Menopause Vocabulary for Therapists: Anatomy and Hormones

Part one of this series covered the perimenopause stages and the menstrual cycle phases. This one goes underneath them — the anatomy involved, and the hormones as the neuroactive compounds they actually are.

I want to start with the reframe, because it changes what the rest of this vocabulary is for.

These are not just reproductive hormones that happen to touch the brain. They are neuroactive steroids. They cross the blood-brain barrier, and the brain also synthesises them locally — meaning the brain is not only a target for these compounds but a maker of them [2]. Estrogen and progesterone act as neuroprotective agents supporting memory consolidation, executive function, emotional regulation, neuronal repair and neurotransmitter balance [4].

This is an example of the importance of language, "it's just hormones" stops being a dismissal and becomes a understanding of experiences.

Menopause vocabulary for mental health therapists — the anatomy and the hormones

Menopause vocabulary for mental health therapists: the anatomy

Clients name these organs in session, often after surgery, and often without having been told what was taken or what it did.

1. Ovaries — the endocrine engine. They hold the follicle pool and produce estradiol, progesterone and a meaningful share of a person's testosterone. Everything else in this series follows from what the ovaries are doing.

2. Fallopian tubes — the passage from ovary to uterus. Not hormone-producing, but relevant because they are removed alongside the ovaries in risk-reducing surgery.

3. Uterus — the muscular organ that builds and sheds a lining. It does not produce the hormones often attributed to it. Removing it ends menstruation without ending the endocrine transition, which matters enormously and is covered in part three.

4. Cervix — the lower opening of the uterus. Relevant to pain, to sexual function and to the experience of pelvic examination, which for trauma survivors is frequently its own clinical topic.

5. Pelvic floor — the sling of muscle and connective tissue supporting the pelvic organs. It is estrogen-responsive, which is why urinary urgency, leakage and pain with penetration cluster in this transition — and why they belong in the differential alongside anxiety and ordinary aging. Pelvic floor physical therapy exists, and most clients do not know it exists. That referral is one of the more concretely useful things you can offer.

The hormones as neuroactive compounds

As you review these 5 terms, note how each one is doing something in mood, cognition, sleep or relational life, and each gives you a different question.

Follicle-stimulating hormone (FSH) -

Pituitary hormone that signals the ovaries to recruit follicles. As the follicle pool depletes, FSH rises — and in the early transition it is elevated but highly variable [1].

• FSH is not a symptom hormone. It is the sound of the pituitary raising its voice at ovaries that can no longer answer, which is a useful image to offer a client who has been told her numbers are normal. Its variability is also why a single blood draw settles very little during perimenopause.

Anti-Müllerian hormone (AMH) -

Produced by small ovarian follicles and used as a marker of ovarian reserve. It falls as the pool depletes and is low in premature ovarian insufficiency [1]. AMH speaks to remaining reserve, not to how someone feels. Its clinical weight in our room is usually grief — it is often the number that ends a fertility conversation.

The estrogens -

There are four, and the distinctions carry real clinical weight. Estradiol (E2) is the potent one and the dominant estrogen through the reproductive years. Estrone (E1) becomes the principal estrogen after menopause. Estriol (E3) and estetrol (E4) are fetal estrogens present during gestation [2].

• So the postmenopausal body is not estrogen-free. It has shifted to a weaker primary estrogen — a more accurate and less bleak thing to be able to tell a client.

• Mental health: estradiol supports mood regulation, verbal memory, processing speed and sleep architecture. Its withdrawal and fluctuation — not simply its level — track with symptoms, which is why the middle of the transition is often harder than the end of it.

• Relational and sexual: estradiol maintains genital tissue integrity, lubrication and sensation. Irritability and a shortened tolerance for noise, touch and demand often show up as conflict at home well before anyone calls it a symptom.

Progesterone and allopregnanolone

Progesterone rises in the luteal phase and, critically for us, metabolises into allopregnanolone — a neurosteroid that is among the most potent naturally occurring positive allosteric modulators of the GABA-A receptor, with anxiolytic and sedative properties comparable in kind to benzodiazepines [3].

• Losing reliable luteal progesterone means losing a monthly endogenous sedative. That is a real, physical explanation for new-onset middle-of-the-night waking and a rising anxiety floor in a woman who used to sleep fine.

• Note the paradox in the literature too: for some, allopregnanolone at luteal-range concentrations is associated with negative rather than calming mood, which is part of why premenstrual dysphoric presentations exist at all [3]. The neurosteroid story is about sensitivity, not simply quantity.

• Relational: sleep loss shortens every fuse in the household, and the person losing the sleep is usually the one being described as difficult.

Testosterone

In the reproductive years roughly half of circulating testosterone comes from the ovaries, with the rest synthesised in other tissues from adrenal and ovarian pre-androgens. After menopause the adrenal pre-androgens become the main source [5]. It is involved in desire, arousal, energy, muscle and bone.

The pattern here is worth having precisely, because a looser version circulates widely. In the Australian Women's Midlife Years Study — 1104 community-recruited participants, sex steroids measured by mass spectrometry, menopausal status staged by STRAW+10 — testosterone declined about 25% between ages 40–44 and 55–59, reached a nadir around 58–59, then rose modestly. It did not vary by menopausal stage. The authors' conclusion: the decline tracks age, not menopause [5].

What does lower it is losing the ovaries. Postmenopausal participants who had undergone bilateral oophorectomy had significantly lower testosterone than those retaining at least one ovary, irrespective of age [5], consistent with earlier work [6].

Clinical use: "my testosterone crashed at menopause" is usually not what happened. "My testosterone dropped when they took my ovaries" usually is.

And desire does fall during this transition — reported desire and arousal difficulties in early perimenopause run at roughly double premenopausal rates [5] — but testosterone is probably not the mechanism. Look instead at estradiol, fragmented sleep, and pain with sex from genitourinary syndrome of menopause, which part four covers.

So the endocrine differential for desire is real, and it is mostly not the hormone everyone names. Holding that differential alongside attachment, attraction and relational history widens what there is to work with, and gives the partner with lower desire an account that is not about the relationship.

One limitation worth naming: that sample was 88% of European ancestry, and the authors flag that the findings may not generalise. Much of this literature has the same shape.

What this vocabulary gives you

Three questions you did not have before.

1. Where in her cycle — because a luteal-phased symptom and a continuous mood state are different clinical objects, and progesterone withdrawal is a mechanism you can name.

2. What happened to her ovaries — because that single fact predicts more about her hormonal picture than her age does.

3. What else could explain the desire change — because the endocrine answer is real and it is usually estradiol, sleep and pain rather than testosterone.

The Neuroactive Hormones and What They D

Next in this series

Coming next: the medical terms clients bring in as fragments — hysterectomy, oophorectomy, ablation, surgical menopause, BRCA and risk reduction, medical menopause and premature ovarian insufficiency. They are not interchangeable, and the differences change the clinical picture.

Continuing education

If you'd like to explore this further, I teach two CAMFT-approved CE courses on the intersection of trauma and hormonal transition:

Bridging the Gap: Perimenopause and Trauma — 2 CE, $33

Menopause and Mental Health: A Comprehensive Framework — 6 CE

Both are self-paced and CAMFT CE–approved (Provider #61115).

To learn more or enroll, visit Courses Page

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About the Author

Julie Cardoza, MS, LMFT is a licensed marriage and family therapist, EMDRIA Approved Consultant, and Certified EMDR therapist specializing in Somatic EMDR, based in California. She is a CAMFT-Approved Continuing Education Provider (#61115) and an IWHI Certified Perimenopause/Menopause Health Coach, and the founder of Heartscapes, LLC.

Julie specializes in the intersection of trauma, neurobiology, and hormonal transition, integrating Somatic EMDR, polyvagal-informed practice, and menopause-informed care. She provides consultation and continuing education for clinicians working where trauma and the menopause transition meet.

Disclaimer

This article is for educational and informational purposes only and does not constitute therapy, medical advice, or a therapeutic relationship. The content reflects the author's clinical perspective as a Licensed Marriage and Family Therapist in California and is not a substitute for individualized medical or mental health care.

Julie Cardoza provides therapy through her licensed private practice (juliecardoza.com) and coaching and education through Heartscapes, LLC (heartscapesllc.com). These services are distinct and offered under separate legal and ethical guidelines.

If you or a client is experiencing a mental health crisis, contact 988 (Suicide and Crisis Lifeline) or go to the nearest emergency room.

Land Acknowledgment

I acknowledge that I live and work on the traditional and ancestral lands of the Yokut and Mono peoples.

AI Acknowledgment

I use AI platforms as research and drafting assistants in developing this material, alongside books, peer-reviewed literature, coursework and consultation. Every source cited here was located and verified by me. The clinical judgment, the framing and the final language are my own.

References

1. Harlow SD, Gass M, Hall JE, et al.; STRAW+10 Collaborative Group. Executive summary of the Stages of Reproductive Aging Workshop +10: addressing the unfinished agenda of staging reproductive aging. Fertility and Sterility. 2012;97(4):843–851. https://www.fertstert.org/article/S0015-0282(12)00187-2/fulltext

2. Sárvári M, et al. The impact of 17β-estradiol on the estrogen-deficient female brain: from mechanisms to therapy with hot flushes as target symptoms. Frontiers in Endocrinology. 2023;14:1310432. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2023.1310432/full

3. Hantsoo L, Epperson CN. Allopregnanolone in premenstrual dysphoric disorder (PMDD): evidence for dysregulated sensitivity to GABA-A receptor modulating neuroactive steroids across the menstrual cycle. Neurobiology of Stress. 2020;12:100213. https://www.sciencedirect.com/science/article/pii/S2352289520300035

4. Del Río JP, Alliende MI, Molina N, et al. Steroid hormones and their action in women's brains: the importance of hormonal balance. Frontiers in Public Health. 2018;6:141. https://pmc.ncbi.nlm.nih.gov/articles/PMC5974145/

5. Wang Y, Islam RM, Bond M, Davis SR. Testosterone and pre-androgens by age and menopausal stage at midlife: findings from a cross-sectional study. eBioMedicine. 2025;121:105972. https://pmc.ncbi.nlm.nih.gov/articles/PMC12552971/

6. Davison SL, Bell R, Donath S, Montalto JG, Davis SR. Androgen levels in adult females: changes with age, menopause, and oophorectomy. Journal of Clinical Endocrinology & Metabolism. 2005;90(7):3847–3853. https://pubmed.ncbi.nlm.nih.gov/15827095/