Low Libido in Women: What Nobody Is Asking You
Low libido in women is rarely investigated properly. Here is what testosterone, cortisol, tissue changes, the pelvic floor and the brain each contribute, and why it deserves more than a shrug.
You have stopped initiating. You have started finding reasons to go to bed later than your partner. When sex does happen it is fine, or it is uncomfortable, or it is something you get through, and afterwards you lie there wondering when exactly you became a person who has to be talked into it.
And somewhere underneath that is a quieter question: what is wrong with me?
You may have mentioned it once, in an appointment, at the end, on the way out the door. And you probably got some version of the same answer every woman gets. You are tired. You have young kids. It is your age. It is normal. Try to make more time for each other.
Then the conversation moved on, because nobody dies of low libido.
That is the actual reason this gets triaged out. Clinical attention follows risk, and low desire does not appear on any mortality statistic. It is not urgent, it is not dangerous, and in a ten minute appointment it loses every time to the blood pressure reading.
But here is what I would say to the woman sitting across from me. Desire is not a service you provide. It is part of how you experience being alive, and its absence is not a character flaw or a relationship failure. It is information. In eighteen years of clinical practice I have almost never found low libido sitting on its own. It arrives with the fatigue, the disrupted sleep, the gut symptoms, the cycle changes. It is usually the first thing to go and the last thing anyone asks about.
Four different problems that all get called "low libido"
Before anything else, some precision. "Low libido" is used as a single label for four distinct things, which have different causes and different treatments. Getting them confused is one of the reasons treatment fails.
1. Desire. Wanting sex. The interest, the thought, the pursuit. This is what most people mean by libido, and it is generated in the brain rather than the body.
2. Arousal. The physical response. Blood flow to the genital tissue, engorgement, lubrication. This depends on vascular function, tissue health and oestrogen status, and it is possible to want sex and not respond physically, or to respond physically without wanting it.
3. Orgasm. The ability to climax, and how easily. Loss here is often neurological or pharmacological rather than hormonal, which is why it behaves differently from the other two.
4. Pain. Discomfort with penetration or arousal. This is treated as its own domain rather than a symptom of the others, because it has its own causes and because it overrides everything above it.
The reason this matters: a woman who says she has lost her libido may have entirely intact desire and an arousal problem. Or intact desire and arousal, and difficulty reaching orgasm. Or she may have stopped wanting sex because it has been hurting for two years, which is not a desire disorder at all. It is a pain problem with a predictable downstream effect.
If you take one thing from this article into your next appointment, take this: be specific about which one has changed. "I've lost my libido" starts a short conversation. "I still want sex, but I've stopped being able to reach orgasm since March" starts a completely different one.
Each section below is marked with which domain it affects. Read for the one that matches yours.
First, something that needs clearing out of the way
This one sits squarely in domain one, desire, and it matters more than any of the physiology below it.
A great many women have never experienced spontaneous desire. They do not get struck by wanting sex out of nowhere, the way it happens in films. Instead, desire arrives after arousal has already begun: after touch, after closeness, after the conditions are right. This is called responsive desire, and it is normal, common, and not a disorder.
If you have spent years believing you are broken because you do not think about sex unprompted, you may not have a libido problem at all. You may have been measured against a template that was never yours.
The question worth asking is not "do I want it spontaneously." It is: has something changed, and does the change distress me? Loss of something you used to have is worth investigating. Never having had it is worth understanding, not treating.
Desire is a discretionary function
Primarily affects: desire.
Here is the frame that organises everything else.
Your body runs a hierarchy. Under sustained threat, it funds the systems that keep you alive right now and defunds the ones that can wait. Reproduction can wait. Digestion can wait. Repair can wait. Desire is not a luxury the body has decided you do not deserve. It is a discretionary function, and a body that believes it is under threat does not fund discretionary functions.
The hypothalamus is running both systems. The stress axis and the reproductive axis sit in the same building, and when the first is activated continuously, it suppresses the second. This is not a malfunction. It is the system working exactly as designed, in a life it was never designed for.
The relevant threat is rarely dramatic. It is a decade of being the one who holds everything together. It is a job with high demand and low control, a parent who needs you, a child who is struggling, a marriage that takes managing. The body does not distinguish between running from something and carrying something for fifteen years.
Cortisol and the sex hormones also compete for the same upstream resources and the same regulatory attention. A body producing stress hormones continuously is not prioritising the production of anything else.
Which is why "just make more time for each other" so often fails. The problem is not scheduling. The problem is that a nervous system in threat mode does not switch to desire because there is a gap in the calendar.
Testosterone: genuinely overlooked, and often oversold
Primarily affects: desire. Some effect on arousal.
Women produce testosterone. Not as much as men, but it is present, it is active, and it declines gradually from the late twenties onward, with a further drop where the ovaries stop functioning or are removed.
It is overlooked clinically, and there is a real gap here. But the story is more complicated than the internet suggests, and the complications matter.
The most comprehensive guidance available is the 2019 Global Consensus Position Statement on testosterone therapy for women, developed by a task force from ten international societies including the Endocrine Society of Australia and RANZCOG. Its conclusion was narrow: the only evidence-based indication for testosterone therapy in women is hypoactive sexual desire disorder in postmenopausal women.
Two things follow from that.
First, a blood test will not settle this. Testosterone levels in women correlate poorly with sexual desire, and no threshold defines deficiency. A woman with a level at the bottom of the range may have no complaint at all, and a woman in the middle may have lost desire entirely. Anyone offering to diagnose your libido from a serum result is overreaching.
Second, for the right woman it can work. Australia is unusual here. AndroFeme 1, a testosterone cream formulated specifically for women, was approved by the TGA in November 2020 and has been available on private prescription since April 2021. It remains the only testosterone product in the world licensed specifically for women, and it is made in Perth. It is not on the PBS, so expect to pay somewhere in the range of one hundred to one hundred and forty dollars per tube. It is prescription only and that conversation belongs with a doctor experienced in menopause care.
The thing almost nobody mentions: the combined oral contraceptive pill raises sex hormone-binding globulin, which binds circulating testosterone and reduces the free fraction available to tissue. For some women, this has a marked effect on desire, and it can persist for a period after stopping the pill. Given how routinely the pill is prescribed to young women for period pain, acne and endometriosis, this is a conversation that should be happening far more often than it is. Many young women are being placed on the OCP before they’re even familiar with their baseline sexual function and libido, and staying on it until they’re well into their 20’s and 30’s and then feeling disconnected from their sexual function and what a ‘normal’ libido is for them.
Tissue change: the part that turns into pain
Primarily affects: arousal and pain. Desire only indirectly.
This is the clearest example of why the distinction matters. A woman with significant tissue change has not lost her desire. She has lost her capacity to respond comfortably, and desire has withdrawn afterwards, in response. Treating that as a desire problem misses it entirely.
Oestrogen receptors are distributed through vaginal, vulvar and urethral tissue. As oestrogen falls through perimenopause and after menopause, that tissue becomes thinner, less elastic and less well lubricated, blood flow reduces, and vaginal pH shifts. The clinical term is genitourinary syndrome of menopause.
Unlike hot flushes, this does not settle with time. Left alone it progresses.
The reason it belongs in a conversation about desire is simple. Pain is the most efficient destroyer of libido there is. If sex has hurt, even a few times, the brain does the arithmetic. Anticipation of discomfort suppresses arousal; reduced arousal means less lubrication, less lubrication means more discomfort. It becomes self-reinforcing, and by the time a woman says she has lost her libido, what she often has is a body that has learned to brace.
This one is highly treatable, and it frustrates me that so many women are never told so.
The pelvic floor: usually too tight, not too weak
Primarily affects: pain. Secondarily arousal.
Pelvic floor conversations in this country are dominated by weakness. Do your Kegels. Postnatally, that is often appropriate.
But in the women I see with pain and low desire, the more common picture is the opposite: a pelvic floor that is chronically overactive and cannot let go. Muscles that will not release produce pain with penetration, reduced blood flow, and a pelvis braced against anticipated discomfort.
Two groups are particularly affected.
Postnatally, tissue change, scarring, birth injury and the sheer physical demand of the early years all contribute. So does something less often named: a body that is touched all day by a small person and has no remaining appetite for being touched at all.
In endometriosis, years of severe cyclical pain train the pelvic floor to guard. Deep dyspareunia is extremely common and frequently goes unmentioned, partly because women with endometriosis have often already been told that pain is simply their situation.
A pelvic floor physiotherapist is the appropriate referral, and downtraining rather than strengthening is often what is needed. Note also the loop back to the section above: a pelvic floor that will not release in a woman whose nervous system will not stand down is not a coincidence.
The brain: where desire is actually decided
Primarily affects: desire and orgasm.
Desire is not generated in the pelvis. It is generated in the brain, and the dopaminergic reward pathways are central to it. Dopamine drives wanting and anticipation, the pursuit part of desire rather than the pleasure part.
Those same pathways are the first to flatten in burnout and depression. When a woman tells me she has lost interest in sex, and I ask what else she has lost interest in, the answer is frequently everything. Food she used to look forward to. Music. Plans. Desire was not selectively removed. It went with the rest.
The clearest evidence for the brain's role is pharmacological, and it is significant enough to deserve its own section below.
It also helps to understand that the brain runs two systems at once: one that responds to sexual cues and one that inhibits. Low desire is at least as often a matter of too much inhibition as too little excitation. Stress, distraction, body shame, resentment, fear of pain and a mental list of unfinished tasks are all inputs to the brake. You cannot press the accelerator hard enough to overcome a brake that is fully applied, which is why advice focused entirely on generating desire so often fails.
Medication: the cause that gets missed most often
Affects all four domains, and orgasm most distinctively.
Before anything else on this list is investigated, the medication cabinet is worth opening.
Sexual dysfunction is one of the most common side effects of SSRIs and SNRIs, and the reported rates tell you almost everything about how it is handled. When researchers rely on patients mentioning it spontaneously, rates come out around ten percent. When researchers ask directly, rates rise into the range of forty to seventy percent.
Same drugs. Same patients. The entire difference is whether anyone asked.
The combined oral contraceptive pill is the other big one. It raises sex hormone binding globulin, which binds circulating testosterone and reduces the free fraction available to tissue. Given how routinely it is prescribed to young women for period pain, acne and endometriosis, this is badly under-discussed.
Also on the list: anti-androgens such as spironolactone and cyproterone, GnRH agonists used in endometriosis, aromatase inhibitors and tamoxifen after breast cancer, opioids, beta blockers, antipsychotics and antihistamines.
None of that is a reason to stop anything, and nothing here should be changed without the prescriber involved. But if something has shifted and you are taking one of these, that deserves naming specifically rather than being absorbed as a fact about you.
I have written about this in full, including how to tell the drug effect from the depression and how to raise it so it gets taken seriously: Antidepressants and Libido: The Side Effect You Probably Weren't Warned About.
What this looks like in practice
Details changed and shared with permission.
She was in her late forties, and she came in because of a weekend away.
It had been a good weekend, at a beautiful place, with a partner she loved and a relationship that was not in trouble. And she had spent most of it engineering reasons not to have sex. On the Saturday, she went for a walk around the grounds and pretended to get lost, because being lost for forty minutes was easier than going back to the room.
She told me this through tears. Not because the weekend had been ruined, but because of what she had become willing to do to avoid her own partner, and what that seemed to say about her.
What we ruled out first. No pain, no discomfort, no tissue or structural findings. That matters, because it told us which domain we were dealing with. Her arousal and her capacity for orgasm were intact. What had gone was desire, on its own, which is a narrower and more specific problem than "low libido."
What the history gave us. Two years in a job she described as relentless. A mind that would not switch off. Evenings spent rehearsing the following day, lying in bed running through conversations that had not happened yet.
That history is not incidental detail. It is the diagnosis.
What the testing showed. Cortisol very high. Testosterone very low.
I want to be careful here, because I have spent this article arguing that a testosterone result does not diagnose anything on its own, and I am not about to contradict myself. The result did not tell us what was wrong. The history had already told us that. What the testing did was confirm the shape of it and give her GP something concrete to work with.
The two findings also belong together. A body producing cortisol continuously, for two years, in a woman who cannot stand down at night, is a body that has deprioritised a discretionary function. The low testosterone was not a separate problem sitting alongside the high cortisol. It was downstream of it.
And there was a third factor neither of us could ignore. At her age she was almost certainly in the perimenopausal transition, which means her hormonal buffer was thinning at precisely the moment her stress load was at its highest. Neither of those things on its own would necessarily have taken her desire. Arriving together, they did. This is a pattern I see constantly: a woman who coped with a demanding life for twenty years and then, somewhere in her forties, suddenly cannot. The transition did not cause it. It removed what had been absorbing it.
What we did. Several things at once, deliberately:
A referral to her GP to consider testosterone therapy.
Targeted nutritional and herbal support aimed at the stress axis
A topical sea buckthorn oil for local tissue support- despite her not having major symptoms I went with this intervention because I wanted to preempt the changes on the horizon for vaginal tissue.
A nightly wind-down ritual, built around red light and a body oiling practice with essential oils. Not necessarily with her partner, but it gradually and organically evolved into something they shared on many evenings.
A note on the testosterone, because I am not going to gloss over it. AndroFeme's approved indication in Australia is hypoactive sexual desire disorder in postmenopausal women, and this patient was perimenopausal. That makes it off-label use, and her GP would have weighed that in deciding whether to prescribe. I supplied a letter to help support this as an intervention.
That last one deserves explaining, because it looks like the softest intervention on the list and it may well have been the most important. A woman who cannot stop rehearsing tomorrow does not need to be told to relax. She needs a physical sequence that signals to her nervous system that the day has ended. The oiling ritual also did something else: it was the first time in two years she had touched her own body for a reason that had nothing to do with anyone else wanting something from it. While eventually it did evolve into something she shared with her husband, this was not the intention- it was her own time and space, which she decided she was happy to include her husband in.
At six weeks. I could see it before she sat down.
She was not back to her baseline, and she said so. But she was initiating again, engaging with her partner, and the dread had gone. That was her word. Not the desire returning first, but the dread leaving.
What I cannot tell you is which element did it. Five things changed at once, and I am not going to pretend I can separate them. What I can say is that at six weeks, testosterone therapy has not reached its full effect, so whatever moved first was most likely the nervous system work rather than the hormone support.
Which is the point of this entire article. It was never one cause, and it was never going to be one fix.
I told her to expect another two to three months before we would know how far the protocol would take her. She was, in her own words, already happy.
What actually needs to happen
Low libido has never once, in my clinic, turned out to have a single cause. It is usually four or five things at modest scale: some tissue change, some stress load, some sleep debt, a medication, a pelvic floor that has been guarding since a birth eleven years ago.
A proper assessment looks at all of it. Which of the four domains has actually changed? Thyroid function, iron, the stress axis, the cycle. A full medication review including the pill, antidepressants and anything on the list above. Sleep, pain history, birth history. And the relational and psychological context, which matters as much as anything above it.
What it does not look like is a single hormone test and a shrug.
If any of this is yours, the thing I would ask you not to do is wait until it is bad enough to count. You will be waiting a long time, because on every clinical triage list this sits near the bottom. Nobody dies of it.
But something does die. Not your marriage, necessarily. The part of you that wanted things.
That is reason enough.
Krystle Alves is a naturopath, nutritionist and yoga therapist with eighteen years of clinical experience, based in Miranda, NSW. She works with women through perimenopause and beyond on fatigue, burnout, hormonal change and complex unresolved presentations.