"My brain went from black and white to technicolor."

“You know that scene from The Wizard of Oz where it goes from black and white to technicolor? That’s my brain on testosterone.”

That’s a patient of Dr. Kelly Casperson’s, speaking about starting testosterone therapy.

Then Casperson herself, at the same event:

“Picture 108 million women energized, focused, and ambitious. Not in spite of their age, but because they are supported through it.”

These two sentences were said in a federal hearing room, to the FDA Commissioner of the United States, by a board-certified urologist who has spent her career watching women’s quality of life collapse from something treatable — and then watching those women be told nothing was wrong.

Let that land.

This hearing, on July 17, 2025, was officially about removing the black box warnings from hormone therapy products. But tucked inside it was something else — a reckoning about testosterone, and how completely medicine has failed women on this one.

This is not just a libido hormone

The first thing to dismantle is the stereotype. When most people hear “testosterone for women,” they assume the conversation is about sex drive. That’s a half-truth that has done a lot of damage.

Here’s what Casperson actually told the FDA panel:

“Testosterone stereotype is that it’s just for libido. It’s a half-truth. It’s a neurohormone critical for mitochondria, nerve function, muscle, bone, and brain function. Libido improves because dopamine and blood flow in the brain improve.”

Read that again. Libido improves as a downstream consequence of the brain working better — not because testosterone is some aphrodisiac switch. The brain has testosterone receptors throughout. When testosterone is restored to physiologic levels, dopamine signaling improves, blood flow improves, mitochondrial function improves, and the whole system runs more efficiently. Better sex drive is a side effect of better brain function.

Here’s what testosterone actually does in the female body:

In your brain: It’s a neurohormone that supports dopamine production, nerve conduction velocity, and cerebral blood flow. It drives what researchers call “goal-oriented behavior” — the ambition, focus, and motivation to pursue things. Women who are deficient don’t just feel tired; they feel flat. Uncaring about things they used to care about.

In your bones: Testosterone directly stimulates osteoblasts, the cells responsible for building new bone. This is distinct from estrogen’s role in protecting existing bone. You need both.

In your muscles: Testosterone drives muscle protein synthesis and recovery. It’s why resistance training becomes harder to yield results in perimenopause — not just because you’re training differently, but because the anabolic signal supporting repair is declining.

In your mitochondria: This is the cellular energy piece. Testosterone is involved in mitochondrial biogenesis — the production of new mitochondria. Less testosterone, less efficient energy production at the cellular level. This is why the fatigue that comes with deficiency doesn’t respond to more sleep.

Here’s a number that surprises most women: you make four times more testosterone than estrogen. Not a little testosterone. Four times more. It is not a trace hormone that barely registers. It is foundational to your baseline biochemistry — and it starts declining around age 25, dropping roughly 50% by the time you hit 40. Before the hot flashes start. Before the cycle irregularities begin. Before anything announces itself as menopause.

A regulatory failure, plainly named

There are zero FDA-approved testosterone products for women in the United States.

Zero.

There are more than twelve FDA-approved testosterone products for men.

Approximately two million off-label testosterone prescriptions are written for women in the US every year. Think about what that means: doctors across the country know this therapy works, know women need it, and are prescribing it anyway — just without legal infrastructure to support them. They’re doing workarounds because the FDA never built the road.

Two formal applications for women’s testosterone products were submitted and denied. Intrinsa, a low-dose transdermal patch, was rejected in 2004 over long-term cardiovascular safety data concerns — despite more than 36 randomized clinical trials demonstrating testosterone’s effectiveness for postmenopausal women. Australia approved the cream AndroFeme in 2020. The US still has nothing.

Casperson at the hearing:

“Testosterone has been used in women since the 1940s. Trans men receive 10 times the dose. What other drug do we have where we give people 10 times the dose for 50 years and publish it and then we’re still asking if it’s safe? Meanwhile, male testosterone products were approved with just six months of safety data. That is not a lack of evidence. It’s a regulatory and equity failure.”

She’s right. The safety data on testosterone in female bodies is extensive, if you count the decades of research on trans men — who receive male doses, far exceeding anything prescribed for perimenopausal women, and for whom the long-term outcomes are well documented. The claim that we don’t have enough evidence to approve a product at physiologic female doses is hard to defend with a straight face.

The FDA and the missing twelve words

In December 2004, Procter & Gamble submitted a formal application to the FDA for approval of Intrinsa — a low-dose testosterone patch specifically designed for women. The company had run the trials. The data was there. The committee convened to evaluate it.

Fourteen of seventeen advisory committee members agreed: the benefits were clinically meaningful.

The vote was not close. The benefit signal was real. The committee members knew it.

So what happened?

A committee member named Dr. Steven Nissen — at the time perhaps the most influential cardiologist in America — said the following, on the record:

“I don’t want to expose several million American women to the risk of myocardial infarction and stroke in order that they can have one more sexual episode a month.”

Read that again slowly.

One more sexual episode a month.

That sentence did more damage to women’s testosterone access than any single piece of negative research. It captured, in twelve words, exactly how medicine had chosen to frame the question — as a narrow, almost trivial convenience, a slight bump in one metric of one function, weighed against catastrophic cardiovascular risk. Not cognitive function. Not dopamine. Not mitochondrial health, bone formation, muscle integrity, anhedonia, or the neurological machinery of ambition. One more sexual episode a month.

The FDA demanded what they did not demand for men: five or more years of safety data on more than 5,000 women before approval. Male testosterone products were approved on six months of data.

Procter & Gamble did the math. Testosterone is a generic molecule. There is no patent on it. There is no intellectual property moat that would allow them to recoup a billion-dollar safety study — the kind it would take to satisfy the FDA’s demand. If you run a $1 billion clinical trial and it proves a generic molecule is safe, any competitor can immediately manufacture the same molecule under a different name and capture the market you paid to create.

So P&G did the only rational thing: they got Intrinsa approved in Europe in 2006, where the evidentiary bar was different, and then abandoned the U.S. application entirely.

And that is why, as of 2026, there are still zero FDA-approved testosterone products for women in the United States.

↑ This is where the email ends. What follows is the full article — the research methodology failures, the SHBG problem your doctor isn’t testing for, every side effect you deserve to know about before you start, and the decades of safety data hiding in plain sight.

[Continue reading on the web →]

The international landscape is a useful contrast. Australia approved a testosterone cream for women (AndroFeme) in 2020. The UK approved one in 2026. A company called Aviva Bio received FDA guidance in January 2026 on their AVA-291 product — the first real regulatory movement in twenty-two years.

But in the country that spent the most time deciding, the answer is still no.

In 2023, Nissen himself chaired the TRAVERSE trial — a large randomized controlled trial that found bioidentical testosterone does not increase major adverse cardiovascular events (MACE) even in men with pre-existing cardiovascular disease. Healthy postmenopausal women at one-tenth the male dose were the population he was supposedly protecting in 2004. His own subsequent research made that protection look like it was never needed.

Dr. Nissen’s quote is not an anomaly. It’s a summary. It reflects how an entire institution had framed the question, and what it had decided the answer was worth. Not “what does testosterone do to the female nervous system?” Not “what happens to the dopamine pathways when a neurohormone declines 50% between ages 25 and 40?” Just: is one more sexual episode a month worth the cardiovascular risk?

That’s not the right question. It never was.

Why the research missed it

Here is something that is true and important to understand: the clinical research on testosterone in women was, in many cases, methodologically broken in ways that had nothing to do with whether the hormone works.

This is not a conspiracy claim. It’s a quality-of-measurement claim. The studies used the wrong thermometer, measured the wrong thing, and stopped before the effects could establish themselves. What they found — or didn’t find — tells us more about study design than it does about testosterone.

The measurement problem. The standard lab assay used to measure testosterone — called an immunoassay — performs far worse than its reputation suggests at female-range concentrations. On the Beckman immunoassay — one of the most commonly used — the correlation with reference-method measurements drops to R² = 0.16 below 37.6 ng/dL. R² = 0.16 means the test explains only 16% of the variance at female-range concentrations. That is not a measurement with error bars. That is essentially no reliable measurement at all. The Endocrine Society has recommended LC-MS/MS (liquid chromatography-tandem mass spectrometry) as the gold standard for measuring testosterone in women since 2007 — eighteen years of official guidance that most commercial labs still don’t act on by default. Both LabCorp (test code 070001) and Quest Diagnostics (test code 15983) now offer LC-MS/MS specifically for women; you may need to request it explicitly. Researchers were, in many cases, literally unable to determine whether two women had meaningfully different testosterone levels. A study designed to detect dose-response relationships in a population cannot find those relationships if it can’t accurately measure the dose. You cannot conduct a valid thermometer study with a broken thermometer — and R² = 0.16 makes that metaphor literal.

Total vs. free testosterone. Studies almost uniformly measured total testosterone — the amount circulating in the blood. But as covered elsewhere in this article, total testosterone is not what your cells use. SHBG — sex hormone binding globulin — captures testosterone with high affinity and holds it unavailable. The biologically active form is free testosterone. A woman with high SHBG and “normal” total testosterone may have near-zero free testosterone and will feel every symptom of deficiency. Most studies never measured SHBG at all. The studies weren’t measuring the thing that matters.

Studies ran too short. The majority of clinical trials on testosterone in women ran twelve to twenty-six weeks. Twelve weeks. Brain function, motivational circuitry, and dopaminergic tone are slow systems. The neuroscientists who study how testosterone modulates dopamine receptor density and tyrosine hydroxylase activity will tell you that meaningful neurological adaptation takes four to six months or longer to establish. A twelve-week study looking for changes in motivation and brain function is the equivalent of planting a tree in October and checking for fruit in December. The absence of fruit is not evidence that the tree doesn’t bear fruit.

The endpoints were wrong. In study after study, the primary outcome measure was sexual function. Sometimes specifically: number of satisfying sexual events per month. This is a legitimate outcome to measure. But it is a narrow slice of what testosterone does in the female body. Anhedonia — the loss of interest and pleasure in things you used to care about — was never a primary endpoint in any randomized trial. Motivation, creative drive, gym performance, willingness to initiate things, the quality of ambition — none of these were ever primary endpoints. The studies were looking at the corner of the room and concluding the whole house was empty.

The 56% number. A 2024–2025 UK observational study of 510 women — the largest cohort ever assembled to look specifically at non-sexual testosterone outcomes — found something remarkable. When women reported symptom improvement on testosterone therapy, the symptom with the highest response rate wasn’t libido. It was anhedonia. Fifty-six percent of women in the cohort reported improvement in anhedonia — loss of interest in things they used to care about. That is the highest response rate of any symptom measured. No randomized controlled trial has ever used anhedonia as a primary endpoint. The thing women experience most powerfully was never the thing researchers were measuring.

The placebo problem. In testosterone studies, anywhere from 31 to 49 percent of women in placebo arms report symptomatic improvement. This is not unusual for trials involving subjective symptom measures — it reflects the complexity of expectation, therapeutic attention, and the natural variability of symptoms over time. But it means you need very large studies, very precise measurement tools, and appropriate study duration to detect the signal above the noise. Most testosterone studies were not designed that way. They were underpowered, used imprecise assays, ran too short, and measured the wrong endpoints.

Put it together: the research didn’t fail to find robust effects because robust effects don’t exist. It failed to find robust effects because it used a broken thermometer, measured the wrong thing, for too short a time, in too small a population, with the wrong outcomes. That is not evidence of absence. It is evidence of poor study design.

The 56% anhedonia response rate in 510 women, from a single observational study, is more clinically meaningful than most of the randomized trial literature — because it’s the first time someone asked the right question with a large enough sample to see the answer.

Why your levels might be lower than you think — the SHBG problem

Here’s where it gets technically interesting, and where most women are being failed at the lab level.

Most doctors who test testosterone in women test total testosterone. But total testosterone is not what your cells actually use. Your cells use free testosterone — the fraction not bound to a carrier protein called sex hormone binding globulin, or SHBG. SHBG grabs testosterone with high affinity and holds it in circulation, unavailable to tissues. When SHBG is high, free testosterone crashes even if total testosterone looks normal.

A woman can have a “normal” total testosterone reading — technically in the reference range — while her free testosterone is near zero. She will feel every symptom of deficiency. Her doctor will look at her labs and tell her everything is fine.

Now add one more layer: oral contraceptive pills dramatically elevate SHBG. The synthetic estrogen in combined pills signals the liver to massively ramp up SHBG production — by 200 to 300% with some formulations, or roughly four times higher than never-users by some measures. Pills containing drospirenone (Yaz, Yasmin) are particularly aggressive because the progestin also has direct anti-androgenic properties, suppressing testosterone at the receptor level. Double the problem.

And — critically — this elevation can persist for six months or more after stopping the pill. Research by Panzer and colleagues published in the Journal of Sexual Medicine found that SHBG remained significantly elevated in women who had discontinued OCPs, even after months off. The liver learns to overproduce it from years of synthetic estrogen stimulation, and doesn’t immediately normalize when the stimulus stops.

Now run the scenario: a woman who was on the pill for fifteen years stops in her early 40s. Her total testosterone is already declining naturally with age. Her SHBG is still elevated from the pill era. The result: free testosterone at or near zero, with labs that show total testosterone in the “normal” range. She gets told she’s fine. She is not fine.

What to ask your doctor: Request total testosterone, free testosterone (specify equilibrium dialysis — the most accurate method), and SHBG together, as a panel. A morning blood draw gives you peak levels. This isn’t exotic testing; it’s just asking for the right thing.

What testosterone actually does to your brain (it’s about dopamine)

I covered the full neuroscience of this in Part 1 — My Antidepressant Couldn’t Fix This. Testosterone Did. — including the VTA, the mesolimbic pathway, tyrosine hydroxylase, and anhedonia as a dopamine-system problem. If you haven’t read it, start there; the brain science is the foundation for everything that follows.

The short version for context: testosterone acts directly at the origin point of the brain’s two major dopamine pathways. Both carry androgen receptors at the VTA. Testosterone supports dopamine synthesis, receptor density, and reward-circuit function. When it declines, the system that generates motivation, pleasure, and the desire to pursue things runs at reduced capacity. This is why the clinical presentation of testosterone deficiency and anhedonia overlap so heavily — they share the same underlying mechanism.

What I want to focus on here is the measurement problem — because the studies that “failed to find” these effects weren’t measuring the right thing, with the right tools, for long enough to see it.

The side effects you deserve to know about — all of them

This section exists because you deserve complete information before you start anything, not after you’ve noticed something. A good menopause specialist will walk through all of this with you proactively. If they don’t, ask.

Clitoromegaly. Testosterone stimulates androgenic tissue, and the clitoris contains androgen receptors. Enlargement — ranging from barely noticeable to clearly visible — is a documented effect at any dose, though mild to moderate is most common at physiologic female doses. It is generally considered permanent once it occurs; it does not fully reverse if you stop the hormone. I have experienced this. I don’t find it problematic — the nerve density in that tissue is unchanged, so if anything, increased surface area is not the worst outcome. But some women feel differently, and that is a legitimate individual response. Know this before you start.

Voice deepening. Testosterone affects the larynx. At supraphysiologic doses — as trans men on male doses routinely experience — voice changes can be dramatic and permanent. At physiologic female doses, any change is generally subtle. I’ve experienced mild deepening; my voice was already on the higher end and the shift is small enough that I don’t notice it in daily conversation. For women in voice-dependent professions (singers, public speakers, broadcast journalists), this deserves a specific conversation about dose and monitoring.

Hair loss — and what you can actually do about it.

This one is the most complicated, so it gets more space.

The mechanism: testosterone is converted in peripheral tissues (including the scalp) into dihydrotestosterone (DHT) by an enzyme called 5-alpha reductase. DHT is approximately five times more potent than testosterone at the androgen receptor. In hair follicles that are genetically susceptible, DHT binding shortens the growth phase of the hair cycle and progressively miniaturizes follicles — turning thick terminal hairs into thin vellus hairs. This is androgenic alopecia. Not everyone gets it. Genetic predisposition determines who is vulnerable.

Risk indicators: a father with male pattern baldness, or a mother/sisters with visible female pattern thinning. If that’s your family history, have a direct conversation with your prescriber before starting testosterone, take baseline photographs of your hairline and part width, and discuss monitoring frequency.

If you are susceptible, the good news is that hair loss and testosterone’s systemic benefits run through different pathways — which means you can potentially protect the hair without defeating the purpose of the therapy.

Here’s how:

Finasteride is a 5-alpha reductase inhibitor that blocks the conversion of testosterone to DHT at the follicle level, reducing scalp DHT by roughly 60–70%. What it does NOT block: testosterone itself. Your testosterone still circulates. It still binds androgen receptors in your brain (supporting dopamine, drive, focus), muscle (supporting protein synthesis and strength), and bone (supporting bone formation). The benefits of testosterone largely come from testosterone directly — not from its conversion to DHT. Blocking 5-alpha reductase cuts off hair-loss risk without pulling away the floor underneath everything else. Finasteride is used off-label in postmenopausal women for female pattern hair loss at doses of 2.5–5 mg daily, with documented efficacy. Important note: it is contraindicated in premenopausal women who could become pregnant.

Dutasteride blocks both Type 1 and Type 2 5-alpha reductase (finasteride only blocks Type 2), reducing serum DHT by approximately 98% vs finasteride’s 71%. More complete DHT suppression, same logic about preserving testosterone’s direct benefits. A 3-year study found dutasteride outperformed finasteride for women under 50, with improvement in up to 80% of patients. Same pregnancy contraindication.

Minoxidil works through an entirely different pathway — vasodilation. It’s a potassium channel opener that increases blood flow to hair follicles, extends the anagen (growth) phase, and stimulates growth factor production. It doesn’t touch the androgen system in a clinically meaningful way at standard doses, which means it can be used alongside testosterone therapy without interfering. Low-dose oral minoxidil (0.5–1 mg/day for women) has shown strong results for female pattern hair loss in recent RCTs and is increasingly the preferred formulation over topical for compliance reasons.

What about spironolactone? Spironolactone is sometimes prescribed for androgen-related hair loss or acne in women, and it works — but by blocking androgen receptors throughout the body. Not just at the hair follicle. This means it blocks testosterone’s action at the brain, muscle, and bone, too. It reverses exactly what you’re trying to accomplish. Spironolactone is the wrong tool for women who want testosterone’s cognitive and physical benefits while protecting their hair.

The practical takeaway: hair loss risk on testosterone is real, genetic, and not universal. If you’re susceptible, it’s manageable with finasteride, dutasteride, or minoxidil — none of which require you to give up the reason you started. This is a conversation to have with your prescriber at the outset, not after you notice your part widening.

The safety data is hiding in plain sight — trans men

The argument that we don’t have enough safety data to support testosterone therapy in perimenopausal women deserves a direct response. Because we have more data than most people realize. We’re just looking in the wrong place.

Trans men — individuals assigned female at birth who receive gender-affirming testosterone therapy — have been receiving testosterone at male doses for decades. Not physiologic female doses. Not the 50–100 ng/dL target range a menopause specialist is aiming for. Male doses: bringing their serum testosterone from female physiologic range (15–70 ng/dL) up to male physiologic range (300–1000 ng/dL). We’re talking about five to twenty times higher than what any menopause physician is prescribing.

And we have approximately 30 to 50 years of published data on this population.

Kelly Casperson said it at the FDA hearing in July 2025, and the logic is worth sitting with:

“Testosterone has been used in women since the 1940s. Trans men receive 10 times the dose. What other drug do we have where we give people 10 times the dose for 50 years and publish it and then we’re still asking if it’s safe? Meanwhile, male testosterone products were approved with just six months of safety data. That is not a lack of evidence. It’s a regulatory and equity failure.”

So what does the data actually show?

On breast cancer: The largest published cohort is the Dutch nationwide study (de Blok et al., 2019, BMJ), which followed 1,229 trans men for up to 17 years on male-dose testosterone. Four cases of breast cancer were diagnosed. Four. The standardized incidence ratio compared to cisgender women was 0.2 — one-fifth the expected rate. Not elevated. If anything, lower than background female risk. The mean testosterone level in trans men who did develop breast cancer was lower than the cohort median — suggesting the cases were not associated with higher testosterone exposure.

A 2023 systematic review confirmed: trans men have lower breast cancer risk than cisgender women and higher risk than cisgender men. The signal is not there.

On cardiovascular outcomes: A 2026 systematic review in Frontiers in Endocrinology analyzed 13 observational cohort studies covering 7,837 trans men, documenting 34 cardiovascular deaths over years of follow-up. In parallel, 13 randomized controlled trials of testosterone in cisgender women (at physiologic doses) reported zero major adverse cardiovascular events. The cardiovascular picture at female physiologic doses — the doses we’re actually discussing — is clean in the short-to-medium term data.

Known parameters to monitor in trans men on male doses: polycythemia (elevated red blood cell count), lipid profile, blood pressure. These are standard monitoring items, not surprise adverse events. They’re manageable and well-characterized.

The argument structure here is straightforward: if we were worried about testosterone safety in female bodies, we have a large, long-duration, high-dose natural experiment that has been running for decades, published repeatedly in peer-reviewed literature, and it does not show the cancer or cardiovascular catastrophe that has been used to justify regulatory paralysis at physiologic female doses.

Casperson’s formulation elsewhere: pellets tend to run supraphysiologic — levels in the 200–400 ng/dL range rather than the 50–100 ng/dL that most specialists target. Even this overshoot, common in the pellet world she cautions against, doesn’t show the feared outcomes. The fears are not tracking the evidence.

For perimenopausal and menopausal women being offered low-dose testosterone to restore physiologic levels? We are, as Casperson put it, fighting about whether to give someone a glass of water while watching people swim safely in the ocean for fifty years.

My own experience — the honest version

Here is what I can tell you from the inside.

Before testosterone, I had textbook anhedonia. Didn’t want to get out of bed in the morning. Couldn’t summon the pull toward things I used to care about. This is worth naming precisely: I’ve been on an antidepressant for 30 years. It was doing its job on the serotonin side of things. But SSRIs and SNRIs address serotonin pathways, not the dopamine-mediated anhedonia that comes from testosterone deficiency. Those are different systems. Someone can be “treated” for depression and still experience the flat, motivationless quality of testosterone-deficiency anhedonia, because the antidepressant isn’t touching that pathway at all. That’s exactly what was happening to me.

On testosterone, I wake up actually wanting to get out of bed. Not in a “I should get up” way, but in the way I felt at 30, when the day felt like it held something worth getting to. I have the drive to finish things I start, which is different from discipline. Discipline is pushing yourself. This is pull. The creativity that built adoption.com from nothing in 1995 — the kind that has you thinking about a new business at 7am before coffee, genuinely excited about the problem — came back. Hard things started feeling worth doing again rather than optional. At the gym, I’m not negotiating with myself to get through it; I want to be there. That quality of wanting is what I had lost, and I hadn’t realized how much it shaped the texture of a day until it returned.

The neuroscience explains this exactly. Testosterone is a neurohormone that supports dopamine signaling and blood flow in the brain. What Casperson said at the FDA hearing about libido improving “because dopamine and blood flow in the brain improve” — I felt that before I understood the mechanism. The goal-directed behavior researchers measure in studies, the ambition and motivation to pursue things, isn’t vague. It’s the literal experience of waking up with somewhere you want to go. The cellular energy piece connects too: testosterone is involved in mitochondrial production. Less testosterone means less efficient energy generation at the cellular level, and that explains why the fatigue that goes with deficiency doesn’t fix with more sleep. I have been both versions of myself. The difference is not subtle.

I can tell you all of this with confidence because I can feel the cycle. My current dosing makes that unavoidably clear. I started exploring testosterone in London as a patient at Newson Health, Louise Newson’s clinic. They prescribed AndroFeme, a testosterone cream originally developed in Australia and prescribed through Newson Health. Follow-up blood tests showed insufficient absorption — my working theory is that it was related to being overweight at the time, since skin thickness and body composition genuinely affect how much of a topical crosses into circulation. I felt nothing.

I moved to injectable. I’ve been using Despamen, a combination injectable available over the counter at Mexican pharmacies — testosterone enanthate 100mg plus estradiol valerate 5mg in one pre-filled syringe.

[ANNETTE TO-DO: Photograph your Despamen pre-filled syringe kit when you open your next one — this photo is needed for the article and the Despamen guide article] And when it works, it works the way I described above. All of it.

Here is the problem: testosterone enanthate has a half-life of about 4.5 days. Injected once a month, levels peak in the first days and crash through subtherapeutic ranges by weeks two and three. That means roughly ten to fourteen days of essentially no hormone on board before the next dose. I can feel that window. The drive goes quiet. The excitement in the morning flattens out. Everything that hinges on whether I get my injection becomes visible precisely because it disappears on a predictable schedule.

This is not a complaint — it is actually useful information. The fact that I can feel the cycle means the hormone is doing what it’s supposed to do when it’s present. It also means the monthly schedule was designed for convenience, not for my physiology. My goal is to move to a formulation dosed more frequently — twice weekly or every other day at smaller amounts — to maintain stable therapeutic levels rather than one good week followed by two weeks of decline.

This is not a perfect story. I’m still figuring out what works for me. Which is, I think, the honest experience for most women navigating this without the FDA having done the regulatory work to make it straightforward.

Your delivery options — an honest assessment

Since no FDA-approved product exists for women, you’re working in the world of off-label and compounded. Here’s what the options look like:

Topical cream or gel is where most specialists start. Applied daily to a consistent site — inner wrist, inner thigh, upper arm. Absorption varies significantly by individual; skin thickness, body composition, and application site all affect how much actually crosses into circulation. For women who absorb well, it’s the gentlest entry point with the easiest titration. You can adjust dose quickly. For women who don’t absorb well (like me), it produces good labs for some and nothing for others.

Subcutaneous injection is the option most intimidating to women who haven’t considered it — and the one most likely to change their minds once they understand the needle. We’re talking about a 27 to 31 gauge needle, half an inch long, going into belly fat or thigh fat. A 2017 study published in the Journal of Clinical Endocrinology & Metabolism by Spratt and colleagues confirmed that subcutaneous testosterone achieves therapeutic levels effectively, with patients strongly preferring it over intramuscular injection for comfort and convenience.

Here’s the frame shift that helps: if you have ever injected Ozempic, Wegovy, or Mounjaro — you have already done this. The GLP-1 pen needles are 31 to 32 gauge, 4 to 6 millimeters long. Subcutaneous testosterone uses a 27 to 31 gauge needle, about 12 to 16 millimeters. They’re in the same category. If you’ve pulled off a weekly Ozempic shot, the “I can’t inject myself” belief doesn’t survive the comparison. The skill set is identical.

Weekly or twice-weekly small subcutaneous injections also solve the pharmacokinetics problem — you maintain stable, steady levels rather than the spike-and-crash cycle that monthly injections guarantee.

Pellets — subcutaneous pellets inserted under the skin every three to six months — are frequently promoted at hormone clinics. I will share what Kelly Casperson says about them: “Pellets tend to run supraphysiologic and that means hair loss and side effects. You need to earn your pellet. Don’t go from zero to Mount Everest.” The practical problem is irreversibility — you cannot remove a pellet if the dose is wrong. You wait months for it to dissolve. ACOG recommends against pellets as first-line therapy. My guidance: test the hormone in a removable form first, establish that you respond well and aren’t prone to side effects, and then revisit pellets as a convenience option.

The complete side effects discussion — including clitoromegaly, voice deepening, and the hair loss question with its management options — is covered in detail in the “The side effects you deserve to know about” section above. Scroll up if you skipped ahead.

If you think you might be deficient

The symptom picture for low testosterone in women overlaps heavily with perimenopause: fatigue that sleep doesn’t fix, brain fog, low libido, difficulty building muscle despite consistent effort, low motivation, mood flatness, a reduced sense of ambition or competitive drive. If you’re in the 40-to-65 range and have several of these, it’s worth investigating.

The right labs: total testosterone, free testosterone by equilibrium dialysis, and SHBG. Tested together. Morning draw. Also useful: DHEA-S, estradiol, and FSH to see the full picture.

Find a menopause specialist rather than a general practitioner. The North American Menopause Society has a provider finder at nams.org. You are asking for off-label treatment — there is no FDA-approved product, so you need a doctor who knows how to navigate that landscape. A GP who hasn’t been trained in this territory may be unfamiliar with what’s available or uncomfortable prescribing it; a menopause specialist won’t be.

If you’ve been on oral contraceptives for years, ask specifically about SHBG and its persistence after stopping. That’s a conversation most doctors aren’t initiating. You may need to start it.

Back to the Wizard of Oz

That patient’s brain going from black and white to technicolor isn’t a metaphor. It’s mitochondria. It’s dopamine. It’s a neurohormone her body stopped making in adequate quantities, and when it was restored, her brain came back online. The cognitive flatness, the fatigue, the sense of operating at partial capacity — those are symptoms with a mechanism, not the normal price of getting older.

108 million women. Energized, focused, ambitious. Not in spite of their age, but because they are supported through it.

The question isn’t whether women deserve this. The question is why it took until 2025 for anyone in a federal hearing room to say it out loud — and then mean it.

Annette Thompson is 57, the founder of adoption.com, and a menopause advocate writing about evidence-based women’s health.

This article is educational and does not constitute medical advice. Talk to a physician before starting any hormone therapy.

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