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Can You Take Hormone Therapy With Ozempic, Zepbound, or Other Weight Loss Medications?

On November 13, 2026October 30, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

Yes, in most cases you can. Hormone therapy and weight loss medications are not forbidden together, and neither the Zepbound nor the Wegovy label lists hormone therapy as a contraindication (1,2). What changes the answer is the form of estrogen you take, your clot and gallbladder history, and what you expect the hormones to do, because they are prescribed for hot flashes, vaginal symptoms and bone loss, not for weight.

That last point trips people up, so it gets its own section first.

Does hormone therapy make weight loss drugs work better?

Maybe. The evidence is thin, and it is observational.

The first signal came from a 2024 retrospective cohort in Menopause: 16 postmenopausal women on hormone therapy and 90 not on it, all taking semaglutide. At 12 months the hormone therapy group had lost 16 percent of body weight versus 12 percent, and the gap survived adjustment for confounders (3). A Mayo Clinic cohort followed with tirzepatide. After matching, 40 women using hormone therapy were compared with 80 who were not, and at a median of 18 months the hormone therapy group had lost 17 percent versus 14 percent. Forty-five percent of them reached a loss of 20 percent or more, against 18 percent of the others (4,5).

A larger analysis presented at the 2026 Menopause Society meeting in October, led by Regina Castaneda at Mayo Clinic Florida, covered nearly 2,400 women on semaglutide and nearly 1,500 on tirzepatide. Hormone therapy was linked to greater, sustained loss with semaglutide. With tirzepatide, users lost more early, but the final difference was not statistically significant (6).

Here is where I part ways with the headlines. Women who choose hormone therapy differ from women who do not. They may sleep better once the night sweats stop, which makes diet and exercise easier, and the Mayo authors say plainly that they cannot say hormone therapy caused the extra loss (4). A Spanish Menopause Society position statement calls the association hypothesis-generating and says weight loss alone is no reason to start hormone therapy (7). A 2026 clinical review lands in the same place (5). I agree.

A randomized answer is on the way. A registered trial of 96 early postmenopausal women compares Wegovy alone, a transdermal estradiol patch with micronized progesterone alone, and the two together (8). Until it reports, treat the synergy as an interesting idea rather than a plan. Tirzepatide already works at every reproductive stage, with about 23 percent loss in the peri- and postmenopausal groups of SURMOUNT-1 against 3 percent on placebo (9).

Will a weight loss medication stop my estrogen or progesterone from absorbing?

It might for a few weeks, and the answer depends on the drug and on whether the hormone is swallowed.

GLP-1 and dual agonist drugs slow gastric emptying. With tirzepatide the delay is largest after the first dose and fades with continued use (1). That matters for anything taken by mouth. The Zepbound label tells women on oral hormonal contraceptives to switch to a non-oral method or add a barrier method for 4 weeks after starting and for 4 weeks after each dose increase, and says non-oral hormonal contraceptives should not be affected (1). The data come from one 5 mg tirzepatide dose given with a combined pill of ethinyl estradiol and norgestimate. Peak levels fell 55 to 66 percent, but total exposure fell only 20 to 23 percent, and peak time slipped 2.5 to 4.5 hours (1).

Does that apply to menopausal doses? Nobody has tested it. Lilly states there is no information on tirzepatide in people taking oral hormone replacement therapy (10). A 2026 Maturitas review looked at tirzepatide and oral progestogens specifically and called an interaction biologically plausible but unproven, noting that no pharmacokinetic data exist for the progestogens used in menopause care and that any risk would cluster around initiation and dose escalation (11). There is one published case report, a 51-year-old woman on oral estrogen whose hot flashes and mood worsened during semaglutide titration and settled when the titration was slowed (12). One case proves nothing, but it fits the mechanism.

The other drugs differ. Wegovy’s label reports no clinically significant change in ethinyl estradiol or levonorgestrel levels with semaglutide tablets at steady state, and says semaglutide injection at 1 mg weekly did not affect absorption of oral medications in its clinical pharmacology trials (2). The same label tells patients to wait at least 30 minutes after the tablet before taking any other oral medication, which in practice means the morning estradiol pill waits (2). Foundayo, the orforglipron tablet I prescribe, can be taken with or without food, yet its label also warns about delayed gastric emptying and gives the same 30-day backup advice for oral contraceptives. Lilly calls that precautionary: modeling predicted a minor drop in peak level and no change in total exposure, and no trial has measured it (13,14).

My practical read is an extrapolation, so weigh it that way. If a woman needs systemic estrogen while starting a GLP-1 or tirzepatide, a patch, gel or spray skips the stomach entirely and the question goes away. If she prefers oral estradiol, starting it is reasonable, but watch for hot flashes or breakthrough bleeding creeping back during titration, and slow the escalation before raising the estrogen, which is what resolved the one reported case. Progesterone deserves a quiet eye too. A woman with a uterus whose bleeding pattern changes at dose steps on oral progesterone should be asked about it, because protecting the lining is the progestogen’s whole job.

I start most women on transdermal estradiol, usually a 0.025 mg patch changed twice a week, and go higher if the symptoms are more disruptive. A patch bypasses the gut and carries less clotting risk than oral estrogen. If she still has a uterus, she needs endometrial protection. For most women I start with separate products, usually a low-dose estradiol patch plus micronized progesterone, because I can adjust each hormone independently. The weight loss drug can change that. I draw a distinction between semaglutide and Foundayo or tirzepatide, where the concern about oral progesterone absorption is greater because of slowed gastric emptying. With Foundayo or tirzepatide, I discuss a levonorgestrel IUD or a combined estrogen-progestin patch to avoid uncertain oral progesterone absorption. The combined patch can be prescribed by telemedicine, which is why it is the one I normally use in that situation, but its lowest strength delivers 0.05 mg of estradiol per day, twice my usual starting dose. That trade-off needs to be discussed rather than treated as an automatic choice.

At the 8 to 12 week follow-up, I adjust for symptoms, bleeding, or side effects. If she feels well, I don’t change anything. If hot flashes or night sweats persist, we may raise the estradiol one step. I don’t adjust the dose for weight loss, and I don’t check routine hormone levels.

Why the route of estrogen matters more than the brand of weight loss drug

Setting absorption aside, route changes two other risks that run high in women with obesity.

Clots first. In a UK nested case-control study of more than 80,000 women with venous thromboembolism, oral hormone therapy raised the odds by 58 percent (adjusted OR 1.58), while transdermal preparations did not (OR 0.93, 95% CI 0.87 to 1.01). Estradiol carried less risk than conjugated equine estrogen, and medroxyprogesterone combinations were worst (OR 2.10) (15). Women with obesity carry a higher baseline clot risk on their own (5), which is why a joint FIGO and World Heart Federation paper calls transdermal estrogen with micronized progesterone or dydrogesterone the safest regimen for women at high thromboembolic risk (16). That is not a reason to refuse hormones to a woman with a BMI of 38. It is a reason to reach for the patch first.

Gallbladder second, and this one is a true stacking problem. The labels for tirzepatide and semaglutide both warn about acute gallbladder disease. In the Zepbound weight trials cholecystitis occurred in 0.7 percent versus 0.2 percent on placebo, and in Wegovy injection trials cholelithiasis ran 1.6 percent versus 0.7 percent, with the excess persisting even after accounting for how much weight was lost (1,2). Foundayo’s cholelithiasis rate was 1.0 versus 0.7 percent (13). Oral estrogen piles on. An estradiol tablet label cites a 2 to 4 fold increase in gallbladder disease requiring surgery (17), and in the Million Women Study current oral users had a relative risk of 1.74 for gallbladder admission against 1.17 for transdermal users (18). Rapid weight loss itself promotes stones (2). Three pushes in one direction is a good argument for the transdermal route in any woman with gallstone history.

Do the side effects overlap?

Mostly in the stomach. In Foundayo’s pooled obesity trials, nausea ran 26 to 35 percent by dose against 10 percent on placebo, vomiting 13 to 24 percent against 4, constipation 20 to 27 against 9, and diarrhea 21 to 25 against 11, mostly during dose escalation and easing afterward (13). Oral estradiol lists nausea, vomiting, abdominal cramps and bloating among its reported effects (17). Start both in the same week and feel awful, and nobody can say which pill is responsible. Staggering the starts, or choosing a patch, keeps the picture readable.

Thyroid medication is the interaction people forget. Estrogen raises thyroid-binding globulin, so a woman on levothyroxine may need more of it (17). Oral semaglutide raised levothyroxine exposure by 33 percent in the Wegovy label (2), and a 2026 case report describes thyrotoxic over-replacement after 48 pounds of weight loss on tirzepatide (19). Opposing forces act on the same woman, so a TSH recheck a few months in is cheap insurance.

What happens to muscle and bone?

This is the part of the combination with a plausible upside, and the least data.

Weight loss on these drugs costs lean mass along with fat. In the SURMOUNT-1 DXA substudy about 75 percent of the weight lost was fat and 25 percent lean, the same split as placebo (20). A 2026 meta-analysis found a consistent drop in lean mass with GLP-1 drugs that mostly tracked the weight loss, with no significant effect on bone outcomes and low certainty about whether the lean mass change harms function (21).

Bone is the open question for postmenopausal women. In the Look AHEAD substudy of postmenopausal women with type 2 diabetes, a 14 percent fall in estradiol during intensive lifestyle weight loss mediated a decline in whole-body bone density (22). Hormone therapy has proven bone effects, and the 2022 Menopause Society statement says it prevents bone loss and fracture (23). Whether it protects bone specifically during GLP-1 weight loss has not been tested. That protection is a reasonable inference, not a finding. For muscle, a 2019 meta-analysis of 12 trials found only a nonsignificant trend toward preserved lean mass with hormone therapy (5).

So I would not start hormones to protect muscle. I would protect muscle on purpose: protein at 80 to 120 grams a day, resistance training, and a bone density scan through her primary care provider when she qualifies. I do not routinely recommend multivitamins, so the effort goes into the food and the weights. If a woman already qualifies for hormone therapy, any skeletal benefit during weight loss is a bonus.

I can’t order a DXA scan myself, so that falls to the patient’s primary care provider. I recommend one if she is old enough to qualify, has a family history, or has another clinical reason, and I suggest she ask her primary care physician for it.

Naltrexone-bupropion and menopause

I use naltrexone only as naltrexone-bupropion (Contrave) for weight, and bupropion is where the menopause questions live.

Start with symptoms. In the Contrave label’s pooled trials, hot flush occurred in 4.2 percent versus 1.2 percent on placebo, hyperhidrosis in 2.6 versus 0.6 percent, and insomnia in 9.2 versus 5.9 percent (24). Those are three things a woman with perimenopausal night sweats already has too much of. The absolute numbers are small, but in fragile sleep they count. Nausea (32.5 versus 6.7 percent) and constipation (19.2 versus 7.2 percent) overlap with GLP-1 and oral estrogen effects (24).

Then safety. Contrave is contraindicated with a seizure disorder, bulimia or anorexia nervosa, chronic opioid use, uncontrolled hypertension, and abrupt discontinuation of alcohol, benzodiazepines, barbiturates or antiepileptic drugs (24). That alcohol line matters in midlife, because a woman who uses wine to fall asleep and then quits cold to start a weight loss program is exactly who the label warns about. The label also notes increases in blood pressure and heart rate, so a home cuff reading before and after starting is reasonable (24). The Contrave label does not mention estrogen, but it asks for caution with drugs metabolized by CYP2D6, which is worth a medication-list check (24).

Bupropion and naltrexone can make it harder to sleep. For a woman who is already sleeping poorly in the middle of perimenopausal changes, I might lean toward a GLP-1 instead.

Where metformin fits

Metformin is the quiet one.

It has no FDA weight loss indication, and the effect is modest. A 2024 meta-analysis of 49 randomized trials in adults with overweight or obesity and no diabetes found a BMI reduction of about 0.56 kg/m2 against placebo, no significant difference from lifestyle modification alone, and low-quality trials overall (25). I prescribe it for weight when a GLP-1 is unwanted or unaffordable and naltrexone-bupropion is unwanted or contraindicated, always alongside diet and exercise.

Interactions are mild. The metformin label lists estrogens among drugs that tend to raise blood glucose, and long-term use can lower vitamin B12 (26). A 2025 review calls for randomized trials of metformin in perimenopausal women, since few exist (27).

Who should not combine them, or should wait?

A few situations call for pausing rather than prescribing at visit one. Unexplained vaginal bleeding comes first. The estradiol label lists undiagnosed abnormal genital bleeding as a contraindication, along with breast cancer history, estrogen-dependent neoplasia, active or past deep vein thrombosis or pulmonary embolism, recent stroke or heart attack, and liver disease (17). A personal or family history of medullary thyroid carcinoma or MEN 2 rules out Zepbound and Wegovy (1,2). A history of gallstones or pancreatitis calls for extra caution on the weight loss side, since the labels warn about both (1,2,13).

What about the boxed warning? In November 2025 the FDA announced it was removing the boxed warnings for cardiovascular disease, breast cancer and probable dementia from menopausal hormone therapy labels, while keeping the endometrial cancer warning on estrogen-alone products (28). The first six products were approved in February 2026 (29). Updates are rolling out batch by batch, and a generic estradiol tablet label posted this month still carries the older boxed language (17). The change shifts the tone of the conversation. It does not change the clot and gallbladder arithmetic above. The Menopause Society’s 2022 statement still describes a favorable benefit-risk balance for women under 60 or within 10 years of menopause onset, and a less favorable one beyond that (23).

For patients

Tell whoever prescribes your weight loss medication that you take hormones, and tell whoever prescribes your hormones what weight loss drug you are on. Those two conversations often happen on different platforms.

If you take estrogen by mouth and start a weekly injection or a pill like Foundayo, watch for hot flashes, mood swings or spotting returning in the first weeks and after each dose increase. Report it rather than assuming the hormones stopped working, and ask whether a patch, gel or spray makes sense. Know the warning signs of gallbladder trouble and clots: pain under the right ribs after eating, a swollen painful calf, sudden shortness of breath.

And do not ask for hormones to lose weight. Ask for them because your sleep, your sweats or your bones need them.

For clinicians

Three points to carry. First, the combination data are retrospective and confounded, so treat established indications as the reason to prescribe MHT and do not use it as an obesity drug (5,7). Second, default to transdermal estradiol when a woman has obesity, gallstone history or other thrombotic risk (15,16,18), and treat oral estrogen during GLP-1 titration as a time to watch for symptom recurrence, recognizing that the concern is extrapolated from contraceptive pharmacokinetics (1,11). Third, recheck TSH in anyone on levothyroxine, and ask about alcohol before prescribing bupropion (17,24).

One question colleagues ask: do the menopause and the weight get handled in the same visit? It depends on whether the patient wants to address the menopause symptoms or the weight first. The two are usually handled at separate visits. Sometimes I see the same patient for both, and sometimes a different clinician handles one of them, depending on scheduling and the patient’s preference.

The Bottom Line

Hormone therapy and weight loss medications can be taken together. The combination is plausible and not prohibited by the Zepbound or Wegovy labels, but the idea that hormones boost GLP-1 weight loss rests on small retrospective studies, and the randomized trial is still pending (3,4,7,8).

The real differences are practical. A patch or gel avoids the stomach-emptying problem behind the contraceptive advice on the Zepbound and Foundayo labels, and carries lower clot and gallbladder risk than oral estrogen, which matters because the weight loss drugs raise gallbladder risk too (1,13,15,18). Naltrexone-bupropion adds hot flashes, sweating and insomnia and is a poor fit for some midlife sleepers. Metformin changes little in either direction. Protect muscle with protein and lifting, and use hormones for menopause symptoms, not as a weight loss supplement.

Sources

ZEPBOUND (tirzepatide) prescribing information. DailyMed, Eli Lilly and Company. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=487cd7e7-434c-4925-99fa-aa80b1cc776b
WEGOVY (semaglutide) injection and tablets prescribing information. DailyMed, Novo Nordisk. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=ee06186f-2aa3-4990-a760-757579d8f77b
Weight loss response to semaglutide in postmenopausal women with and without hormone therapy use. Menopause. 2024;31(4). https://pubmed.ncbi.nlm.nih.gov/38446869/
Mayo Clinic. New study links combination of hormone therapy and tirzepatide to greater weight loss after menopause (Lancet Obstetrics, Gynaecology & Women’s Health, 2026). News release, January 22, 2026. https://www.eurekalert.org/news-releases/1113701
Clinical review: Menopause hormone therapy in weight management. Obesity Pillars. 2026 Jun. https://pmc.ncbi.nlm.nih.gov/articles/PMC13010941/
The Menopause Society. Hormone therapy may increase weight loss effectiveness of GLP-1s. Press release for the 2026 Annual Meeting. https://menopause.org/press-releases/hormone-therapy-may-increase-weight-loss-effectiveness-of-glp-1s
Incretin-based therapies in peri- and postmenopausal women with obesity: an expert position statement from the Spanish Menopause Society. Maturitas. 2026 Oct. https://pubmed.ncbi.nlm.nih.gov/42664617/
ClinicalTrials.gov NCT06715514. Effects of combined menopausal hormone therapy and GLP-1 receptor agonist therapy on glucose and energy homeostasis in early postmenopausal women with or at risk of diabetes. https://clinicaltrials.gov/study/NCT06715514
Body weight reduction in women treated with tirzepatide by reproductive stage: a post hoc analysis from the SURMOUNT program. Obesity. 2025. https://pubmed.ncbi.nlm.nih.gov/40074721/
Eli Lilly Medical. Can Zepbound (tirzepatide) be used with oral contraceptives or hormone replacement therapy? https://medical.lilly.com/us/products/answers/can-zepbound-tirzepatide-be-used-with-oral-contraceptives-or-hormone-replacement-therapy-211019
Tirzepatide and oral progestogens: a hypothesis-generating review of a biologically plausible pharmacokinetic interaction in gynaecologic disease control and menopausal hormone therapy. Maturitas. 2026 Sep. https://pubmed.ncbi.nlm.nih.gov/42721915/
Worsening vasomotor symptoms in the setting of estradiol and semaglutide: a case report. Menopause. 2025. https://pubmed.ncbi.nlm.nih.gov/40729307/
FOUNDAYO (orforglipron) tablets prescribing information. Eli Lilly and Company. https://uspl.lilly.com/foundayo/foundayo.html
Eli Lilly Medical. Can Foundayo (orforglipron) be used with contraceptives? https://medical.lilly.com/us/products/answers/can-foundayo-orforglipron-be-used-with-contraceptives-314529
Vinogradova Y, Coupland C, Hippisley-Cox J. Use of hormone replacement therapy and risk of venous thromboembolism: nested case-control studies using the QResearch and CPRD databases. BMJ. 2019;364:k4810. https://pubmed.ncbi.nlm.nih.gov/30626577/
Menopause hormone therapy in women with cardiovascular risk factors or established ischemic heart disease: a joint FIGO and WHF position paper. Global Heart. 2026. https://pubmed.ncbi.nlm.nih.gov/42799440/
Estradiol tablets, USP prescribing information. DailyMed (label posted October 2, 2026). https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=9333d92f-2585-4b99-aaea-87c01c95125e
Gallbladder disease and use of transdermal versus oral hormone replacement therapy in postmenopausal women: prospective cohort study (Million Women Study). BMJ. 2008;337:a386. https://pubmed.ncbi.nlm.nih.gov/18617493/
Thyroid dysfunction following tirzepatide use in a post-thyroidectomy patient on stable levothyroxine therapy: a case study. Cureus. 2026. https://pubmed.ncbi.nlm.nih.gov/42109981/
Body composition changes during weight reduction with tirzepatide in the SURMOUNT-1 study of adults with obesity or overweight. Diabetes Obes Metab. 2025. https://pubmed.ncbi.nlm.nih.gov/39996356/
GLP-1 receptor agonists and musculoskeletal outcomes: a systematic literature review and meta-analysis. Drugs. 2026. https://pubmed.ncbi.nlm.nih.gov/42730869/
Sex hormones mediate intensive lifestyle intervention-induced bone mineral density changes: Look AHEAD Sex Hormone Study. J Clin Endocrinol Metab. 2026. https://pubmed.ncbi.nlm.nih.gov/40576264/
The 2022 hormone therapy position statement of The North American Menopause Society. Menopause. 2022;29(7). https://pubmed.ncbi.nlm.nih.gov/35797481/
CONTRAVE (naltrexone HCl and bupropion HCl) extended-release tablets prescribing information. DailyMed. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=485ff360-32c8-11df-928b-0002a5d5c51b
The impact of metformin on weight and metabolic parameters in patients with obesity: a systematic review and meta-analysis of randomized controlled trials. Diabetes Obes Metab. 2024. https://pubmed.ncbi.nlm.nih.gov/38468148/
Metformin hydrochloride extended-release tablets prescribing information. DailyMed. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=356b02d0-d239-4441-bb33-c4c54166fcd7
Metformin use in prediabetes: a review of evidence and a focus on metabolic features among peri-menopausal women. Diabetes Obes Metab. 2025. https://pubmed.ncbi.nlm.nih.gov/40329646/
FDA. HHS advances women’s health, removes misleading FDA warnings on hormone replacement therapy. November 10, 2025. https://www.fda.gov/news-events/press-announcements/hhs-advances-womens-health-removes-misleading-fda-warnings-hormone-replacement-therapy
FDA. FDA approves labeling changes for menopausal hormone therapy products. February 12, 2026. https://www.fda.gov/news-events/press-announcements/fda-approves-labeling-changes-menopausal-hormone-therapy-products

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New Guidelines Say Estrogen Is First-Line for Hot Flashes: What Changed?

On October 23, 2026October 8, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

Yes. On October 5, 2026, the American College of Physicians published a guideline telling clinicians to start with estrogen for menopausal hot flashes and night sweats, adding a progestogen if you still have a uterus (1)(2). Antidepressants, gabapentin and the newer non-hormonal drugs move to the back-up positions for women who cannot take estrogen or do not tolerate it.

That is a clear change in tone from what many women have heard in clinic. Here is exactly what the guideline says, what it leaves open, who should still stay away from estrogen, and what to bring up at your next visit.

What the ACP actually recommended

The document is titled “Pharmacologic Treatments for Females With Menopausal Vasomotor Symptoms,” and it appeared in Annals of Internal Medicine. It is written for internal medicine physicians and other clinicians who see women in outpatient settings (1). The College built it on systematic reviews of benefit, harm, patient values and cost, graded with the GRADE method.

The structure is a three-step ladder. The wording below comes from the published abstract, since the full text was not accessible for this review (1).

First line, a strong recommendation: start estrogen plus a progestogen if the woman has a uterus, or estrogen alone if she does not. Both carry high-certainty evidence. Second line, a conditional recommendation: an SNRI, either desvenlafaxine or venlafaxine, for women with contraindications to estrogen or who do not tolerate it. Moderate-certainty evidence. Third line, also conditional, for women who cannot use or tolerate the first two: an SSRI (escitalopram or paroxetine) or gabapentin, both on low-certainty evidence, or a neurokinin receptor antagonist (elinzanetant or fezolinetant) on moderate-certainty evidence (1).

One more line from the guideline matters as much as the ladder. Clinicians are told to use informed decision-making and talk through benefits, harms, contraindications, other medical conditions, the patient’s values and preferences, cost, and whether the treatment is actually available (1)(2). The ladder is a default, not a mandate.

What the guideline did not settle

Three things do not appear in the abstract or the press release. It does not rank oral estrogen against a patch. It does not set a dose or a stopping date. And it does not say why the neurokinin drugs sit on the third rung even though their evidence is graded moderate, the same as the SNRIs (1)(2). Coverage of the full paper reports that the authors describe avoiding a start after age 60 or more than 10 years past the final period, and stopping at 3 to 5 years, as common practice rather than a formal recommendation, and that an accompanying editorial argues age over 60 should not be an absolute contraindication (3).

Why this is a bigger deal than it sounds

Menopause societies have said for years that hormone therapy is the most effective treatment for hot flashes. The Menopause Society’s 2022 position statement says exactly that, and it called the benefit-risk balance favorable for women under 60 or within 10 years of menopause onset who have no contraindications (4). So the science is not new.

What is new is who is saying it. This guideline comes from a major internal medicine society, and its stated audience is internal medicine physicians and other outpatient clinicians (1), the people who also handle blood pressure, diabetes and refills. That is my interpretation, but I think it matters: a woman who has been told “let’s try an antidepressant first” by a well-meaning primary care office now has a guideline to point to.

Context helps. The US Preventive Services Task Force gave a grade D in 2022 to hormone therapy for preventing chronic disease in postmenopausal women, and people sometimes cite that as if it covered hot flashes. It does not. The statement explicitly excludes treatment of menopausal symptoms from its scope (5). The ACP guideline is about symptoms, and that is the gap.

The regulatory ground moved too. An FDA expert panel met on July 17, 2025, and most members called the boxed warnings on estrogen outdated, though the panel took no formal vote (6). On November 10, 2025, the FDA announced it was starting to strip the boxed-warning language on cardiovascular disease, breast cancer and probable dementia from menopausal hormone products. The endometrial cancer warning stays on systemic estrogen-alone products (7). By February 12, 2026, the agency had approved revised labels for the first six products, out of 29 whose manufacturers had submitted changes (8).

The same November announcement included approval of a non-hormonal hot flash drug (7). That was elinzanetant (Lynkuet), approved October 24, 2025, for moderate to severe hot flashes in postmenopausal women (9). It blocks both NK1 and NK3 receptors (9). The ACP puts it and fezolinetant in the same third-line group (1).

Who should still not take estrogen

Estrogen is first-line, not universal. The standard US prescribing information for an estradiol patch lists these as contraindications: unexplained vaginal bleeding, current or past breast cancer, estrogen-dependent tumors, active or past DVT or pulmonary embolism, active or past arterial thromboembolic disease such as stroke or heart attack, liver impairment or disease, known clotting disorders such as protein C, protein S or antithrombin deficiency, and prior serious allergic reaction to the product (10).

That list is why the second and third rungs exist. For a woman with a prior clot or a history of breast cancer, the SNRI and neurokinin options are the real plan, not a consolation prize. In my view the gray zone (a strong family history, high blood pressure, a smoking history, a borderline cardiovascular risk estimate) is where the informed decision-making language earns its keep.

Patch or pill?

The ACP did not choose. The Menopause Society’s summary of its 2022 statement says transdermal routes and lower doses may reduce the risk of venous thromboembolism and stroke (11). Note the word “may.” I would not promise anyone a patch is risk-free. But when a woman has migraine with aura, I lean toward a low-dose transdermal estradiol. Migraine with aura rules out combined hormonal contraception, which uses much higher estrogen doses, and it does not automatically rule out menopausal hormone therapy.

Practical wrinkle: the patch has been hard to find in 2026. If you are told to start one, ask your pharmacy about supply before the visit ends.

Is there still a window, and what about age 60?

The FDA’s own framing is to start systemic therapy within 10 years of menopause onset or before age 60, with the start and the duration decided together by prescriber and patient (7). The Menopause Society says the benefit-risk balance looks less favorable beyond that window because the absolute risks of heart disease, stroke, clots and dementia are higher (4). It also says treatment need not be routinely stopped at 60 or 65 when symptoms persist, though randomized data on long use are thin (11).

My interpretation: the window is a risk gradient, not a cliff. A woman at 58 and one at 64 are not in different universes, but the 64-year-old who has never taken estrogen deserves a more careful cardiovascular conversation, and the SNRI rung may be the better first step.

I usually start with a non-hormonal option, because beginning systemic estrogen after age 60 or more than 10 years past menopause carries more cardiovascular, clotting, and stroke risk, even though age alone is not an absolute contraindication. If all of her risk factors are low, she may be offered low-dose transdermal estradiol. I refer if there is prior cardiovascular disease, a history of thrombosis, cancer, unexplained bleeding, or anything else that makes the decision less clear.

For patients and for clinicians

For patients. If your hot flashes are disrupting sleep or work, you are allowed to ask about estrogen directly. Know whether you have a uterus, because that decides whether you need a progestogen. Know your clot, stroke, breast cancer and liver history, and your family history of the same. Expect to be asked about unexplained bleeding and blood pressure. If estrogen is off the table, ask which of the second and third rung drugs fits you, and whether insurance covers it.

For clinicians. Ask about vasomotor symptoms, because some women will not raise them (3). Screen the contraindication list above before prescribing, and document the discussion the guideline asks for. A progestogen is required with systemic estrogen in a woman with a uterus. And if a patient reports bleeding after menopause or an unexplained change in pattern, evaluate it before starting anything. The label itself warns about diagnostic work-up for persistent abnormal bleeding (10).

How this plays out in a video visit

Menopause visits with me are by video and run about 45 minutes. When the history is straightforward, I prescribe at the first visit and follow up at 8 to 12 weeks. At that second visit we judge relief, bleeding and side effects and adjust the dose or the formulation.

I usually start with a generic transdermal estradiol patch at 0.025 mg per day, changed twice a week. If the hot flashes are frequent or wreck her sleep, I may start at 0.0375 mg per day. With an intact uterus, I add oral micronized progesterone: 100 mg at bedtime every night for a woman whose periods have stopped, or 200 mg at bedtime for 12 to 14 days each month for a woman who is still having periods. After a hysterectomy, progesterone is usually unnecessary.

I use a non-hormonal medication when estrogen is contraindicated, when the patient strongly prefers to avoid hormones, or when she is starting treatment after 60 or more than 10 years past menopause, especially with meaningful cardiovascular risk. An SNRI is especially useful when hot flashes travel with anxiety or depression, and I usually start venlafaxine XR at 37.5 mg daily. For isolated hot flashes, Veozah 45 mg daily or Lynkuet 120 mg at bedtime may be a better fit, though both require liver blood tests and a careful drug interaction review. Cost matters too. Generic venlafaxine is fairly inexpensive and usually covered, while Veozah and Lynkuet commonly require prior authorization.

You also need a blood pressure reading before we start. A home cuff is fine.

Questions to bring to your visit

Do I have a reason I cannot take estrogen? Do I need a progestogen? Is a patch or a pill better for my history, and can I actually get the patch this month? What bleeding is normal, and what means I should call? When do we check in, and what would make us change course? And if estrogen is not right for me, which of the other options would you pick first, and why?

The Bottom Line

The ACP now says estrogen, with a progestogen if you have a uterus, is the first treatment to consider for menopausal hot flashes, and it rates that evidence high-certainty (1)(2). SNRIs come second. SSRIs, gabapentin, elinzanetant and fezolinetant come third. Those back-up options are real, and they matter for women who cannot take estrogen.

The guideline is a default that still asks for a conversation about your history, your preferences and your access. If hot flashes are costing you sleep, bring this to your next visit.

Sources

Qaseem A, et al. Pharmacologic Treatments for Females With Menopausal Vasomotor Symptoms: A Clinical Guideline From the American College of Physicians. Ann Intern Med. October 6, 2026 (abstract). https://pubmed.ncbi.nlm.nih.gov/42832802/
American College of Physicians. ACP recommends hormonal therapy as a first-line treatment for menopausal vasomotor symptoms. October 5, 2026. https://www.acponline.org/acp-newsroom/acp-recommends-hormonal-therapy-as-a-first-line-treatment-for-menopausal-vasomotor-symptoms
Healio. ACP: Use hormone therapy as first-line treatment for menopausal vasomotor symptoms. October 5, 2026. https://www.healio.com/news/womens-health-ob-gyn/20261005/acp-use-hormone-therapy-as-firstline-treatment-for-menopausal-vasomotor-symptoms
The 2022 hormone therapy position statement of The North American Menopause Society. Menopause. 2022;29(7):767-794. https://pubmed.ncbi.nlm.nih.gov/35797481/
US Preventive Services Task Force. Menopausal Hormone Therapy: Preventive Medication. November 1, 2022. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/menopausal-hormone-therapy-preventive-medication
Patient Care. FDA advisory panel urges revised black box warnings on hormone replacement therapy. July 2025. https://www.patientcareonline.com/view/fda-advisory-panel-urges-revised-black-box-warnings-on-hormone-replacement-therapy
US FDA. HHS Advances Women’s Health, Removes Misleading FDA Warnings on Hormone Replacement Therapy. November 10, 2025. https://www.fda.gov/news-events/press-announcements/hhs-advances-womens-health-removes-misleading-fda-warnings-hormone-replacement-therapy
US FDA. FDA Approves Labeling Changes to Menopausal Hormone Therapy Products. February 12, 2026. https://www.fda.gov/news-events/press-announcements/fda-approves-labeling-changes-menopausal-hormone-therapy-products
Contemporary OB/GYN. FDA approves elinzanetant (Lynkuet) for vasomotor menopausal symptoms. October 24, 2025. https://www.contemporaryobgyn.net/view/fda-approves-elinzanetant-lynkuet-for-vasomotor-menopausal-symptoms
DailyMed. Estradiol Transdermal System (Sandoz), prescribing information. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=c714974b-766f-42f2-a846-b0c1f5a60560
Highlights From the 2022 Hormone Therapy Position Statement of The Menopause Society. https://letstalkmenopause.org/our-articles/nams-2022-hormone-therapy-position-statement

A woman seen from behind at a pharmacy counter talking with a pharmacist

Why Can’t You Get an Estrogen Patch? The 2026 Estradiol Shortage, Explained

On October 5, 2026October 5, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

Several of my patients are having a hard time filling their estradiol patches right now. Not one pharmacy being out for a week. Calling four places, getting a different strength than was prescribed, driving across town, running out before the next box arrives.

So let us go through the explanations people are offering, in order, and then what the evidence actually supports.

Hypothesis one: everyone started using them at once

This one is true, and the numbers are not subtle.

Estradiol patch prescriptions went from about 594,000 in June 2024 to 1.6 million in May 2026 (1). Among women aged 45 to 54, prescribing rose 184 percent, and by February 2026 roughly one in twenty women in that age group had an estrogen prescription (2). Patches now account for a large share of all estrogen prescriptions, and they were never the volume product the supply chain was built around.

The accelerant was regulatory. On November 10, 2025, the FDA announced it was removing the boxed warnings about cardiovascular disease, breast cancer and dementia from menopausal hormone therapy, with Commissioner Marty Makary saying the agency intended to “stop the fear machine steering women away from this life-changing, even lifesaving, treatment” (3). Those warnings had suppressed use for two decades. Pull them off, and a very large number of women who had been told no for years hear a different answer in the same month.

I wrote about that decision when it happened and I thought it was defensible. I did not expect it to empty the shelves.

Hypothesis two: something broke in manufacturing

This one is mostly false, and it is worth saying so clearly because it is the version that frightens people.

There is no recall behind this. No contamination finding, no plant shutdown, no safety problem with the patches that are reaching pharmacies. The FDA’s position, repeated through the summer, is that all the manufacturers are producing at full capacity (4).

What is true is that patches are hard to make more of quickly. A transdermal patch is a drug-in-adhesive matrix that has to deliver a precise dose through skin for three or four days. The production lines are specialized, and companies describe expansion timelines in years rather than months. Add thin generic margins, and nobody is rushing to build a new line for a product that might be a fad.

So: not a manufacturing failure. A manufacturing capacity ceiling, which is a different thing and gets solved on a much slower clock.

Hypothesis three: RFK Jr. and the administration did this

This is the one I keep seeing in comment sections, and the honest answer is more interesting than either the accusation or the denial.

There was no sabotage. Nobody restricted estrogen. If anything, this administration’s FDA pushed hormone therapy harder than any in twenty years, and the demand surge is a direct downstream consequence of that push. You cannot simultaneously argue that they suppressed access and that they promoted the drug into a shortage.

Where policy does have fingerprints is slower and less dramatic. HHS cut roughly 3,500 FDA positions in 2025 as part of a larger restructuring (5). The agency said reviewers and inspectors were protected. Reporting since has described reviewers absorbing administrative work and longer, less predictable timelines. None of that caused the shortage. All of it makes a nimble response harder, and a nimble response is exactly what a demand shock requires.

And there is a specific, consequential decision sitting right in the middle of this.

The part that actually matters: the FDA has not declared a shortage

Pharmacists have been listing estradiol patches as short since January 30, 2026. ASHP’s bulletin has grown to roughly 17 affected packages across five manufacturers, including Dotti, Lyllana, and the Noven, Sandoz, Viatris and Zydus generics (6).

The FDA has acknowledged that women are having trouble and says it is working with manufacturers to expand supply (7). It has not added the patches to its official shortage list.

That gap is not bureaucratic trivia. A formal shortage designation changes what other parties are allowed and incentivized to do. It can ease the path for additional manufacturers, it supports compounding in some circumstances, and it affects how insurers handle a prescription that has to be split across strengths or pharmacies. An Arizona gynecologist, Dr. Suzanne Hackenmiller, started a petition asking for the declaration, and Democratic members of the House have written to the agency asking the same (8).

So the fair summary of the policy question is this. The administration did not cause a shortage by restricting anything. It drove demand deliberately and then declined to use the one administrative tool that would most directly help the women it told to ask for treatment.

Two more explanations worth naming

Fragmentation makes it worse. When a patient cannot get one 0.1 mg patch, the workaround is often two 0.05 mg patches, or a different brand at a different pharmacy. Every one of those workarounds consumes more units of a constrained product and can generate a second copay. Scarcity plus substitution produces more scarcity.

Stockpiling is rational and corrosive. A woman who has been told to ration her patches will fill three months when she can get three months. I do not blame anybody for that. It also means supply reaches fewer people in any given week.

What to do if you are caught in this

First, do not simply stop. Vasomotor symptoms come back fast once estrogen is withdrawn, and the people who suffer most in a shortage are the ones who quietly go without and assume there was no alternative.

There are several, and most of them keep you on transdermal delivery, which matters if the reason you were on a patch in the first place was migraine with aura, a clot history, or anything else that argued against oral estrogen.

Gels and sprays are the closest substitute: EstroGel, Divigel, Evamist. Same route, same avoidance of first-pass liver metabolism, different daily routine. Oral estradiol is reasonable for many women and is widely available and cheap, though it is not the right swap for everyone. A different patch brand or a weekly patch instead of a twice-weekly one is often available when your usual one is not. If your symptoms are limited to vaginal dryness and painful sex, local vaginal estrogen is a different supply chain entirely and is not caught up in this.

Practical things that work: ask the pharmacy to check the strengths they do have rather than just saying no, call independent pharmacies because they order through different channels than the big chains, ask for a 90-day fill when you find stock, and have your clinician send the prescription with the substitution permitted so the pharmacist can act without a second call.

For clinicians

Write the alternative into the prescription up front. A patch prescription with no permitted substitution turns every stockout into a phone call, and in a shortage that is where the days get lost.

Know which of your patients actually need transdermal delivery rather than merely prefer it, because that determines whether oral is an acceptable bridge or a bad idea.

And counsel on the rebound explicitly. A patient who runs out and waits two weeks does not experience that as a supply problem. She experiences it as hormone therapy failing, and some of them do not come back.

The Bottom Line

The estrogen patch shortage is a demand shock, not a manufacturing failure and not a conspiracy.

The FDA removed a twenty-year-old warning, prescriptions nearly tripled in two years, and a small, low-margin, slow-to-expand corner of the generic industry could not absorb it. The policy criticism that holds up is not that anyone blocked access. It is that the agency drove the demand and has still not declared the shortage that would help unlock supply.

If you are affected, you have options, and most of them keep you on the same route of delivery. Call before you run out rather than after.

Sources

Estrogen patch shortage prompts doctors, lawmakers to seek FDA action. CBS News, September 3, 2026. https://www.cbsnews.com/news/estrogen-patch-shortage-fda-declaration-hormone-replacement-therapy/
Menopause Estrogen Patches Are in Short Supply. What Are the Alternatives? Healthline, April 15, 2026. https://www.healthline.com/health-news/menopause-estrogen-patch-shortage-after-fda-endorsement
HHS. HHS Advances Women’s Health, Removes Misleading FDA Warnings on Hormone Replacement Therapy. November 10, 2025. https://www.hhs.gov/press-room/hhs-advances-womens-health-removes-misleading-fda-warnings-hormone-replacement-therapy.html
Estrogen patches are in short supply as women seek menopause support. CNBC, June 26, 2026. https://www.cnbc.com/2026/06/26/estrogen-patches-are-in-short-supply-as-women-seek-menopause-support.html
HHS to cut 10,000 staff in major restructuring. BioPharma Dive. https://www.biopharmadive.com/news/hhs-layoffs-restructuring-kennedy-fda-cms-trump/743694/
ASHP Drug Shortage Detail: Estradiol Transdermal System. https://www.ashp.org/drug-shortages/current-shortages/drug-shortage-detail.aspx?id=1206
FDA acknowledges estrogen patch shortage, says it’s working to increase supply. Stateline, September 16, 2026. https://stateline.org/2026/09/16/fda-acknowledges-estrogen-patch-shortage-says-its-working-to-increase-supply/
FDA claims there’s no estrogen patch shortage as women struggle to get prescriptions filled. NBC News. https://www.nbcnews.com/health/womens-health/fda-estrogen-patch-shortage-hormone-therapy-alternatives-rcna344233
FDA removes menopause hormone therapy black box warnings. Harvard Health. https://www.health.harvard.edu/womens-health/fda-removes-menopause-hormone-therapy-black-box-warnings

A made bed below a bedroom window with autumn leaves visible outside in daylight

Menopause and Sleep: What Is Actually Waking You Up

On September 30, 2026September 30, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

It is almost always three in the morning. You were asleep, and then you were not, and now you are doing arithmetic about how many hours are left before the alarm.

Somewhere along the way you decided this is menopause. It might be. But I have learned not to assume that, and the reason is that four or five different problems all arrive wearing the same costume.

The first thing I ask

What does not sleeping mean for you?

Trouble falling asleep is one thing. Waking up drenched at two in the morning is another. Waking at three for no reason you can name and lying there until five is a third. Those three answers send me down three different roads, and a woman who tells me only that she is not sleeping well has not yet told me the thing I need.

So we start there, before anyone says the word estrogen.

The one I do not want to miss

Here is what surprises patients: I do not automatically blame estrogen.

Menopause genuinely does fragment sleep. It also happens to be the stretch of life when obstructive sleep apnea stops being a mostly male problem. Prevalence climbs sharply after the transition, and in some series the majority of postmenopausal women have at least some degree of it (1). Surgical menopause, after both ovaries come out, roughly doubles the risk, and early menopause raises it as well (2).

The reason it gets missed is that everyone is looking for the wrong thing. The picture in most clinicians’ heads is a heavyset man who snores like a chainsaw and whose wife has watched him stop breathing. Women often do not present that way at all. They present with fatigue, morning headaches, trouble concentrating, waking to urinate, and insomnia (3). Every one of those gets filed under hormones, or stress, or getting older.

I use STOP-BANG. Not everyone does, and I know its performance in women is not what it is in men, but I would rather run a screen that is imperfect than rely on whether somebody’s husband has mentioned snoring.

Now the honest part, and it is a limitation of how I work rather than a clinical opinion. On the platform I currently practice through, I cannot order a home sleep apnea test. I would like that to change. What I can do is recognize the pattern, tell the patient plainly what I think is going on, and get her to someone who can test her. That is not as good as ordering it myself. It is considerably better than calling it menopause and moving on.

When the hot flashes really are the problem

Sometimes the story is simple. She wakes because she is soaked, three or four times a night, and has been for a year.

When vasomotor symptoms are driving the awakenings, treating the vasomotor symptoms usually fixes the sleep. That is the cleanest version of this problem and the most satisfying to treat. Hormone therapy works. Among the non-hormonal options, elinzanetant (Lynkuet) is worth knowing about: approved October 24, 2025, it blocks NK1 in addition to NK3, and the OASIS trials picked up an effect on sleep disruption rather than only on flash frequency (4). Fezolinetant, approved in 2023, works on NK3 alone.

If somebody’s nights are being destroyed specifically by the waking rather than the flashes themselves, the drug with a sleep signal behind it is the more logical place to start.

When insomnia has taken on a life of its own

The other pattern is the one where the hot flashes have settled down, or were never that bad, and she still cannot sleep. The insomnia has detached from whatever started it and become its own condition.

For that, cognitive behavioral therapy for insomnia is first-line. Not a suggestion, not an alternative to try if the pill does not work. It is what the American Academy of Sleep Medicine and the European Sleep Research Society both put ahead of medication for chronic insomnia, and that holds for menopausal women specifically (5).

I refer out for it. We have psychologists who work with us, which makes that referral considerably easier than it is in a lot of settings. I mention that because “CBT-I is first-line” is easy to write and genuinely hard to act on when there is nobody to send people to.

What I will prescribe, and what I will not

I am conservative with sleep medication, and more so after 60.

Before I write anything I want to know what is actually breaking the sleep. Night sweats. Sleep apnea. Restless legs. Alcohol. Pain. Another medication already on the list. Fix the cause and you often do not need the hypnotic at all.

When falling asleep is the main problem and medication is warranted, I may prescribe ramelteon 8 mg. It is not controlled, weight gain is not a typical adverse effect, and it has little dependence potential. The benefit is modest, and I say so upfront rather than letting somebody discover it themselves.

Melatonin can be reasonable when the timing of sleep is part of the problem. I do not present it as a strong treatment for chronic insomnia, and more is not better. Higher doses tend to buy morning grogginess and vivid dreams without buying much additional sleep. Magnesium comes up constantly. I am comfortable discussing a cautious trial when kidney function is normal, particularly if dietary intake is low, but the evidence in insomnia is weak and I will not pretend otherwise.

The list of things I do not do is longer. I do not start chronic benzodiazepines for sleep. I generally avoid zolpidem and the other Z-drugs in older women. Diphenhydramine and doxylamine, no. Quetiapine as a sleeping pill, no. Sedating antidepressants used purely as hypnotics, no. I avoid tricyclics here too, because anticholinergic effects and weight gain are a poor trade for a modest sleep benefit.

After 60 I want the treatment to improve the next day as well. Eight hours of sedation followed by fogginess, a bigger appetite, or a fall is not successful insomnia care.

For clinicians

Three things worth holding onto.

Ask what the sleep complaint actually is before reaching for a hormonal explanation. Sleep onset, vasomotor awakenings and maintenance insomnia are different problems and the history separates them in about ninety seconds.

Screen for apnea in this population, and do not wait for a snoring history to prompt you. STOP-BANG underperforms in women relative to men, which is an argument for screening more of them rather than fewer.

And when you tell a patient CBT-I is first-line, have somewhere to send her. The recommendation is only worth what the referral pathway behind it is worth.

The Bottom Line

Menopause can genuinely wreck your sleep, and it is not the only thing that does.

Start by working out what kind of not-sleeping you have. If night sweats are waking you, treating them usually fixes the nights. If the insomnia has become its own problem, cognitive behavioral therapy comes before a prescription. And if you are exhausted, foggy, waking to urinate and getting headaches in the morning, somebody should be thinking about sleep apnea rather than writing it all off to hormones.

That last one is the one I most want not to miss.

Sources

Advances in the Diagnosis and Treatment of Obstructive Sleep Apnea in Women. https://pmc.ncbi.nlm.nih.gov/articles/PMC12992857/
Type of Menopause, Age at Menopause, and Risk of Developing Obstructive Sleep Apnea in Postmenopausal Women. American Journal of Epidemiology. https://academic.oup.com/aje/article/187/7/1370/4819319
Sleep Apnea in Women Often Missed After Menopause. Medscape. https://www.medscape.com/viewarticle/sleep-apnea-women-often-missed-after-menopause-2026a1000cri
FDA Approves Elinzanetant as First Nonhormonal Therapy for Menopause Vasomotor Symptoms. Pharmacy Times, October 2025. https://www.pharmacytimes.com/view/fda-approves-elinzanetant-as-first-nonhormonal-therapy-for-menopause-vasomotor-symptoms
Insomnia in Postmenopausal Women: How to Approach and Treat It? https://pmc.ncbi.nlm.nih.gov/articles/PMC10816958/

A wooden bedside table with a closed notebook, reading glasses, and a mug beside an unmade linen bed in soft morning window light

Should Women Take Testosterone After Menopause?

On September 11, 2026September 18, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

Update, September 18, 2026: What Came Out of the FDA Workshop

The workshop happened yesterday. Nothing was approved, and approval was never on the table. What changed was the tone. Admiral Brian Christine, the Assistant Secretary for Health, opened by calling the lack of an FDA-approved testosterone product for women “unacceptable” when Australia has one. The FDA’s own position was more measured: the approval standard is the same for every drug, data from other countries will be judged case by case, and the agency says it stands ready to review an application (10).

That last point matters most. Nothing changes for patients until a company actually files. Products made for women are already approved in the UK, Australia, New Zealand and South Africa, so the data exists. The question is whether anyone brings it here.

The science presented matched what I wrote below. Dr. Rajita Patil of UCLA’s menopause program said the evidence supports testosterone for postmenopausal women with low sexual desire and is insufficient for mood, cognition or general well-being. She also cautioned against oral testosterone because of what it does to cholesterol (10).

My own practice hasn’t changed. Until there’s an approved product I can prescribe, I refer patients out. Public comments are open until October 19, 2026.

On September 17, 2026, the FDA holds its first public workshop on testosterone use in menopausal women. It is a hybrid session, in person at the agency’s White Oak campus and online at the same time, filed under docket FDA-2026-N-5479, with the public comment period open through October 19 (1). Right now, no testosterone product is FDA-approved for use in women in the United States. Every prescription written for a woman is off-label, borrowed from a product built and dosed for men. When I think a patient would benefit, my role right now is to refer her to someone who can prescribe it, not to write it myself.

That gap has been widening for a decade, and the FDA is only now catching up to it.

Why the Agency Is Paying Attention Now

Prescribing tells the story better than any regulatory notice could. Testosterone prescriptions to women in the US rose roughly 2.6-fold between 2016 and 2025, from 50.0 to 130.8 per 100,000 eligible women (2). In 2025 alone, 90,482 prescriptions went out, up 58.7 percent from the year before. About three in five, 62.2 percent, went to women between 45 and 64. More than half, 51.2 percent, already carried at least one documented cardiometabolic risk factor (2).

Rapid off-label growth in a population that already carries meaningful cardiovascular risk, for a drug whose long-term safety in women is still not established: that combination is what put a federal workshop on the calendar.

The Evidence That Actually Holds Up

Low sexual desire is where testosterone has real trial support. A 2019 systematic review and meta-analysis by Islam and colleagues in The Lancet Diabetes & Endocrinology pooled 36 randomized controlled trials and 8,480 women (3). In postmenopausal women, testosterone significantly improved desire, arousal, orgasm, and sexual pleasure, and reduced the distress that comes with low libido. The Global Consensus Position Statement, released the same year, reached the same conclusion from a different angle: the only evidence-based indication for testosterone therapy in women is hypoactive sexual desire disorder, confirmed only after a genuine biopsychosocial assessment rules out the other usual explanations, a strained relationship, untreated depression, a medication doing this to her (4).

I put it this way when the subject came up this week:

“Low desire is where the evidence is strongest, and that alone is reason not to dismiss it. A lot of women also just feel better on it. We cannot fully explain why yet, but at a physiologic dose with honest counseling about what is proven, that is a reasonable place to stand.”

What the Data Still Cannot Explain

The same Islam review found no measurable effect of testosterone on general wellbeing, cognition, body composition, or musculoskeletal outcomes. No real change in bone density. No change in lean mass or strength. The consensus statement says it plainly: no effect on general wellbeing has been demonstrated in trials to date.

That sits awkwardly next to what a lot of women report once they are actually on it: more energy, sharper focus, a sense of being back in their own body. That reported experience deserves to be taken seriously rather than waved off, and I am not going to claim an energy or cognition benefit I cannot point to a trial for either. The evidence has not caught up to the experience yet.

What a Reasonable Dose Looks Like

The goal is a physiologic premenopausal testosterone level. The dose I would want a patient on is about one-tenth of the standard male dose of a regulated 1 percent testosterone gel, roughly 5 mg applied to the skin daily, off-label since nothing is approved for women. Pellets and high-dose injections push levels into supraphysiologic territory that a properly dosed gel does not reach. Compounded products are a different problem: no consistent evidence backs their dosing, efficacy, or safety, whatever the label promises (4).

Monitoring is not complicated. Check a baseline total testosterone level, recheck at three to six weeks to confirm the dose landed where it should, and stop by six months if there is no symptomatic benefit. Formulation matters for one specific reason: oral testosterone raises LDL cholesterol, while a transdermal patch or gel leaves the lipid panel essentially untouched. Side effects run mild and cosmetic more often than dangerous, acne and unwanted hair growth chief among them. The same 2019 review also recorded an overall increase in weight with testosterone treatment. Worth knowing if weight is already part of the conversation.

Where Estrogen Usually Fits First

Estrogen treats hot flashes, night sweats, disrupted sleep, and vaginal dryness, none of which testosterone has been shown to fix, and it has a much longer safety record behind it. When I treat patients, estrogen usually comes before testosterone.

Without a need for contraception, the regimen I reach for is transdermal 17-beta-estradiol 0.025 to 0.05 mg per day, paired with micronized progesterone 100 mg nightly, continuously, if she still has a uterus. With a need for contraception, I use continuous ethinyl estradiol 20 mcg with levonorgestrel 100 mcg daily instead. About a quarter of the women I see on video visits arrive already started on hormone therapy from somewhere else, so a fair amount of my job is auditing a regimen I did not write.

Flibanserin, sold as Addyi, is worth knowing about too. On December 15, 2025, the FDA expanded its approval to cover postmenopausal women under 65 with HSDD; before that it had only been approved for premenopausal women, since 2015 (5). It is a separate, FDA-approved option aimed specifically at low desire rather than at hormone levels.

Getting Any of This Through a Screen

Testosterone is a Schedule III controlled substance. Under the DEA and HHS telemedicine flexibilities extended through December 31, 2026, a DEA-registered practitioner can currently prescribe it after a video visit alone, with no prior in-person exam, and generally without a separate DEA registration in the patient’s state, as long as both states’ laws allow it (6, 7). That is temporary: it rests on an extension already renewed four times, and the permanent replacement, a special-registration system that would keep Schedule III drugs like this one in an easier tier than Schedule II, has been in White House OMB review since August 25, 2026 with no final version yet (8, 9).

So federal law is not what stops me right now. Some telemedicine platforms do let a DEA-registered clinician prescribe controlled substances after a video visit. The platforms I work through don’t give me that ability at the moment, so when I think a patient would genuinely benefit, I refer her to an in-person clinician who can prescribe it. If that changes, or the DEA’s pending rule settles things for good, I may be able to write it myself.

For Patients

Before a video visit about this, bring your current medications and any hormone therapy already written down. Know what has changed for you, specifically, rather than a general “I don’t feel like myself.” And say what you want treatment to do: “I want my desire back” and “I want more energy” point toward different conversations, and only one has real trial data behind it.

One red flag worth knowing: pellets. The consensus statement is direct about this. Any testosterone preparation that produces supraphysiologic levels, pellets and high-dose injections included, is not recommended, in part because there is no way to adjust or remove the dose once a pellet is implanted. If a clinic is pitching pellets alongside language about restoring youthful vitality, that is worth questioning.

For Colleagues

A total testosterone level should never be the test that diagnoses HSDD. It does not correlate reliably with symptoms; this is a clinical diagnosis built on history and distress, other causes ruled out along the way. There is no data supporting use in premenopausal women, so keep the indication where the evidence lives, and screen for cardiometabolic risk before starting anything, given how much of the current prescribing population already carries it (2).

The Bottom Line

Low desire is where the evidence for testosterone is strongest in postmenopausal women, and that alone is reason not to dismiss it. Many women report feeling better on it, and nobody can fully explain why yet. If I were prescribing, the dose would be physiologic: about one-tenth of the standard male dose of a regulated 1 percent gel, roughly 5 mg on the skin daily, and estrogen usually comes first. Right now I am not the one writing that prescription. Testosterone is a Schedule III controlled substance, and the platforms I work through don’t currently let me prescribe it, so when a patient would benefit, I refer her to an in-person clinician who can. That could change once the DEA finalizes its pending rule or my platforms add the capability. The comment window on the FDA’s workshop closes October 19, 2026.

Sources

1. FDA. Public Meeting: Testosterone Use in Menopausal Women. September 17, 2026. Docket FDA-2026-N-5479. https://www.fda.gov/consumers/womens-health-events/fda-public-meeting-testosterone-use-menopausal-women-09172026

2. Avivi I, Stuenkel CA, Sampath-Kumar R, Ben-Yehuda O. Accelerating Testosterone Prescribing for U.S. Women: Implications for Cardiovascular Safety. JACC Adv. 2026;5(6 Pt 1):102724. PMID 42095794. https://pmc.ncbi.nlm.nih.gov/articles/PMC13309321/

3. Islam RM, Bell RJ, Green S, Page MJ, Davis SR. Safety and efficacy of testosterone for women: a systematic review and meta-analysis of randomised controlled trial data. Lancet Diabetes Endocrinol. 2019;7(10):754-766. PMID 31353194. https://pubmed.ncbi.nlm.nih.gov/31353194/

4. Davis SR, Baber R, Panay N, et al. Global Consensus Position Statement on the Use of Testosterone Therapy for Women. J Clin Endocrinol Metab. 2019;104(10):4660-4666. PMID 31498871. https://pmc.ncbi.nlm.nih.gov/articles/PMC6821450/

5. Historic First in Women’s Sexual Health: FDA Grants Approval for Addyi (flibanserin) in Postmenopausal Women. BioSpace, December 15, 2025. https://www.biospace.com/press-releases/historic-first-in-womens-sexual-health-fda-grants-approval-for-addyi-flibanserin-in-postmenopausal-women

6. Fourth Temporary Extension of COVID-19 Telemedicine Flexibilities for Prescription of Controlled Substances. Federal Register, December 31, 2025. https://www.federalregister.gov/documents/2025/12/31/2025-24123/fourth-temporary-extension-of-covid-19-telemedicine-flexibilities-for-prescription-of-controlled

7. Drug Enforcement Administration, Diversion Control Division. Telemedicine: State Registration Q&A (EO-DEA192, DEA-DC-044). https://www.deadiversion.usdoj.gov/GDP/(DEA-DC-044)(EO-DEA192)_Telemed_State_Reg_QA_(Final).pdf

8. Special Registrations for Telemedicine and Limited State Telemedicine Registrations. Federal Register, January 17, 2025. https://www.federalregister.gov/documents/2025/01/17/2025-01099/special-registrations-for-telemedicine-and-limited-state-telemedicine-registrations

9. DEA Prescribing of Controlled Substances via Telemedicine. Alliance for Connected Care. https://connectwithcare.org/dea-prescribing-of-controlled-substances/

10. Mahatole S, Ananthan P. US regulators urge more research on testosterone therapy for women. Reuters (via GV Wire), September 17, 2026. https://gvwire.com/2026/09/17/us-regulators-urge-more-research-on-testosterone-therapy-for-women/

A bedside table in soft morning light with a folded linen cloth, a glass of water and two books

Vaginal Dryness After Menopause: Why It Doesn’t Go Away

On August 29, 2026September 11, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

Half the women who have it have never used a single treatment. Among the never-treated, close to three quarters have never mentioned it to a clinician. Both come from EMPOWER, a survey of 1,858 postmenopausal American women with genitourinary symptoms; most who stayed quiet assumed it was aging they had to live with (1).

That assumption is wrong in one specific way. Hot flashes usually fade. This does not.

Why the name changed in 2014

Genitourinary syndrome of menopause was coined at a 2013 ISSWSH and NAMS conference and endorsed by both boards in 2014 (2). It replaced vulvovaginal atrophy and atrophic vaginitis. Those terms implied an infection that is not there, and left out the urethra and bladder entirely (2).

Somewhere between 27% and 84%

That is the range cited by The Menopause Society and the 2025 AUA/SUFU/AUGS guideline (1)(3). A three-fold spread is less a number than a confession that case definitions vary wildly. One firmer figure: 84% of women six years past menopause had it (1).

Then the sentence that belongs on every package insert, verbatim from the 2020 position statement: “In contrast to vasomotor symptoms (VMS) that usually improve over time, GSM is generally progressive without effective therapy” (1). Generally, not always, but the direction is the point, and the 2025 guideline treats GSM as chronic (3). Untreated, it is also associated with women avoiding Pap smears (3). A complaint nobody raised becomes a screening gap.

What I can settle over video. What I can’t.

I practice entirely by telemedicine, so let me be direct about limits. The Menopause Society says diagnosis “requires the presence of both characteristic examination findings and bothersome symptoms” (1), and the 2025 guideline requires a genitourinary examination (3). No camera does that half.

Nearly everything else works remotely: the focused history, a medication review catching aromatase inhibitors and GnRH agonists, self-administered instruments like the Cervantes-GSM (3). And one free question: did the symptoms start before menopause? If so, another diagnosis is likelier (1). The mimics are the problem. Lichen sclerosus reads like GSM in a history and carries carcinoma risk. Postmenopausal bleeding I never close out on video. No guideline addresses telemedicine for GSM, so that division of labor is my own reasoning, not a society position.

So here is my position, and it diverges from the letter of the guideline. I recommend that a patient be examined in person for these symptoms. I also do not hesitate to treat her when what she describes is clearly GSM to me. The exam still needs to happen, and I say so. It does not have to happen first.

Red flags are where I hold the line. Bleeding after menopause, a visible lesion, or symptoms that predate menopause need eyes on them before anything else.

Start in the drugstore aisle

Lubricants and moisturizers get confused constantly. A lubricant goes on at the time of sex to cut friction. A moisturizer goes on a schedule, sex or no sex, to rehydrate tissue over time (1). Oil-based lubricants erode condoms. Hyaluronic acid sells at a premium with no evidence it beats products without it (1).

The humbling part. MsFLASH randomized 302 postmenopausal women to a 10-microgram vaginal estradiol tablet, a moisturizer, or dual placebo. At 12 weeks nothing beat placebo (P = .25 and .31) (4). The Menopause Society notes the placebo gel likely lubricated (1). The lesson survives: plenty improve on a drugstore moisturizer, which is why the guideline recommends them (3).

Low-dose vaginal estrogen

Most evidence, strongest recommendation (3). Vagifem (10 micrograms) and Imvexxy (4 or 10) run daily two weeks, then twice weekly; the Estring ring lasts 90 days; creams taper to two or three times weekly (1). After 14 days of daily use, serum estradiol on the inserts measured 3.6 and 4.6 pg/mL against 4.3 on placebo (1). Across 20 trials and 2,983 women exposed up to a year there was one endometrial cancer, and no progestogen is needed (1)(3).

The gap nobody advertises: the longest randomized trial of any vaginal estrogen ran 52 weeks (1), and this needs years of treatment. Reassurance past that is observational: 18 years of Nurses’ Health Study data found no excess chronic disease (5). Cochrane graded 30 trials low to moderate quality (6). Consistent direction, mediocre trials.

My own preference is the vaginal tablets. That is my preference and nothing stronger, and Cochrane found no efficacy difference between the preparations anyway (6). What decides it is what the patient prefers and what it costs her.

About that boxed warning, precisely

On November 10, 2025, FDA announced it was initiating removal of boxed warning language on menopausal hormone therapy, including low-dose vaginal estrogen, covering cardiovascular disease and breast cancer, plus probable dementia (7). The Menopause Society agreed, calling the warning a likely deterrent to a safe, effective therapy (8).

Implementation is running product by product. As of August 29, 2026, FDA’s updated-labeling list holds six drugs, and Estring is the only vaginal estrogen among them, its label updated April 27, 2026 (9)(10). Vagifem, Imvexxy and Premarin Vaginal Cream still carry the full boxed warning (11)(12)(13). Fill a prescription this week and you may find that warning in your own package. The paperwork has not caught up. Two things not to conflate: systemic estrogen-alone products keep a boxed warning for endometrial cancer, and ospemifene was never part of this action (7)(14).

DHEA, ospemifene, and the limits of systemic therapy

Vaginal DHEA (prasterone, Intrarosa) is a 6.5 mg insert used once daily, and endometrial sampling stayed inactive or atrophic in all 422 women studied for 52 weeks (1). It has never carried a boxed warning, and that predates the recent FDA action (15). Ospemifene (Osphena), the only oral option at 60 mg daily, holds the guideline’s weakest recommendation grade (3), causes hot flashes in 7.2% versus 2% on placebo (1), and its own boxed warning for endometrial cancer and cardiovascular disorders stands (14).

If you take systemic hormone therapy for hot flashes, do not assume it covers this. Some get inadequate GSM relief from it, and the guideline recommends adding local estrogen or DHEA (3). You will see percentages quoted for this. I could not trace one to a primary source, so I am not repeating one. The add-on rests on expert opinion, with no data on the combination’s risk (3).

Lasers

In a sham-controlled trial, 85 women were followed 12 months after three CO2 laser or sham treatments. Symptom severity fell 17.2 points with laser and 26.6 points with sham (16). Read that again. The point estimate favored sham, and the biopsy histology showed no difference either, so the collagen-remodeling mechanism they are sold on was never shown in tissue. The 2025 guideline calls them experimental outside trials (3), and no energy-based device is FDA-cleared for any gynecologic indication (17). Cash pay, expensive, and the widest gap between marketing and data here.

The best evidence here is about UTIs

Recurrent UTI means two culture-proven infections in six months, or three in a year (1). Vaginal estrogen for prevention is the only Grade B statement in the 2025 guideline; every other one is Grade C or expert opinion (3). Raz and Stamm, 1993: 93 postmenopausal women randomized to intravaginal estriol or placebo, infections falling to 0.5 episodes per patient-year against 5.9 (18). Estriol, oddly, is not sold as an FDA-approved product here (3), so the field’s cleanest result came from a drug Americans cannot prescribe. Pelvic floor physical therapy suits coexisting pelvic floor dysfunction, though its direct GSM evidence is one single-arm feasibility study (3).

After breast cancer, especially on an aromatase inhibitor

Aromatase inhibitors produce what the 2020 statement calls a profound estrogen-deficiency state, and severe GSM in most survivors (1). ACOG’s 2021 clinical consensus, which replaced its 2016 committee opinion: nonhormonal treatment first line; if that fails, low-dose vaginal estrogen may be used after breast cancer, including on tamoxifen, and in aromatase inhibitor users after shared decision-making between patient, gynecologist and oncologist (19). ACOG reviewed seven studies covering more than 4,000 survivors, median follow-up two to seven years, tamoxifen and aromatase inhibitor users alike, with no increased recurrence, and calls low-dose vaginal estrogen safe in women with hormone receptor-positive disease at low risk of recurrence (19).

The caution traces to one Danish cohort: 8,461 women with early ER-positive breast cancer, 1,957 of them vaginal estrogen users. Overall recurrence risk was not raised, relative risk 1.08 (95% CI 0.89 to 1.32); in the subgroup on adjuvant aromatase inhibitors it was 1.39 (95% CI 1.04 to 1.85), with no rise in mortality (20). The finding is contested; JNCI published four separate comments responding to it. It is an observational subgroup, and a 2024 meta-analysis of eight studies found no such increase (3). I will not tell you it is settled. Neither ACOG nor the urology panel did. Both put the oncologist in the room.

So who starts that conversation. She raises it with her oncologist, and I make sure that conversation starts from evidence rather than a package insert. ACOG puts that squarely on the prescriber: provide “data on the safety of low-dose vaginal estrogen to patients and their medical oncologists” (19). It matters because the warning FDA only began removing in November 2025 is still printed on three of the products named above, and an oncologist reading it has every reason to say no.

If you are the patient

Bring it up. That is the whole intervention, and most women never do. Say the words: dryness, burning, painful sex, urgency, recurring infections. Expect any prescription to work over weeks and to continue indefinitely.

Notes for clinicians

The screening question is the treatment. Asking costs thirty seconds. Two habits worth changing: stop ordering estradiol and FSH to diagnose this (3), and warn women about the boxed warning before the pharmacy does (1).

Here is mine, word for word.

“Do you experience vaginal dryness more now than you used to? Sometimes this can be a common side effect of menopause which can be related to painful intercourse.”

The Bottom Line

GSM reaches a quarter to four fifths of postmenopausal women and generally does not improve on its own. Half of affected women have never treated it, mostly because nobody asked. A drugstore moisturizer is a legitimate first step. Low-dose vaginal estrogen barely reaches the bloodstream and has 18 years of observational safety behind it, though most packages still carry a boxed warning FDA has already directed off. Lasers lost to sham. And a woman on an aromatase inhibitor deserves a real conversation with both her physicians, not a blanket no.

Sources

1. Menopause Society 2020 GSM position statement. https://menopause.org/wp-content/uploads/default-document-library/2020-gsm-ps.pdf

2. Portman DJ, Gass ML. Maturitas. 2014;79(3):349-354. https://pubmed.ncbi.nlm.nih.gov/25179577/

3. AUA/SUFU/AUGS GSM guideline, 2025. https://www.auanet.org/guidelines-and-quality/guidelines/genitourinary-syndrome-of-menopause

4. Mitchell CM, et al. MsFLASH. JAMA Intern Med. 2018;178(5):681-690. https://pubmed.ncbi.nlm.nih.gov/29554173/

5. Bhupathiraju SN, et al. Menopause. 2019;26(6):603-610. https://pubmed.ncbi.nlm.nih.gov/30562320/

6. Lethaby A, et al. Cochrane Database Syst Rev. 2016;(8):CD001500. https://pubmed.ncbi.nlm.nih.gov/27577677/

7. FDA labeling change request, 11/10/2025. https://www.fda.gov/drugs/drug-alerts-and-statements/fda-requests-labeling-changes-related-safety-information-clarify-benefitrisk-considerations

8. Menopause Society comment on the FDA announcement. https://menopause.org/press-releases/the-menopause-society-comments-on-the-fda-announcement-on-hormone-therapy

9. FDA list of MHT products with updated prescribing information. https://www.fda.gov/drugs/drug-safety-and-availability/menopausal-hormone-therapies-updated-prescribing-information

10. DailyMed, ESTRING label, Apr 27, 2026. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=110b9865-5a07-4d45-b560-e89947f12600

11. DailyMed, VAGIFEM label, Feb 12, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=e5ad3cf6-dd96-4e64-af21-c1eee38d0b88

12. DailyMed, IMVEXXY label, Sep 18, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=104be9f2-a8f6-430e-9e01-2ee7cc1861f1

13. DailyMed, PREMARIN VAGINAL CREAM label, Jun 02, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=96609623-528e-4aba-cabe-7254aed816d5

14. DailyMed, OSPHENA label, Feb 17, 2025. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9accbcc9-78ee-4f84-9b7e-704f2ab1c413

15. DailyMed, INTRAROSA label, Aug 03, 2026. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ada639d4-bac0-2ad0-e053-2a95a90afce7

16. Li FG, et al. JAMA. 2021;326(14):1381-1389. https://pmc.ncbi.nlm.nih.gov/articles/PMC8511979/

17. FDA CDRH letter to Inmode MD Ltd., July 24, 2018. https://www.fda.gov/files/medical%20devices/published/Inmode%20MD%20Lotd%20IHCTOA%20Letter.pdf

18. Raz R, Stamm WE. N Engl J Med. 1993;329(11):753-756. https://pubmed.ncbi.nlm.nih.gov/8350884/

19. ACOG Clinical Consensus Number 2, December 2021, “Treatment of Urogenital Symptoms in Individuals With a History of Estrogen-dependent Breast Cancer” (replaces Committee Opinion 659, March 2016). https://www.acog.org/clinical/clinical-guidance/clinical-consensus/articles/2021/12/treatment-of-urogenital-symptoms-in-individuals-with-a-history-of-estrogen-dependent-breast-cancer

20. Cold S, et al. J Natl Cancer Inst. 2022;114(10):1347-1354. https://pubmed.ncbi.nlm.nih.gov/35854422/

A wooden table in warm morning light with a coiled cloth tape measure, a small hand weight and a folded linen cloth

Does Menopause Cause Weight Gain, or Is It Just Aging?

On August 29, 2026September 11, 2026 By Dr. Scott RennieIn Menopause & Women's Health, Weight Loss & Metabolic HealthLeave a comment

Your weight has been climbing about a pound a year since your early forties. Then something else changed. Same body, rearranged. The jeans that caught at the hip now catch at the waist.

Aging put the weight on. Menopause moved it.

The scale was never the menopause story

The Study of Women’s Health Across the Nation tracked women through the transition with repeated DXA scans. Weight and BMI gains that begin in premenopause “continue on an unaltered trajectory” through it, then flatten after the final period (1). Menopause does not bend the weight curve. The curve was already bending.

Two SWAN numbers circulate and both are real. In the full cohort of 3,064 women aged 42 to 52, weight rose 2.1 kg over three years, about 0.7 kg a year (2). In the smaller DXA sub-cohort, inside the 3.5-year window around the final period, 0.25 kg a year (1). Call it a pound to a pound and a half a year through midlife, none of it accelerated by menopause.

Where the fat goes

In 380 SWAN women with serial DXA, visceral fat drifted down before the transition at 1.85% a year, then climbed 6.24% a year inside the transition window (95% CI 4.31 to 8.17), settling at 1.47% after (3). Android fat went from 1.21% to 5.54%; the hip and thigh depot only to 2.03%. Lean mass flips sign in the same window, from gaining 0.2% a year to losing 0.2% (1), on top of the 3% to 8% per decade women lose after 30 (4).

Waist girth, meanwhile, rises 0.55% a year before the transition and 0.96% during it (3). Visceral fat moves six times faster than the tape can see, which is why a stable BMI and an unchanged waist are not reassurance.

Your metabolism did not crash at 50

Doubly labeled water, the reference method for what a human actually burns, was applied to 6,421 people across 29 countries. Total expenditure, basal expenditure and fat-free mass were “all stable from age 20 to 60” (5). The break point for adjusted total expenditure sits at 63.0 years, and the decline after it runs 0.7% a year (5).

The estradiol-specific effect is real and modest. Forty-five premenopausal women were randomized to ovarian suppression with placebo or transdermal estradiol add-back. Resting expenditure fell 54 kcal a day on placebo and did not fall at all with estradiol (6). Fifty-four calories. Measurable. Not a collapse.

Why it happens, and how much of that is known

Less than the confidence of the explanations would suggest. Estradiol loss lowers resting expenditure, since add-back prevented it in a randomized design (6), and the redistribution is time-locked to the final period rather than to birthdays (3). Past that it thins out fast. The one randomized ovarian-suppression trial measuring body composition and free-living expenditure together, 34 women over 24 weeks, found no endpoint that differed between groups (7). The Menopause Society says estrogen regulation of energy intake and expenditure “has not been well studied,” with “a paucity of studies” on estrogen and skeletal muscle (8). Falling estradiol, rising FSH, the androgen-to-estrogen shift: nobody has sorted out which drives it.

What shows up on your labs

SWAN modeled cardiovascular risk factors two ways in 1,054 women with a natural final period, once as chronological aging and once as ovarian aging. Only total cholesterol, LDL cholesterol and apolipoprotein B jumped inside the year before and after the final period (9). Glucose, insulin, blood pressure, fibrinogen and CRP fit the plain aging model (9), and the American Heart Association agrees (10).

So insulin resistance is not independently menopause-driven, whatever you have been told. The visceral fat is menopause-linked, and visceral fat drives insulin resistance on its own. A chain, not a shortcut, and it points at different treatment.

Here is where my own practice diverges from the cohort data. I screen lipids and apoB at intake, before starting any medication for weight loss, so my trigger is the visit rather than the menopausal stage. For hormone therapy I don’t routinely order them. I give the patient the options and tell her up front that insurance sometimes will not pay for apoB or apoA testing, which turns out to be a real constraint on what actually gets drawn.

Lift something heavy, then eat enough protein to use it

101 randomized trials, 5,697 postmenopausal women. Training raised fat-free mass 0.66 kg and cut fat mass 1.27 kg, and the modalities split: resistance work won for lean mass (+0.90 kg), aerobic for fat and waist (1.94 kg, 2.30 cm) (11).

Protein partners that work rather than replacing it. In 776 postmenopausal women aged 55 and older, whey improved lower-limb lean mass and strength when paired with resistance training, and had “no significant benefit on muscle strength or lean mass” without it (12). The powder is not the intervention.

Write down 1.2 g of protein per kilogram daily, 150 minutes of moderate activity weekly, strength training twice a week (4). On an incretin, higher: 1.2 to 1.6 g/kg/d, strength work three times weekly (13).

The strongest diet trial here is a prevention trial

The Women’s Healthy Lifestyle Project randomized 535 premenopausal women, mean age 47, and followed them 54 months through the transition. The intervention group finished 0.2 lb lighter. Controls gained 5.2 lb (14). Which diet matters less: 144 centrally obese postmenopausal women randomized to an energy-restricted Mediterranean or Central European diet both lost 7.6 kg and 24.6% of visceral fat in 16 weeks, with no difference between arms (15). Choose the one you will still be doing next year.

Hormone therapy, stated precisely in both directions

A Cochrane review of 28 randomized trials and 28,559 women found no evidence that estrogen alone or estrogen with progestogen affects body weight or prevents the BMI increase normally experienced at menopause (16). That review is old, last published in 2000, and still the largest pooled analysis of that endpoint. Hormone therapy does not cause weight loss, and it does not prevent menopausal weight gain.

What it does is narrower. The Menopause Society’s own key point: hormone therapy “may help attenuate abdominal adipose accumulation and weight gain associated with the menopause transition,” and “the effect is small” (8). In the WHI, no significant slowing of weight gain and a lesser waist increase over three years (8). On muscle, systematic reviews find neither benefit nor harm (8). A 2026 review is blunt: hormone therapy “should not be marketed or prescribed for weight loss or obesity treatment” (17).

Good drug. Vasomotor symptoms, genitourinary syndrome, bone. Abdominal fat is not on that list.

My own practice, stated plainly: I don’t prescribe MHT for patients who want to lose abdominal fat.

GLP-1s and the muscle question

Menopausal status does not blunt these drugs. A post hoc SURMOUNT analysis by reproductive stage found tirzepatide produced 23% weight reduction in postmenopausal women against 3% on placebo, matching premenopausal women at 26% versus 2% (18).

Now the counterintuitive part. In the SURMOUNT-1 DXA substudy, 160 participants scanned at baseline and week 72, tirzepatide produced 21.3% weight loss, 33.9% fat mass loss and 10.9% lean mass loss (19). Of the weight lost, roughly 75% was fat and 25% lean in both the tirzepatide and the placebo arms (19). The lean loss scales with the weight lost rather than with the drug.

DXA lean mass is also not muscle. It counts water, glycogen and organ mass, and modeling puts true muscle loss nearer 10% to 15% of weight reduction in women who are not strength training (13). In a 106-patient semaglutide cohort, grip strength rose 4.1 kg at a year and sarcopenic obesity fell from 49% to 33% (20). Function can improve while the DXA number falls.

Still, nobody has published incident sarcopenia or functional outcomes for postmenopausal women on these drugs. That gap is why protein and lifting belong in the prescription.

When I start a postmenopausal patient on an incretin, the instruction is 1.6 g of protein per kilogram of body weight a day, and strength training two to three times a week. That is the top of the range the evidence supports (13), and I put it there on purpose.

What is oversold

Supplements sold for menopausal weight loss. I looked for a randomized trial of any of them showing meaningful weight or visceral fat reduction and found none. Absence of evidence in one search is not proof of absence, so put it precisely: the marketing category exists; the trial literature does not. The Menopause Society does not recommend supplements or herbal remedies even for hot flashes (21).

Hormone therapy stacked on a GLP-1. Two retrospective cohorts, no randomized trial, and the 2026 review is unambiguous: do not start hormone therapy to boost an obesity medication (17).

And one asymmetry worth getting exactly right. Treating hot flashes or insomnia in order to lose weight has no trial behind it that I can find. The reverse direction is supported: the Menopause Society recommends weight loss for vasomotor symptoms, conceding those studies are small pilots and post hoc analyses (21).

If you are the patient reading this

Stop asking whether menopause made you gain weight. Ask where it went. Your BMI can sit still while visceral fat climbs 6% a year (3), so get lipids and apoB checked around your final period (9). Then put your effort where the randomized evidence is: resistance training, and a deficit you can hold for years.

Which raises the obvious question for a practice that runs entirely over video. So here is what I actually do. Patients get a Withings scale that syncs into the chart on its own and reports weight, BMI and body fat. A blood pressure cuff syncs the same way, automatically. The waist they measure themselves, with a tape, because the scale will not catch what the tape catches. Weight and blood pressure come in at least monthly and often more frequently than that, which means the trend is visible long before an annual visit would have found it.

For the clinicians

Screening beats explaining. The window runs roughly two years before to 18 months after the final period (1), and that is when lipids move and visceral fat accelerates (3)(9). Order the panel with apoB in it, and do not reassure a woman on a stable BMI or an unchanged waist; both understate a 6.24% per year visceral gain (3). When you start an incretin, write the protein target and the strength training into the plan (13). Hormone therapy earns its place on symptoms, bone and the diabetes signal (8), and no line at all on the weight plan.

The Bottom Line

Aging adds the weight, roughly a pound and a half a year through midlife, on a curve menopause does not bend (1)(2). Menopause moves the fat, visceral gain going from minus 1.85% to plus 6.24% a year inside a 3.5-year window (3). Metabolism holds steady to 60 (5). Hormone therapy treats symptoms and bone, not weight (8)(16). What changes the outcome is lifting, protein, a deficit you can sustain, and where indicated, a medication that works as well after menopause as before (11)(18).

Sources

1. Greendale GA, et al. Changes in body composition and weight during the menopause transition. JCI Insight 2019. https://pmc.ncbi.nlm.nih.gov/articles/PMC6483504/

2. Sternfeld B, et al. Physical activity and changes in weight and waist circumference in midlife women. Am J Epidemiol 2004. https://academic.oup.com/aje/article/160/9/912/86561

3. Greendale GA, et al. Changes in regional fat distribution and anthropometric measures. J Clin Endocrinol Metab 2021. https://pmc.ncbi.nlm.nih.gov/articles/PMC8372653/

4. The Menopause Society. MenoNote: Midlife Weight Gain, 2025. https://menopause.org/wp-content/uploads/for-women/MenoNote-Weight-Gain.pdf

5. Pontzer H, et al. Daily energy expenditure through the human life course. Science 2021. https://doi.org/10.1126/science.abe5017

6. Melanson EL, et al. Regulation of energy expenditure by estradiol in premenopausal women. J Appl Physiol 2015. https://pmc.ncbi.nlm.nih.gov/articles/PMC4628992/

7. Gavin KM, et al. Ovarian suppression in premenopausal women: no change in free-living energy expenditure. Obesity 2020. https://pmc.ncbi.nlm.nih.gov/articles/PMC7653843/

8. North American Menopause Society. 2022 hormone therapy position statement. Menopause 2022. https://menopause.org/wp-content/uploads/professional/nams-2022-hormone-therapy-position-statement.pdf

9. Matthews KA, et al. Chronological aging or the menopausal transition? J Am Coll Cardiol 2009. https://doi.org/10.1016/j.jacc.2009.10.009

10. El Khoudary SR, et al. Menopause transition and cardiovascular disease risk. Circulation 2020. https://doi.org/10.1161/CIR.0000000000000912

11. Khalafi M, et al. Exercise training and body composition in postmenopausal women. Front Endocrinol 2023. https://pmc.ncbi.nlm.nih.gov/articles/PMC10306117/

12. Kuo YY, et al. Whey protein supplementation in postmenopausal women. Nutrients 2022. https://pmc.ncbi.nlm.nih.gov/articles/PMC9572824/

13. Mozaffarian D, et al. Nutritional priorities to support GLP-1 therapy for obesity. Am J Clin Nutr 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC12612741/

14. Kuller LH, et al. Women’s Healthy Lifestyle Project: results at 54 months. Circulation 2001. https://doi.org/10.1161/01.cir.103.1.32

15. Bajerska J, et al. Energy-restricted Mediterranean and Central-European diets in postmenopausal women. Sci Rep 2018. https://pmc.ncbi.nlm.nih.gov/articles/PMC6057942/

16. Kongnyuy EJ, et al. Hormone replacement therapy: weight and body fat distribution. Cochrane Database Syst Rev CD001018. https://www.cochrane.org/evidence/CD001018_hormone-replacement-therapy-has-no-effect-body-weight-and-cannot-prevent-weight-gain-menopause

17. Younglove C. Menopause hormone therapy in weight management. Obesity Pillars 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC13010941/

18. Tchang BG, et al. Weight reduction with tirzepatide by reproductive stage: SURMOUNT post hoc analysis. Obesity 2025. https://doi.org/10.1002/oby.24254

19. Look M, et al. Body composition changes with tirzepatide in SURMOUNT-1. Diabetes Obes Metab 2025. https://doi.org/10.1111/dom.16275

20. Alissou M, et al. Semaglutide, fat mass, lean mass and muscle function: SEMALEAN. Diabetes Obes Metab 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC12673431/

21. North American Menopause Society. 2023 nonhormone therapy position statement. Menopause 2023. https://menopause.org/wp-content/uploads/professional/2023-nonhormone-therapy-position-statement.pdf

A flat black rectangle lying on cream linen surrounded by sprigs of dried sage, lit by soft window light.

FDA Removes Black Box Warning From Menopause Hormone Therapy

On August 14, 2026September 11, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

Since the headlines ran, some version of the same question has been opening my video visits. “So it’s safe now, right? I saw it on the news.”

The women asking are usually a few years past their last period, sleeping badly, foggy at work, and frustrated. Somewhere along the way they were told hormones would give them breast cancer, and that was the end of the conversation. Something did change this summer. What changed is not what most people think.

The FDA did not run a new trial. No fresh outcome data landed on anyone’s desk. What happened is better described as a labeling correction: a regulatory acknowledgment that a warning written for one population had been applied, for more than twenty years, to a completely different one. That distinction is the whole story. It tells you how much permission this gives us, and it tells you exactly where the permission stops.

What Actually Happened

On November 10, 2025, HHS and the FDA announced they were initiating removal of the boxed warning from menopausal hormone therapy products containing estrogen. The specific language coming out covered cardiovascular disease, breast cancer, and probable dementia. (1) The move followed a public expert panel the agency convened in July 2025 and a comment period after that.

Then came the slower part, the part that got almost no coverage. Removing a boxed warning is not a press release. It is a product-by-product labeling supplement for every manufacturer. In February 2026, the FDA approved the first batch: labeling changes for six products spanning all four categories of menopausal hormone therapy, including systemic combination therapy, systemic estrogen alone, systemic progestogen for women with a uterus, and topical vaginal estrogen. (2) Twenty-nine companies had submitted proposed changes by that point. (2) More have been approved since.

The new labels also add something that wasn’t there before: age-specific framing, pointing toward initiation within ten years of menopause onset or before age 60 for systemic therapy. (2)

So the headline “HRT is safe now” is doing a lot of work it can’t support. The accurate version is that a warning which never fit a healthy 52-year-old with hot flashes has finally been taken off her prescription.

Why That Warning Was There In The First Place

You cannot understand the correction without understanding the error.

In July 2002, the Women’s Health Initiative stopped its estrogen plus progestin arm early. That trial had randomized 16,608 postmenopausal women with an intact uterus to conjugated equine estrogens plus medroxyprogesterone acetate or placebo. (3) The data safety monitoring board pulled the plug at 5.2 years because the global index crossed a predetermined boundary.

The relative risks made every front page in the country. Invasive breast cancer, hazard ratio 1.26. Coronary heart disease, 1.29. Stroke, 1.41. Pulmonary embolism, 2.13. (3)

What ran in far smaller type, if it ran at all, were the absolute numbers. Per 10,000 women per year of treatment: seven more coronary events, eight more strokes, eight more pulmonary emboli, eight more invasive breast cancers. Also five fewer hip fractures and six fewer colorectal cancers. (3) These are small absolute differences. “A twenty-six percent increase in breast cancer” and “eight additional cases per ten thousand women per year” describe the same finding, and only one of them ended a generation of treatment.

The estrogen-alone arm, which enrolled 10,739 women who had already had a hysterectomy, was stopped separately in 2004. That arm never showed an increase in breast cancer at all. If anything it trended the other direction. (4) The boxed warning went on both.

The dementia language came from WHIMS, the memory substudy. WHIMS enrolled women aged 65 to 79. (5) That is worth reading twice. A finding generated exclusively in women 65 and older became a printed warning handed to women in their early fifties for the next two decades.

The Trial Didn’t Study The Women Who Got The Warning

Mean age at enrollment in WHI was 63.3 years. (3)

Think about who that is. The average American woman reaches menopause around 51. A 63-year-old enrolling in the mid-1990s was, on average, more than a decade out from her final period. Many were two decades out. Most were not symptomatic, which was by design, because WHI was built as a chronic disease prevention trial and not a symptom trial. Participants were also carrying the cardiovascular risk you would expect at that age, including a substantial proportion with hypertension, obesity, and subclinical atherosclerosis nobody had imaged.

Put estrogen into an artery that already has established, possibly unstable plaque and you are not doing the same thing you do when you put estrogen into a 52-year-old’s relatively clean vasculature. That is the biological core of what became known as the timing hypothesis: estrogen appears to be protective, or at least neutral, in healthy endothelium, and potentially destabilizing in diseased endothelium.

The evidence for it isn’t a hunch.

The ELITE trial randomized 643 postmenopausal women to oral estradiol or placebo, stratified by how far out from menopause they were. In women less than six years postmenopause, estradiol significantly slowed carotid intima-media thickness progression. In women ten or more years out, it did nothing. (6) Same drug, same trial, opposite vascular story depending on when you started it.

The Danish Osteoporosis Prevention Study randomized about 1,000 recently postmenopausal women to hormone therapy or no treatment and followed them for ten years. The treated group had a lower composite rate of death, heart failure hospitalization, and myocardial infarction, with no increase in cancer, stroke, or venous thromboembolism. (7) It was open-label, which limits it, and it wasn’t powered as a cardiovascular outcomes trial. But it points the same direction.

And WHI’s own investigators, when they went back and stratified by age, found the pattern sitting in their own data. Women who started in their fifties looked different from women who started in their seventies. (8) The 18-year follow-up of both WHI arms, published in 2017, found no increase in all-cause mortality, cardiovascular mortality, or cancer mortality in either treatment group. (9)

None of this is new. ELITE published in 2016. The mortality follow-up published in 2017. The FDA’s 2025 action was a review of literature that already existed, which is exactly why calling it a labeling correction is fair. The evidence got there long before the label did.

Now The Part Nobody Is Covering: What This Does Not Do

Here is where I want to slow down, because the celebratory version of this story is going to get people hurt.

The endometrial cancer warning did not go away

The FDA explicitly did not seek removal of the boxed warning regarding endometrial cancer for systemic estrogen-alone products. (1) Unopposed systemic estrogen in a woman with a uterus causes endometrial hyperplasia and carcinoma, and the PEPI trial put hard numbers on how fast. Over three years on unopposed conjugated estrogen, 22.7 percent of women developed complex hyperplasia and 11.8 percent developed atypical hyperplasia. Every arm that included a progestogen held hyperplasia under 1 percent. (14) That risk is dose and duration dependent, it is real, and it is almost entirely preventable. Nothing in this label change touched it.

The word doing all the work in that paragraph is systemic, and it is worth slowing down on, because this is the single most muddled point in the entire subject.

Low-dose vaginal estrogen does not need a progestogen. Not for the cream, not for the ring, not for the tablet. A systematic review of 20 randomized trials covering nearly 3,000 women found endometrial cancer in 0.03 percent and hyperplasia in 0.4 percent, which is background noise, and the WHI Observational Study found no association either. (15) The Menopause Society does not recommend adding a progestogen to low-dose vaginal estrogen therapy. Neither do I. If you have a patient on Estring or a small twice-weekly dab of vaginal estradiol cream for dryness and recurrent UTIs, she does not need progesterone, and putting her on it adds side effects for no endometrial benefit.

Here is the part that trips people up. The dividing line is not oral versus topical. It is systemic versus local. A patch, a pump gel, a spray, and a compounded body cream are all systemic estrogen, and they all raise endometrial risk the same way a pill does. Transdermal delivery changes the clot risk, which I will get to in a minute. It does nothing for the endometrium. If she has a uterus and the estrogen is reaching her bloodstream at systemic levels, she needs a progestogen at an adequate dose for as long as she is on it, no matter what the delivery device looks like.

I bring it up because the compounded and direct-to-consumer market blurs exactly that line, and “cream” gets used to mean two completely different products. I have picked up patients well into a compounded systemic estradiol cream, rubbed on the inner arm at a real systemic dose, with no progestogen prescribed and nobody having mentioned that they needed one.

Removing a warning does not remove a risk

Venous thromboembolism with oral estrogen is the cleanest example. The large UK nested case-control analysis of more than 80,000 VTE cases found oral hormone therapy carried an adjusted odds ratio of 1.58 overall, with oral conjugated equine estrogen plus medroxyprogesterone acetate at 2.10. Transdermal preparations showed no increased risk. Head to head, oral was associated with roughly 70 percent higher VTE risk than transdermal. (10)

That finding should change your prescription pad, not your enthusiasm. The route matters here, and this is the one place it does. First-pass hepatic metabolism drives the procoagulant shift, and transdermal estradiol bypasses it. For a woman with obesity, a prior clot, a thrombophilia, migraine with aura, or a family history that makes you uneasy, transdermal isn’t a preference. It’s the answer.

Breast cancer risk was overstated, not erased

The 2019 Lancet collaborative reanalysis of the worldwide epidemiological evidence put it in numbers a patient can actually hold onto. For a woman of average weight starting at age 50 and using therapy for five years, the excess breast cancer incidence through age 69 is roughly one additional case per 50 users of estrogen plus daily progestogen, and about one per 200 users of estrogen alone. (11) Small. Not zero. And dose and duration dependent, which means the conversation at year eight is a different conversation than the one at year two.

For context I give patients, because context is what they are usually missing: that magnitude sits in the same neighborhood as two alcoholic drinks a day, or carrying significant excess weight after menopause. Nobody puts a black box on either of those.

This is still not a primary prevention drug

The approved indications didn’t change. Systemic hormone therapy is indicated for moderate to severe vasomotor symptoms, for moderate to severe genitourinary symptoms of menopause, for prevention of postmenopausal osteoporosis in appropriate candidates, and for hypoestrogenism from hypogonadism or primary ovarian insufficiency. That’s the list.

The USPSTF continues to recommend against menopausal hormone therapy for the primary prevention of chronic conditions, a grade D recommendation. (12) You do not start a 58-year-old on estradiol to prevent her heart attack. If the timing hypothesis eventually earns a prevention indication, it will do so through a trial designed to answer that question, and that trial has not been run.

A boxed warning coming off is not new evidence coming in

There were no new randomized trials behind the November 2025 action. The FDA reviewed what already existed and concluded the label misrepresented it. That is a real and overdue fix. It is not a discovery, and anyone selling it to you as one is probably selling you something else too.

If You’re A Patient: You Can Reopen This

If you were told no in 2009, or 2015, or honestly even in 2023, the answer you got was shaped by a warning that has since been withdrawn. You are allowed to ask again.

A few things worth knowing before that appointment.

The window matters. The risk-benefit math is most favorable for women who are generally healthy, under 60, and within about ten years of their final menstrual period. The further out from that window you are, the more carefully the decision has to be individualized, and for some women the answer will still be no.

Vaginal estrogen is a separate conversation entirely. Low-dose vaginal estrogen for genitourinary symptoms, meaning dryness, painful sex, recurrent urinary tract infections, urgency, has minimal systemic absorption. The Menopause Society specifically welcomed the boxed warning removal for these products, describing them as safe and effective for a condition that affects most menopausal women. (13) If vaginal symptoms are your issue, the systemic risk conversation largely doesn’t apply to you, and you almost certainly do not need to take progesterone alongside it.

There are still real contraindications. A history of breast cancer, an estrogen-dependent tumor, prior stroke or heart attack, active or prior venous thromboembolism, a known thrombophilia, significant liver disease, or unexplained vaginal bleeding that hasn’t been worked up. If any of those apply to you, the answer may genuinely be no, and there are non-hormonal options worth discussing, including the newer neurokinin receptor antagonists for hot flashes.

And bring specifics, even to a twenty minute video visit. How many nights a week you wake up. Whether you have stopped exercising. Whether sex hurts. Whether you are thinking about leaving a job you used to like. A recent blood pressure reading, when your last mammogram was, and what your mother’s and sister’s history looks like. Symptom burden is half the equation, and “I’m having some hot flashes” badly undersells what is usually going on.

If You’re A Colleague: How I’m Counseling Now

I practice entirely by telemedicine, so everything below happens over video, usually in one visit and a follow-up. Here is how I run it in 2026.

I start by asking what she was told before, and by whom. Roughly half of my perimenopausal and postmenopausal patients are carrying a specific prior refusal, and if I don’t surface it, it sits there and quietly undermines everything I say next.

Then I frame the decision around three questions instead of one. Is she in the window? What is her baseline cardiovascular and thrombotic risk? And what is her symptom burden, honestly measured? A woman at 52 with severe vasomotor symptoms and no risk factors is a different patient than a woman at 64 with controlled hypertension and mild night sweats. The label change does not collapse that difference.

The remote setting changes the logistics of that second question, not the standard. Before I start systemic therapy I want a blood pressure I trust, which usually means a home cuff and a few readings rather than one number she remembers from a year ago. I want her mammogram status current, her personal and family history of clot and breast cancer taken carefully rather than checkbox-style, and any abnormal bleeding evaluated in person before we go anywhere near estrogen. None of that requires me to be in the room. All of it requires me to actually ask.

Route selection is where I have gotten more opinionated. Transdermal estradiol is my default for anyone with obesity, hypertriglyceridemia, migraine with aura, gallbladder disease, or any thrombotic history, personal or family. (10) The oral versus transdermal difference in VTE risk is one of the few places in this entire discussion where we can meaningfully reduce absolute harm by changing one line on the prescription.

Progestogen goes with every uterus on systemic estrogen, and only with systemic estrogen. Micronized progesterone is my preference for the metabolic profile and possibly the breast profile, though I will say plainly that the comparative data across progestogens is observational and not as strong as some of the marketing suggests. If she is on vaginal estrogen alone, she does not get a progestogen from me.

I still ask about duration out loud, every year. Not because there is a hard stop at five years, because there isn’t one, and the old “lowest dose for the shortest duration” language has aged badly. But breast cancer risk is duration dependent (11), and the woman who has been on therapy for nine years should be making that choice consciously rather than by inertia.

And I document the shared decision making. Symptom burden, risk factors reviewed, route and rationale, progestogen plan, alternatives discussed. That note protected me before the label change and it protects me now.

One more thing, and it matters more in this setting than any other. The current news cycle is producing a wave of patients who want hormones for reasons that are not on the label. Longevity. Body composition. Cognitive performance. Telemedicine is where most of that demand is landing, and a lot of it is landing on platforms that will ship estradiol after a four-question intake form and never once ask about the uterus. I would much rather have the honest conversation about what the evidence does and does not support than have someone go around me to get a worse version of the same drug.

The Bottom Line

A warning that should never have been applied to a healthy 52-year-old with hot flashes has been removed. That is a genuine correction, and the women who were denied treatment for twenty years deserved it a long time ago.

What did not happen is a change in the underlying biology. Oral estrogen still raises clot risk. Unopposed systemic estrogen still endangers the endometrium, whatever it is delivered in. Breast cancer risk is still small, still real, still duration dependent. Hormone therapy still isn’t a preventive medication.

The label was wrong. The nuance was always right. We just get to have the conversation now without a black box sitting in the middle of the table.

Menopause Care by Telemedicine: What a Virtual Visit Can and Cannot Do

On November 6, 2025September 29, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

You are 51. You have not had a period in fourteen months, you are waking at three in the morning soaked through your shirt, and the first opening with a gynecologist near you is in March. That gap is most of the reason virtual menopause care exists.

The question comes up in the first couple of minutes of a lot of my video visits. Can this actually be done over a screen? Fair question, and the answer is mostly yes, with one category of exception that matters more than everything else on this page combined.

The diagnosis is a conversation, not a lab draw

If you are 45 or older, your periods have stopped or gone erratic, and you are having hot flashes and night sweats, the diagnosis is clinical. No blood test required. For women in that age group with typical symptoms, routine hormone testing is not recommended, and that is not a corner being cut for the sake of convenience (1).

Patients ask me to check their hormone levels constantly. Almost always they have read something first and done real work on their own, and what they are after is a number that explains why they feel the way they do.

I understand that request better than I used to. It is not really about the lab. It is about wanting proof that this is happening and that she is not imagining it.

Which is exactly why ordering it can backfire. FSH swings week to week in perimenopause, so a single value lands wherever it happens to land that morning. Hand a woman a normal result while she is exhausted and soaked at four in the morning, and you have taken away the validation she came for and given her nothing in exchange. So I tell her what the test can and cannot settle, and then I treat the symptoms, which is what she needed either way.

Under 45 is a different conversation. Early menopause and primary ovarian insufficiency change the stakes, and there I do want labs.

What I can prescribe without ever being in the room

Systemic estrogen, as a patch, gel, spray or tablet. A progestogen alongside it if you still have a uterus, because unopposed estrogen is what drives endometrial risk. Low dose vaginal estrogen for dryness and painful sex, which barely registers systemically and is the most underused prescription in midlife women’s health.

The non-hormonal side has moved recently and plenty of people have not caught up. Fezolinetant (Veozah) was approved in May 2023 and blocks the NK3 receptor (2). Elinzanetant (Lynkuet) followed on October 24, 2025, and blocks NK1 as well as NK3, which is why the OASIS trials picked up an effect on sleep disruption and not only on hot flashes. Dosing is 120 mg daily (3). Where sleep is the dominant complaint rather than the flashes themselves, the agent with an actual sleep signal behind it is the more logical place to start.

Paroxetine at 7.5 mg and gabapentin are both still reasonable, particularly for women who cannot take estrogen at all.

One boxed warning came off. One did not.

On November 10, 2025, the FDA moved to strip the boxed warnings for cardiovascular disease, breast cancer and probable dementia from estrogen-containing menopause products (4). The endometrial cancer warning on systemic estrogen-only products stayed exactly where it was, and that is the part the coverage mostly dropped.

My read is that this fixed a labeling problem rather than a science problem. Nothing underneath changed in November. What changed is that a warning drawn from a trial population averaging 63 years old had spent two decades frightening 52 year olds away from a treatment whose risk profile depends enormously on how old you are when you start it. I wrote about that separately.

The thing a video visit cannot do, and it just got harder

Bleeding after menopause needs an in-person evaluation. Not a phone call, not reassurance, not wait and see.

ACOG updated this in April 2026 and it moved in the stricter direction. Transvaginal ultrasound on its own is no longer considered adequate initial triage for postmenopausal bleeding. The recommendation now is ultrasound together with endometrial tissue sampling in most patients (5). Relying on ultrasound alone appears to miss 5 to 12 percent of cancers, and the old 4 mm endometrial thickness cutoff performed especially badly in Black women, with a sensitivity around 47.5 percent (5).

Read that number again. A triage rule that caught fewer than half the cancers in one group of women was standard practice until this year.

So when a patient tells me on video that she is a year past her last period and bleeding again, the visit stops being about hot flashes and becomes about getting her seen and scanned quickly by someone who can put instruments on the problem. That is not telemedicine failing. That is telemedicine doing the one thing it can do in that moment, which is recognizing what it is looking at and moving.

Same goes for a new breast lump, for pelvic pain, and for anything needing a speculum, an IUD, a mammogram or a bone density scan.

What the visit actually looks like

Expect questions, a lot of them. When your last period was. What the flashes are doing to your sleep and your work. Whether sex has become painful, which almost nobody volunteers unless asked directly. Your personal and family history of breast cancer, clotting, stroke and heart disease. Whether you get migraines with aura.

I will ask what your blood pressure has been running, and if you do not own a cuff I will ask you to get one, because starting systemic estrogen without knowing that number is not something I am willing to do. I will ask when your last mammogram was, and I will ask again at follow-up. The biggest failure mode in virtual menopause care is a woman who feels wonderful on therapy and quietly slides three years behind on screening.

Labs, when they are warranted, get ordered to a draw site near you. Prescriptions go to your pharmacy the same day.

For clinicians

Licensure is the whole ballgame. You need a license in the state where the patient is physically sitting during the visit, not where she gets her mail, and telehealth prescribing of estrogen is otherwise permitted across all fifty states on that basis.

On my own panel, roughly 25 percent of the women arrive already on hormone therapy started somewhere else, usually a direct-to-consumer platform. That number tells you what kind of visit you are actually having. Much of the time you are not initiating therapy, you are inheriting it, and the first job is working out what she is on, at what dose, and whether anyone ever screened her for a contraindication.

Two things worth tightening. Document the contraindication screen explicitly rather than letting it sit implicitly in the note, because the labeling change has patients arriving expecting a prescription and expecting it that day. And build a real handoff to a local gynecologist before you need one. After the April 2026 update, a postmenopausal bleeding referral carries a specific expectation about what the workup should include, and telling someone to go see somebody is not a plan.

The Bottom Line

Most of menopause care transfers to video without losing anything. The diagnosis is clinical, the history is the test, and hormone therapy, the two neurokinin antagonists and the non-hormonal alternatives can all be started and adjusted remotely by someone licensed where you are.

What does not transfer is anything needing hands. Bleeding after menopause is the one to take seriously, and as of April 2026 the standard for evaluating it went up, not down.

If you have been waiting until March to ask someone about this, you do not have to.

Sources

1. National Institute for Health and Care Excellence. Menopause: identification and management. https://www.nice.org.uk/guidance/ng23

2. U.S. Food and Drug Administration. FDA Approves Novel Drug to Treat Moderate to Severe Hot Flashes Caused by Menopause. May 12, 2023. https://www.fda.gov/news-events/press-announcements/fda-approves-novel-drug-treat-moderate-severe-hot-flashes-caused-menopause

3. FDA Approves Elinzanetant as First Nonhormonal Therapy for Menopause Vasomotor Symptoms. Pharmacy Times, October 2025. https://www.pharmacytimes.com/view/fda-approves-elinzanetant-as-first-nonhormonal-therapy-for-menopause-vasomotor-symptoms

4. U.S. Food and Drug Administration. HHS Advances Women’s Health, Removes Misleading FDA Warnings on Hormone Replacement Therapy. November 10, 2025. https://www.fda.gov/news-events/press-announcements/hhs-advances-womens-health-removes-misleading-fda-warnings-hormone-replacement-therapy

5. American College of Obstetricians and Gynecologists. ACOG Publishes Updated Guidance on Evaluation of Postmenopausal Bleeding. April 2026. https://www.acog.org/news/news-releases/2026/04/acog-publishes-updated-guidance-evaluation-postmenopausal-bleeding

Why Menopause Care Is Missing From Women’s Checkups

On November 5, 2025September 11, 2026 By Dr. Scott RennieIn Menopause & Women's HealthLeave a comment

I hear some version of the same question most weeks on video visits, patients trying to figure out whether what they’re feeling is actually menopause.

Women often come to me with vague but frustrating symptoms. Trouble sleeping. Brain fog. New anxiety. Irregular or heavy periods. Weight creeping up despite no major changes. Sometimes joint pain, palpitations, or new migraines. Many times, we both suspect something hormonal. The connection to menopause doesn’t always click right away.

Most of us were never taught to see the menopause transition as its own physiologic phase with real preventive implications, not because we don’t care. Medical training gives menopause a brief mention inside reproductive aging, with the emphasis staying on fertility, not on what happens once it ends. Patients ask me about hormone therapy, sleep, mood, or sexual changes, and more often than I’d like, I don’t feel equipped in the moment to explain what’s happening or lay out the options.

The average woman in the United States reaches menopause at about age 51, according to the Mayo Clinic (2024). The years leading up to that point, called perimenopause, can last four to eight years. Hormone levels fluctuate widely during this time. These shifts affect body temperature regulation, brain chemistry, metabolism, and cardiovascular function. Symptoms can begin well before the final menstrual period. A woman in her mid-forties may show up with new anxiety, fatigue, or night sweats. That’s an easy substitution to make instead of perimenopause, and it’s one I watch for now specifically because of how often it happens.

There are several reasons why menopause-related concerns get missed. Many women are still menstruating irregularly and do not yet think of themselves as menopausal; primary care visits are short and filled with competing priorities. The confusion that followed older studies on hormone therapy still lingers. I’d rather be direct about where I land: the newer safety data is solid, and hesitation still rooted in the old fear is outdated. Newer research from The Menopause Society and the National Institutes of Health shows clear safety and benefit for most healthy women under 60 or within 10 years of menopause onset (The Menopause Society, 2023; NIH, Office on Women’s Health, 2024).

I ask every woman in her forties about menstrual changes, hot flashes, sleep, mood, libido, and vaginal or urinary symptoms, because awareness starts with the question, not the answer. Simple questions open the door. If a patient raises the issue herself, I’d rather start the conversation than defer it to a specialist on the spot.

I lean on The Menopause Society’s practical resources and CME, and I’m working through their Menopause Society Certified Practitioner (MSCP) program myself. Reading Menopause Practice: A Clinician’s Guide or reviewing their treatment algorithms has strengthened my own confidence here. Other organizations such as the NIH, AAFP, and Cleveland Clinic also offer free CME courses and case examples.

Treatment doesn’t always mean prescribing systemic hormone therapy right away. I explain the range of choices and personalize them: for some patients that means hormone therapy, for others it’s non-hormonal medications, localized vaginal treatment, or lifestyle interventions. For a symptomatic perimenopausal patient who still needs contraception, I favor continuous combined hormonal contraceptives, since standard menopausal hormone therapy can produce breakthrough bleeding in that setting; a typical low-dose choice is ethinyl estradiol 20 mcg plus levonorgestrel 100 mcg orally once daily, often continuously. If contraception isn’t a factor, my usual starting menopausal regimen is transdermal 17-beta-estradiol 0.025 to 0.05 mg/day plus micronized progesterone 100 mg nightly, continuously, if the uterus is present. Weight-bearing exercise, protein intake, and good sleep remain foundational regardless of what else we add. My job is to know the options well enough to guide that discussion, and to know when a referral actually helps more than I can.

When menopause management becomes part of preventive care, patients feel seen and supported. It becomes a normal part of the health conversation, the same as colon screening or cholesterol management; I try to keep these discussions inside the relationship I already have with a patient, rather than routing her to someone new for something I can manage myself.

Menopause represents a turning point for cardiovascular, metabolic, and bone health, and recognizing it early is a real opportunity to prevent disease later. My honest read on where primary care gets this wrong: it’s decades-old caution about hormone therapy that the newer data no longer supports, not a lack of caring. Women deserve clinicians who treat that caution as outdated and prescribe with the confidence the evidence now allows.

Does hormone therapy make weight loss drugs work better?

Will a weight loss medication stop my estrogen or progesterone from absorbing?

Why the route of estrogen matters more than the brand of weight loss drug

Do the side effects overlap?

What happens to muscle and bone?

Naltrexone-bupropion and menopause

Where metformin fits

Who should not combine them, or should wait?

For patients

For clinicians

The Bottom Line

Related Reading

Sources

What the ACP actually recommended

What the guideline did not settle

Why this is a bigger deal than it sounds

Who should still not take estrogen

Patch or pill?

Is there still a window, and what about age 60?

For patients and for clinicians

How this plays out in a video visit

Questions to bring to your visit

The Bottom Line

Related Reading

Sources

Hypothesis one: everyone started using them at once

Hypothesis two: something broke in manufacturing

Hypothesis three: RFK Jr. and the administration did this

The part that actually matters: the FDA has not declared a shortage

Two more explanations worth naming

What to do if you are caught in this

For clinicians

The Bottom Line

Related Reading

Sources

The first thing I ask

The one I do not want to miss

When the hot flashes really are the problem

When insomnia has taken on a life of its own

What I will prescribe, and what I will not

For clinicians

The Bottom Line

Related Reading

Sources

Update, September 18, 2026: What Came Out of the FDA Workshop

Why the Agency Is Paying Attention Now

The Evidence That Actually Holds Up

What the Data Still Cannot Explain

What a Reasonable Dose Looks Like

Where Estrogen Usually Fits First

Getting Any of This Through a Screen

For Patients

For Colleagues

The Bottom Line

Related Reading

Sources

Why the name changed in 2014

Somewhere between 27% and 84%

What I can settle over video. What I can’t.

Start in the drugstore aisle

Low-dose vaginal estrogen

About that boxed warning, precisely

DHEA, ospemifene, and the limits of systemic therapy

Lasers

The best evidence here is about UTIs

After breast cancer, especially on an aromatase inhibitor

If you are the patient

Notes for clinicians

The Bottom Line

Related Reading

Sources

The scale was never the menopause story

Where the fat goes

Your metabolism did not crash at 50

Why it happens, and how much of that is known

What shows up on your labs

Lift something heavy, then eat enough protein to use it

The strongest diet trial here is a prevention trial

Hormone therapy, stated precisely in both directions

GLP-1s and the muscle question