Sara Szal MD
Susan came to see me when she was 48. Mid-way through our first consultation at my medical office, she lowered her voice the way patients do when they’re about to confess something they’ve decided is shameful: “I just don’t think about sex anymore.”
She seemed relieved to share this disclosure with me.
I had questions. No period for 10 months. No hot flashes. She was taking hormone therapy with estrogen and progesterone and had no contraindications. Sex wasn’t painful, she wasn’t angry at her husband. Twenty-four years together, three kids raised, a mortgage nearly paid off, and she still loved him. She just felt somewhat dead inside, not depressed, but not really alive either.
Somewhere in her 40s, sex fell off the map. Her husband would flirt or reach for her in bed and her first thought was never desire, it was logistics: what time is it, did I answer that email, how early do I have to get up?
She used to be a woman who fantasized, who noticed a stranger across a restaurant, and felt something register below the neck. Now: nothing.
“Right now I feel like I could go the rest of my life without sex,” she explained, then paused, “but I don’t want to be that woman.”
Low sexual desire isn’t automatically a disease. Plenty of women are content wanting less, but Susan wasn’t one of them. She missed her erotic side, as did her husband. For years, it was causing her distress.
We walked through the usual suspects: relationship strain, sleep, stress, medication, mood, estrogen status, vaginal pain and dryness, thyroid, the exhaustion of caregiving for children and/or aging parents, the cognitive tax of running a household and a career. We all know desire is nuanced and there’s not a simple on/off switch.
Her testosterone was also low.
When you look at the scientific literature on women and testosterone, you find that a single blood level of testosterone doesn’t diagnose low sexual desire, and no threshold reliably distinguishes women with diminished libido from those without it.
Testosterone’s relationship to female desire isn’t a simple dose-response the way it is in men; that distinction matters more than people think, and I’ll come back to it. That’s why I check the level anyway, as one input among several.
Susan had the clinical picture, the distress, and a lab value that added one more piece to the puzzle. We talked about hormone therapy generally — I usually recommend starting with estrogen and progesterone for at least six weeks before adding anything else, which she’d already completed. Then we talked about whether to add a testosterone cream or gel: the risks, benefits, and alternatives.
This is the very moment where women’s medicine still embarrasses itself. There’s no FDA-approved testosterone product for women in this country, so I go outside FDA-approved guidance and prescribe what the evidence supports, not just what the agency has sanctioned.
We didn’t chase the number; we treated the whole picture. Within a few months, Susan came back and told me she recognized herself again. Susan’s story isn’t unusual, and the system built around it may finally be catching up.
The status of testosterone for women over 40 may begin to change today as the FDA’s Office of Women’s Health (OWH) and Center for Drug Evaluation and Research (CDER) offer a public hybrid workshop on Testosterone Use in Menopausal Women. You can watch it here for free, from 9 am to 4:30 pm ET.
Men have gels, patches, injections, a new oral pill, and pellets, an entire testosterone shelf, all FDA approved [1]. They have at least 16 options at last count.
Women have zero. There is not a single testosterone product formulated for a woman’s body that has FDA approval in the United States [1].
I have prescribed testosterone to women for 30 years. Every continuing medical education lecture I give on this subject opens with a slide disclosing that the use is off-label. I have read that slide probably 500 times to audiences of clinicians.
Today as the FDA holds their public workshop on that exact question, I’ve been weighing that same evidence in my exam room for decades.
I prescribed Susan a physiologic dose of transdermal testosterone. She had to get it from a compounding pharmacy. Her insurance didn’t cover it, so she paid out of pocket for a hormone her own body used to make for free.
Four weeks later she came back smiling before I could ask any questions.
“I’m thinking about sex again. I feel more alive.”
Her erotic mind had come back online. She started noticing attractive men again. Standing in her kitchen, she caught a glimmer of wanting her husband, and told me about it with the stunned look of someone who found precious jewelry she thought was gone for good.
Nothing about her marriage changed in those four weeks. Her husband hadn’t become more charming. Her inbox was still a battleground.
Susan had changed, or something that already belonged to her had come back within reach, perhaps on different terms.
Medicine taught generations of women to look everywhere for the cause of low desire except the endocrine system. I believe we ask marriages to solve what is sometimes a physiology problem, and ask women’s psychology to compensate for what medicine doesn’t bother to investigate.
Reducing desire to a hormone would be as incomplete as pretending the hormone has nothing to do with it.
Earlier I said no threshold reliably predicts when a woman’s libido collapses. I want to be specific about what that means, because this is exactly where a normal lab result gets used to dismiss a real complaint.
The Endocrine Society’s own guideline is direct about this point. Neither epidemiologic nor clinical studies have found a lower limit of androgens, or their precursors, that reliably identifies diminished sexual function. In their data, nonhormonal variables predicted the severity of low sexual interest and desire, which we used to call hypoactive sexual desire disorder (HSDD). Women with HSDD did not have measurably different serum testosterone than women without it [2].
The newest primary data agree. The Australian Women’s Midlife Years Study, published in 2026, checked this directly. After adjusting for other factors, no hormone was associated with sexual desire or desire difficulty. The study’s own conclusion: these hormones shouldn’t be part of the routine workup for a woman’s sexual concerns [3].
Here is the messay part. A 2022 meta-analysis did find a modest association between total testosterone and desire at the population level [4]. This is real. Population signal and individual diagnostic threshold are different instruments, built for different jobs. Confusing them is how a normal-range lab result gets used to wave off a legitimate complaint.
In my patients, I look for a free or total testosterone in the lower half of the reference range. That’s what I was taught to do, in the absence of data, and to explain to a woman as part of a consent process, that we could run an n-of-1 experiment to see if raising her testosterone within the physiologic range might help her libido.
Other researchers like Rosemary Basson have found the cortisol and DHEA, a precursor to testosterone, can predict HSDD, in a study of 275 women, so I check those hormones too [17] if the patient can afford it.
Female sexual function draws on the nervous system, hormones, physical health, relationship, history, and culture all at once. A single number was never going to carry that much weight [5,6], but it’s a place to start.
The global consensus among endocrine and menopause societies holds that hypoactive sexual desire disorder, HSDD, is the only evidence-based indication for testosterone in women [5].
Physiologic-dose transdermal testosterone improves satisfying sexual events, desire, arousal, and orgasm in postmenopausal women with HSDD, and eases the distress that comes with it [5,7].
It hasn’t been shown to improve mood, cognition, bone density, muscle mass, or general wellbeing at physiologic doses [5].
If someone offers you a body recomposition and a personality upgrade with testosterone, find a new provider who is more evidence informed.
Here is the sentence I want you to remember. The longest safety data we have on physiologic-dose testosterone in women runs only 24 months [5].
So every reassuring thing I’m about to tell you carries that limitation.
Within that window, transdermal physiologic dosing shows no meaningful effect on lipids (oral testosterone is a different story and isn’t recommended) [5], no significant short-term effect on blood pressure, glucose, or A1c [5], and only a nonsignificant clotting trend, confounded by concurrent estrogen use [5].
Two large claims-database studies looked at cardiovascular outcomes in women on testosterone and landed in opposite places.
One found lower rates of major cardiac events, clotting, and breast cancer.
The other found higher rates of cardiovascular disease, coronary disease, and stroke [8,9]. Neither is a randomized trial.
Both carry the kind of bias that makes closely monitored patients look protected and broader, less-selected populations look harmed [8,9].
A 2026 analysis using three separate statistical methods found no difference in heart attack, stroke, or sudden cardiac arrest with testosterone use, and the clotting signal seen in simpler comparisons disappeared once confounding was accounted for [10].
I read these conflicting data as a reason for vigilance, not a reason for confidence in either direction. I don’t use testosterone in women with elevated baseline cardiometabolic risk and I monitor everyone closely with the tests I described last month.
The patients I worry about are not the ones on a careful physiologic dose. They are the women on pellets, and the women with PMOS, formerly known as PCOS, whose androgen levels run high before treatment even starts.
Supraphysiologic testosterone, by any delivery method, was never the goal of the evidence above and isn’t what it was built on [5].
Compounded pellets in particular produce unpredictable, often supraphysiologic levels, and I don’t recommend them [5]. If your clinician can’t tell you your testosterone level before and during treatment, ask why not.
Women ask me regularly whether testosterone will help them hold onto muscle in midlife. My honest answer is we do not know for sure, not at the dose I prescribe.
At physiologic, HSDD-range dosing, guideline-level trial data show no significant effect on lean body mass or strength [5]. The anabolic effect is real, but it shows up mainly at doses well above the physiologic female range.
What I advise is to get adequate protein, at least 100 grams per day, and higher if you’re trending toward sarcopenia, take creatine at 5 to 10 grams per day, lift heavy, and read this essay on the topic. Testosterone may help at the upper half of the physiological range, but we don’t know for sure.
A young-women’s trial using roughly five times the physiologic testosterone level produced measurable muscle-fiber hypertrophy and a rise in protein synthesis [11,12], and the same dose-response pattern shows up in the athletic-performance research on why supraphysiologic testosterone counts as a competitive advantage [13].
One newer observational study links higher endogenous testosterone to lower rates of sarcopenia in postmenopausal women [14], which is suggestive rather than proof.
The Endocrine Society’s own guideline concedes the musculoskeletal evidence base in women is small and underpowered [2]. I don’t prescribe testosterone to build muscle. Of every claim in this essay, this is the one where the evidence is thinnest and my confidence is lowest. We simply need more data.
If you want to explore the topic of female sexuality and testosterone, I am hosting a Master Class for paid subscribers on Wednesday, September 30th, 11 AM PT / 2 PM EST, for 90 minutes: The Vagina Makeover: Tissue, Hormones, Spirit. You can become an annual subscriber for $99 (expires tomorrow), and founding members can submit questions in advance through September 20th. We will send the link to paid subscribers and founding members the day before and when we go live.
Quick summary, since I just handed you two claims back to back that sound like they contradict each other. Testosterone’s only proven benefit in women is sexual desire. Testosterone can also increase muscle mass. Both are true. Neither cancels the other. They describe two different doses and not different facts [2,5].
At the physiologic, HSDD-range dose guidelines endorse and I prescribe, desire improves and muscle mass doesn’t move [2,5,15]. Raise the dose into supraphysiologic territory, and muscle accrual becomes real, along with the androgenic and virilizing risk that comes with it [2,5]. I read a muscle change in a patient on testosterone as a potential sign the dose has drifted somewhere I didn’t intend it to go [2,16].
More than a thousand people wrote to the FDA before today’s workshop even opened. As of this writing, 1,124 public comments sit on the docket, mine among them. So 1,124 people didn’t wait to be asked to testify for or against testosterone.
I don’t know what today’s panel will decide. I know what I’m hoping for: an approved option, so women stop paying out of pocket for compounded products of uneven quality. Clear guidance that keeps dosing physiologic instead of supraphysiologic. And an acknowledgment, on the record, that desire loss in women has a biological substrate worth treating, not just a psychology worth managing.
Tell me in the comments what you hope comes out of today’s meeting, and what your own experience with testosterone, or a doctor who wouldn’t discuss it, has been. Kindly let me know if you want another post, the one where I walk through exactly how I dose and monitor testosterone in my own practice. Comments are open everyone and I read every single one.
xo, Dr. Sara
Notes
[1] U.S. Food and Drug Administration. “Testosterone Information.” fda.gov.
[2] Wierman ME, et al. “Androgen Therapy in Women: A Reappraisal: An Endocrine Society Clinical Practice Guideline.” Journal of Clinical Endocrinology and Metabolism, 2014.
[3] Wang Y, et al. “Associations Between Testosterone and Pre-Androgens and Sexual Function; Findings From the Australian Women’s Midlife Years Study.” Fertility and Sterility. 2026 Sep 1. PMID: 42167520.
[4] Maseroli E, Vignozzi L. “Are Endogenous Androgens Linked to Female Sexual Function? A Systematic Review and Meta-Analysis.” The Journal of Sexual Medicine. 2022;19(4):553–568. PMID: 35227621.
[5] Davis SR, et al. “Global Consensus Position Statement on the Use of Testosterone Therapy for Women.” Journal of Clinical Endocrinology and Metabolism, 2019.
[6] Committee on Practice Bulletins—Gynecology. “Female Sexual Dysfunction: ACOG Practice Bulletin Clinical Management Guidelines for Obstetrician-Gynecologists, Number 213.” Obstetrics and Gynecology, 2019.
[7] Davis SR, et al. “Testosterone for Low Libido in Postmenopausal Women Not Taking Estrogen.” New England Journal of Medicine, 2008.
[8] Agrawal P, et al. “Testosterone Therapy in Females Is Not Associated With Increased Cardiovascular or Breast Cancer Risk: A Claims Database Analysis.” Journal of Sexual Medicine, 2024.
[9] Lopez DS, et al. “Testosterone Replacement Therapy in Relation With Cardiovascular Disease in Cisgender Women and Transgender People.” Journal of Clinical Endocrinology and Metabolism, 2023.
[10] Vo TT, et al. “Effect of Exogenous Testosterone on Cardiovascular, Cerebrovascular, and Thromboembolic Adverse Events: Results of Three Complementary Research Designs.” American Journal of Epidemiology, 2026.
[11] Horwath O, et al. “Fiber Type-Specific Hypertrophy and Increased Capillarization in Skeletal Muscle Following Testosterone Administration in Young Women.” Journal of Applied Physiology, 2020.
[12] Smith GI, et al. “Testosterone and Progesterone, but Not Estradiol, Stimulate Muscle Protein Synthesis in Postmenopausal Women.” Journal of Clinical Endocrinology and Metabolism, 2014.
[13] Hunter SK, et al. “The Biological Basis of Sex Differences in Athletic Performance: Consensus Statement for the American College of Sports Medicine.” Translational Journal of the ACSM, 2023.
[14] Osmancevic A, et al. “Endogenous Sex Hormones, Sex Hormone-Binding Globulin, and Muscle Health: Insights Into Sarcopenia and Sarcopenic Obesity From the Women’s Health Initiative.” Menopause, 2026.
[15] Davis SR. “Sexual Dysfunction in Women.” New England Journal of Medicine, 2024.
[16] Kling JM. “Testosterone for the Treatment of Hypoactive Sexual Desire Disorder in Perimenopausal and Postmenopausal Women.” Obstetrics and Gynecology, 2025.
[17] Basson R, et al. “Dehydroepiandrosterone and Cortisol as Markers of HPA Axis Dysregulation in Women With Low Sexual Desire.” Psychoneuroendocrinology. 2019.
