insulin regulates blood glucose. Thyroid hormones influence metabolism, while melatonin helps time the sleep–wake cycle. Perimenopause does not automatically make any of them abnormal.
They can nevertheless influence the experience. Poor sleep and chronic stress affect cortisol regulation. Changes in sleep, activity and body composition can influence metabolic health. Thyroid disease can also produce symptoms resembling menopause and should not be overlooked.
An interconnected body does not mean that every hormone is “out of balance.”
Which hormones create the greatest disruption?
During perimenopause, the largest disturbance comes from variable oestradiol, inconsistent ovulation and unpredictable progesterone exposure. FSH and LH are largely responding to those changes.
After menopause, the pattern shifts. Fluctuation reduces, but the body is now functioning with much lower oestradiol and without cyclical progesterone.
That is not one hormone creating every symptom. It is a communication system moving from one biological pattern into another.
The hormones have not turned against you.
The conversation between the brain and ovaries is changing. Understanding who is sending each message—and why—allows us to stop blaming every hormone and begin interpreting the signals more accurately.
Further reading and evidence
NICE: Menopause—identification and management
https://www.nice.org.uk/guidance/ng23
Endocrinology of the menopause
https://pmc.ncbi.nlm.nih.gov/articles/PMC6983294/
Reproductive hormones and the menopause transition
https://pmc.ncbi.nlm.nih.gov/articles/PMC3197715/
The normal menstrual cycle and the control of ovulation
https://www.ncbi.nlm.nih.gov/books/NBK279054/
Changes in androstenedione, DHEAS, testosterone and oestrone around the final menstrual period