Author: Dr. Scott Rennie

I am board certified by the American Board of Obesity Medicine and the American Board of Family Medicine. I am also an active member of The Menopause Society. I am located in Nevada, licensed to practice medicine in all 50 U.S. states and Guam. My focus is on providing expert medical care with personalized service in the realms of telemedicine, weight loss, urgent care, primary prevention, and whole-body wellness. In obesity medicine I prescribe medication when it is the right fit for the patient, alongside nutrition, activity and dietary changes tailored to the individual.

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Does Mounjaro Lower Your Risk of Heart Attack and Stroke?

On September 18, 2026September 18, 2026 By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

On August 28, 2026, the FDA approved a new use for Mounjaro (tirzepatide): lowering the risk of cardiovascular death, nonfatal heart attack, and nonfatal stroke in adults with type 2 diabetes who are at high risk for those events (1). That is a real change written into the drug’s FDA-approved label. The short version is this: tirzepatide matched, but did not beat, a diabetes drug that already had proven heart benefits of its own. Whether that counts as exciting news depends on what you were expecting going in.

What the Label Now Says

Mounjaro’s original approval covered blood sugar control in adults, later extended to children age 10 and up with type 2 diabetes in December 2025 (3). The new cardiovascular indication sits on top of that one. It reads, in the FDA’s language, as lowering the risk of major adverse cardiovascular events, meaning cardiovascular death, nonfatal heart attack, or nonfatal stroke, in adults with type 2 diabetes who are already at high risk for those events (1, 2). That population matters: this approval is specific to people with type 2 diabetes who already carry meaningful cardiovascular risk, largely established atherosclerotic disease.

An outcomes indication like this one is a different category of claim than glycemic control. It says the drug changed what happens to a person’s heart and vessels over years, something a lab value at three months cannot tell you on its own. That distinction is the entire reason a cardiovascular outcomes trial exists.

The Trial Behind It

The approval rests on SURPASS-CVOT, a randomized, double-blind trial that enrolled more than 13,000 adults with type 2 diabetes and established atherosclerotic cardiovascular disease across 640 sites in 30 countries (4). Participants were assigned to tirzepatide, titrated up to 15 mg weekly or their highest tolerated dose, or dulaglutide (Trulicity) 1.5 mg weekly, followed for a median of roughly four years. Dulaglutide was not a placebo. A drug with its own proven cardiovascular track record from the REWIND trial, chosen deliberately as a harder comparator than sugar water.

The primary outcome, a composite of cardiovascular death, heart attack, or stroke known as three-point MACE, occurred in 12.2 percent of the tirzepatide group and 13.1 percent of the dulaglutide group. That is a hazard ratio of 0.92, with a 95.3 percent confidence interval of 0.83 to 1.01 (4). Tirzepatide met the prespecified bar for noninferiority (p=0.003). It did not meet the bar for superiority (p=0.09). Read plainly: tirzepatide did not fall behind a drug already known to protect the heart, and it numerically edged ahead, but the trial cannot say with statistical confidence that it beat dulaglutide on this endpoint.

Two other numbers are worth knowing even though they sit outside the approved claim. All-cause mortality was 16 percent lower with tirzepatide than with dulaglutide, hazard ratio 0.84, 95 percent confidence interval 0.75 to 0.94, per Lilly’s topline results release (5). And the weight difference was large: about 11.6 percent body weight reduction with tirzepatide against 4.5 percent with dulaglutide (4), which tracks with everything already known about how the two drugs differ on that front. Neither of those numbers was the tested primary endpoint, so treat them as suggestive rather than proven.

I do not read this trial as evidence that tirzepatide is the better heart drug. I read it as evidence that choosing tirzepatide over an active cardioprotective comparator costs you nothing on the cardiovascular side, while it still outperforms on weight and blood sugar. That is a useful thing to know, and it is a smaller claim than the headlines will make it sound.

Where This Leaves Ozempic, Wegovy, and Zepbound

Semaglutide already has cardiovascular outcomes data of its own, built from different comparators and different populations, which matters when you start comparing hazard ratios across trials. SUSTAIN-6 tested injectable Ozempic against placebo in type 2 diabetes at high cardiovascular risk and found a hazard ratio of 0.74 (6). Ozempic tablets, oral semaglutide, picked up their own cardiovascular indication in October 2025 based on the SOUL trial, hazard ratio 0.86, in a population with type 2 diabetes and atherosclerotic disease, chronic kidney disease, or both, broader than “established cardiovascular disease” alone (7). Wegovy’s SELECT trial went further still: adults with overweight or obesity and established cardiovascular disease, no diabetes required at all, hazard ratio 0.80 against placebo (8).

Four trials went into these numbers, each built around its own comparator and its own patient population. Lining the hazard ratios up side by side and picking a winner overstates what any single number can tell you. SURPASS-CVOT is the only one of the four tested against an active drug with its own proven benefit, a harder bar to clear even when the resulting number looks smaller.

Zepbound carries no such indication yet. Zepbound and Mounjaro are the same molecule, tirzepatide, at the same doses. The difference is entirely regulatory. Mounjaro is approved for type 2 diabetes, and its new cardiovascular claim comes from a trial that specifically enrolled people with diabetes. Zepbound is approved for obesity and, separately, moderate to severe obstructive sleep apnea. Its own cardiovascular outcomes trial, SURMOUNT-MMO, is still enrolling, expected to include roughly 15,000 adults with obesity who do not have diabetes, and has not reported results (9). Tirzepatide’s heart benefit currently exists on the books only under the Mounjaro name, for a population that has diabetes.

For Patients

If you have type 2 diabetes and known heart disease and you are already doing well on dulaglutide, this trial should reassure you. Superiority was not shown, so nothing in the data requires a change if your current regimen is working. If your blood sugar or weight has been harder to manage, this approval gives your clinician a documented, FDA-recognized reason to discuss tirzepatide.

Coverage is worth asking about directly. An outcomes-based indication sometimes changes how an insurer’s prior authorization process treats a drug, because it can be framed as reducing a documented risk of death rather than only managing a lab value. That is not guaranteed, and formularies vary by plan. Ask specifically whether this new indication affects your prior authorization, rather than assuming it automatically will.

Patients on my video visits do ask about switching from semaglutide to tirzepatide after news like this. I tell them to stay on semaglutide if it’s working. Superiority was not shown here, so a regimen that is already working has no data forcing a change.

The Practical Question for Prescribers

For a patient with type 2 diabetes and established cardiovascular disease, tirzepatide’s larger effect on weight and A1c, paired with a trial showing it keeps pace on cardiovascular safety against an already-protective drug, makes a reasonable case for choosing it first. That is my opinion, and it deserves the caveat the superiority test earned: the point estimate favored tirzepatide, but the confidence interval did not exclude the possibility of no difference at all.

The active-comparator design is also worth sitting with. Because there was no placebo arm, SURPASS-CVOT cannot independently quantify tirzepatide’s benefit against doing nothing. It borrows dulaglutide’s REWIND-established benefit and shows tirzepatide keeps that benefit intact. Proving a brand new benefit from scratch would have required a placebo arm, and this trial did not have one.

When type 2 diabetes is the indication, I prescribe Mounjaro.

The Bottom Line

Tirzepatide gives up nothing on heart safety when measured against a drug that already protects the heart, and it does more for weight and A1c along the way. That is the real result of SURPASS-CVOT, even though the trial stopped short of proving superiority: the noninferiority bar was met (p=0.003), the superiority bar was not (p=0.09). If you have type 2 diabetes and heart disease, ask your prescriber whether tirzepatide fits your regimen better than what you are on now, and ask whether this new indication changes what your insurer will approve. The August 28, 2026 approval gives that conversation a documented reason to happen (1).

Sources

1. FDA approves Lilly’s Mounjaro (tirzepatide) to reduce cardiovascular risk in adults with type 2 diabetes. Eli Lilly and Company, August 28, 2026. https://investor.lilly.com/news-releases/news-release-details/fda-approves-lillys-mounjaro-tirzepatide-reduce-cardiovascular

2. FDA Expands Tirzepatide Label to Reduce Cardiovascular Risk in Type 2 Diabetes. AJMC. https://www.ajmc.com/view/fda-expands-tirzepatide-label-to-reduce-cardiovascular-risk-in-t2d

3. FDA approval letter, supplement 215866/S-039 (pediatric type 2 diabetes indication, age 10 and older). U.S. Food and Drug Administration, December 19, 2025. https://www.accessdata.fda.gov/drugsatfda_docs/appletter/2025/215866Orig1s039ltr.pdf

4. Cardiovascular Outcomes with Tirzepatide versus Dulaglutide in Type 2 Diabetes (SURPASS-CVOT). New England Journal of Medicine, December 2025. PMID 41406444. https://pubmed.ncbi.nlm.nih.gov/41406444/

5. Lilly’s Mounjaro (tirzepatide), a GIP/GLP-1 dual agonist, demonstrated cardiovascular protection in landmark head-to-head trial. Eli Lilly and Company, July 31, 2025. https://investor.lilly.com/news-releases/news-release-details/lillys-mounjaro-tirzepatide-gipglp-1-dual-agonist-demonstrated

6. Marso SP, Bain SC, Consoli A, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes (SUSTAIN-6). N Engl J Med. 2016;375:1834-1844. https://www.nejm.org/doi/full/10.1056/NEJMoa1607141

7. McGuire DK, Marx N, Mulvagh SL, et al. Oral Semaglutide and Cardiovascular Outcomes in High-Risk Type 2 Diabetes (SOUL). N Engl J Med. 2025. https://www.nejm.org/doi/full/10.1056/NEJMoa2501006

8. Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes (SELECT). N Engl J Med. 2023;389:2221-2232. PMID 37952131. https://pubmed.ncbi.nlm.nih.gov/37952131/

9. Tirzepatide for Reduction of Morbidity and Mortality in Adults with Obesity (SURMOUNT-MMO). ClinicalTrials.gov, NCT05556512. https://clinicaltrials.gov/study/NCT05556512

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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/

An amber prescription bottle tipped over on a pale wooden table with pink and white antibiotic capsules spilling out, beside a folded paper card, in bright window light

You Probably Are Not Allergic to Penicillin

On August 31, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

About one in ten Americans carries a penicillin allergy in their chart (1). When those people are actually tested, the large majority are not allergic.

That gap is one of the most consequential unforced errors in medicine, and almost nobody goes back and checks.

Where the label usually comes from

Most penicillin allergy labels were applied in childhood, by someone who is no longer involved, based on something that happened once.

The classic story is a rash during a course of amoxicillin at age four. Here is the problem with that story. Viral illnesses cause rashes. Children with viral illnesses get prescribed antibiotics. When a rash appears on day three, the antibiotic is the thing everyone is looking at, so the antibiotic gets the blame and the label goes in the chart. It never comes out.

The other common origins are a family member’s allergy transferred onto the patient, and side effects filed as allergy. Nausea is not an allergy. Diarrhea is not an allergy. A yeast infection is not an allergy. They are all reasons to dislike a drug and none of them are reasons to avoid it for life.

Even genuine allergy fades. IgE-mediated penicillin sensitivity wanes over time, and a substantial proportion of people who really were allergic at twenty are not allergic at fifty.

The label is not free

This is the part I want to land, because people assume that avoiding penicillin is the cautious choice and therefore the safe one.

It is not. Blumenthal and colleagues followed 64,141 adults carrying a penicillin allergy label against 237,258 matched comparators for a mean of six years (2). The people with the label had an adjusted hazard ratio of 1.69 for MRSA and 1.26 for Clostridioides difficile.

The mechanism is not mysterious, and the authors show it. Those patients received far more of the alternatives: macrolides at over four times the rate, clindamycin at nearly four times, fluoroquinolones at twice (2). Those drugs do more collateral damage to the gut and select harder for resistance. The excess MRSA and C. difficile were mediated by that substitution.

So the label does not sit there harmlessly. It quietly buys worse antibiotics for the rest of a person’s life.

There is a score for this, and it runs on history alone

The thing that changed my thinking here is that you do not need a skin test to identify most of the people who are low risk. You need four questions.

PEN-FAST was derived and validated by Trubiano and colleagues (3). It scores like this:

Five years or fewer since the reaction: 2 points. Anaphylaxis or angioedema, or a severe cutaneous adverse reaction: 2 points. Treatment required for the episode: 1 point.

A score under 3 means low risk. In the derivation cohort, only 17 of 460 low-risk patients tested positive, giving a negative predictive value of 96.3 percent (3).

Read the criteria again and notice what is not in them. No skin prick. No specific IgE. No blood work at all. Every input is something the patient tells you.

That is why this belongs in a conversation rather than a laboratory, and it is why I think most clinicians could be doing more of this than they are.

What I actually do with this on a video visit

I ask everyone about allergies before I prescribe anything. That part is unremarkable. What is worth describing is what happens next, because it is where most of these labels give themselves away.

When somebody tells me they are allergic to amoxicillin, I ask what the reaction was.

Two answers come back more than any others. The first is that they do not really remember, because they were a baby and their parents told them. The second is some version of “I think I am allergic because my mom is.”

Neither of those is an allergy history. The second one is not even about the patient.

Here is where I part company with the enthusiastic version of this argument. A person who is sick today and needs an antibiotic today is not in a good position to test a theory about their own immune system. If there is any real concern about anaphylaxis in what I am hearing, I do not push it. I pick something else and move on, and I am comfortable with that.

I also do not send people off for an oral challenge as a matter of course. That is a real procedure with a real indication, and routing every vague childhood label into an allergy clinic is not a good use of anyone’s afternoon.

What I do instead is tell them the label is worth reopening properly, and that the time to do it is when they are well rather than in the middle of an infection. It belongs with whoever manages their ongoing care, in a visit where nobody is waiting on a prescription.

The distinction matters. The label deserves to be examined. The examination should not happen while someone is sick and I am trying to treat them.

What a real reaction looks like, and what has changed about treating it

None of the above applies to someone who has had a genuine severe reaction. Anaphylaxis, angioedema, or a severe cutaneous adverse reaction such as Stevens-Johnson syndrome or DRESS means the label stays. Those people are not candidates for de-labeling and should not be challenged.

Worth knowing what has changed on the treatment side. For decades the only option for anaphylaxis outside hospital was an intramuscular auto-injector. There is now an FDA-approved epinephrine nasal spray, neffy, the first intranasal adrenaline product to reach the market (4). Pharmacokinetic studies show plasma concentrations comparable to or exceeding intramuscular injection, and, counterintuitively, nasal congestion does not appear to impair absorption (5).

I mention it because needle avoidance is a real reason people leave their epinephrine at home, and a device you will actually carry beats a better device you will not. If someone genuinely needs to carry epinephrine and the needle is the barrier, that conversation is now worth having.

It does not change the rule that epinephrine is the treatment and antihistamines are not.

For patients

If your penicillin allergy dates from childhood and you cannot remember what happened, it is worth reopening. Ask specifically to be assessed rather than mentioning it in passing, because in passing it stays in the chart.

Before that conversation, work out three things: roughly when it happened, what you or your parents remember seeing, and whether anyone treated it. That is most of the assessment.

Raise it when you are well. A visit for an infection is the wrong moment, because whoever is treating you needs to choose an antibiotic today and will reasonably play it safe. Bring it to a routine appointment instead, when nobody is waiting on a prescription.

If you have taken amoxicillin, Augmentin or any similar antibiotic since the original reaction and were fine, say so early. It is the single most useful thing you can tell your clinician.

And if your reaction involved breathing trouble, swelling of the face or throat, or a blistering rash, the label is real and it stays.

For colleagues

PEN-FAST costs four questions and identifies low-risk labels at the point of care with a negative predictive value of 96.3 percent (3). We are not short of the tool. We are short of anyone taking ownership of the conversation.

Frame it as a safety intervention rather than a convenience one, because it is. The hazard ratios in the Blumenthal cohort are for MRSA and C. difficile, not for inconvenience (2).

And ask the question that costs nothing: has this person taken a penicillin since. A meaningful share of these labels fall over on that answer alone.

The Bottom Line

Roughly ten percent of people carry a penicillin allergy label and most of them are not allergic, usually because a childhood viral rash got blamed on an antibiotic. The label is not harmless. Carrying it is associated with a 69 percent higher risk of MRSA and a 26 percent higher risk of C. difficile, driven by the broader antibiotics used instead. Four questions, scored as PEN-FAST, identify most low-risk labels without any testing at all, which makes this one of the few things in medicine that is fixed by a conversation. If your reaction was anaphylaxis, angioedema or a blistering rash, the label stays and you keep your epinephrine, which now comes as a nasal spray as well as an injector.

Sources

1. Shenoy ES, Macy E, Rowe T, Blumenthal KG. Evaluation and management of penicillin allergy: a review. JAMA. 2019;321(2):188-199. PMID 30644987. https://pubmed.ncbi.nlm.nih.gov/30644987/

2. Blumenthal KG, Lu N, Zhang Y, Li Y, Walensky RP, Choi HK. Risk of meticillin resistant Staphylococcus aureus and Clostridium difficile in patients with a documented penicillin allergy: population based matched cohort study. BMJ. 2018;361:k2400. PMID 29950489. https://pubmed.ncbi.nlm.nih.gov/29950489/

3. Trubiano JA, Vogrin S, Chua KYL, et al. Development and validation of a penicillin allergy clinical decision rule. JAMA Intern Med. 2020;180(5):745-752. PMID 32176248. https://pubmed.ncbi.nlm.nih.gov/32176248/

4. Hernandez-Trujillo V, Tachdjian R, et al. Successful administration of neffy (epinephrine nasal spray) by patients and caregivers. Ann Allergy Asthma Immunol. 2026. PMID 42476303. https://pubmed.ncbi.nlm.nih.gov/42476303/

5. Takahashi K, Yanagida N. Intranasal adrenaline: a new treatment for anaphylaxis. Pediatr Allergy Immunol. 2026;37(3):e70316. PMID 41796069. https://pubmed.ncbi.nlm.nih.gov/41796069/

Two empty medical vials and syringe beside an illustrated human brain

Does the Shingles Vaccine Lower Dementia Risk? What the Evidence Shows

On August 30, 2026August 31, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

I wrote about shingles here in 2012. Back then the vaccine question was simple and slightly boring: there was one shot, it worked reasonably well, and most people over 60 were told to consider it.

The question I get now is different. People do not ask me whether the shingles vaccine prevents shingles. They ask whether it protects the brain.

That is a fair question, the evidence behind it is more interesting than most vaccine headlines, and it has a catch in it that almost nobody reporting on it mentions.

Start with the boring part, because it is the part that matters

Shingles is the chickenpox virus waking up. It sat in a nerve root for decades and then came back out along that nerve, which is why the rash arrives in a band on one side and stops at the midline.

The rash heals. The nerve pain is the problem. Postherpetic neuralgia is burning, electric pain in the same distribution that can outlast the rash by months, occasionally years, and it is genuinely difficult to treat once it settles in. That, not the rash, is the reason to care about this.

The current vaccine is Shingrix, given as two doses. In the ZOE-50 trial across more than 15,000 adults aged 50 and over, efficacy against shingles was 97.2 percent (1). In ZOE-70, in adults 70 and older, it was 89.8 percent, and in the pooled analysis of everyone over 70 across both trials, efficacy against postherpetic neuralgia specifically was 88.8 percent (2).

Those are very good numbers. Vaccines rarely perform like that in the age group where you most want them to work.

It is a reactogenic shot. Roughly one in six people feels properly unwell for a day or two after a dose, sore arm, tired, achy, sometimes feverish. I tell people that in advance, because a person who was warned takes the second dose and a person who was ambushed does not.

The dementia finding, and the catch

Here is where it gets interesting.

In 2025, a group at Stanford published a study in Nature that used an accident of Welsh policy (3). When Wales rolled out the shingles vaccine, eligibility was set by exact date of birth. Anyone born before 2 September 1933 was ineligible, permanently. Anyone born on or after that date was eligible.

Think about what that creates. A person born on 1 September 1933 and a person born on 3 September 1933 are, on average, identical in every way that matters. Same generation, same health, same everything. The only systematic difference between them is that one could get the vaccine and one could not. Uptake went from 0.01 percent in the group one week too old to 47.2 percent in the group one week younger.

That is as close to a randomized trial as you will ever get out of routine health records without running one.

Over seven years, the vaccinated group had a 3.5 percentage point lower probability of a new dementia diagnosis, which works out to a 20 percent relative reduction (3). The effect was stronger in women. The authors then reproduced it in a separate population using death certificates rather than diagnoses, which guards against the finding being an artifact of who happens to get diagnosed.

Now the catch.

Wales was using Zostavax, the old live-attenuated vaccine. That product was withdrawn from the US market in November 2020. It is not what you would be offered today, and the study does not tell you what Shingrix does.

A separate group looked at exactly that, using the rapid switchover from live to recombinant vaccine as its own natural experiment, and found the recombinant vaccine associated with a 17 percent increase in dementia-free time, about 164 extra days without a diagnosis among those who went on to be diagnosed, over six years (4). Again larger in women. I will note, because they note it, that the senior author consults for the manufacturer, and that GSK had no involvement in the study and did not know about it until after acceptance.

What I actually think about it

I think the signal is real and I do not think it should be the reason you get the shot.

Those are compatible positions. The dementia work is observational in design even when it is cleverly built, the mechanism is unproven, and no randomized trial has tested it. Something could still be wrong with it. Meanwhile the case for Shingrix rests on two large randomized controlled trials showing it prevents a disease that causes months of nerve pain, and that case was already sufficient on its own.

So my framing is this. Get it because postherpetic neuralgia is miserable and largely preventable. If the dementia finding holds up, you will have gotten that for free.

What the finding does change is urgency. I used to be relaxed when someone in their early fifties wanted to put it off a few years. I am less relaxed now, because if there is a neurological benefit it presumably accrues with time, and there is no advantage to waiting.

The part that belongs to my day job

Most of my practice is metabolic, and shingles turns out to sit closer to that than it looks.

A meta-analysis of sixteen studies put the risk of shingles in people with diabetes at a pooled relative risk of 1.38 compared with the general population (5). A separate population cohort found that people with diabetes had roughly 1.45 times the risk of postherpetic neuralgia, and that when they got it, it tended to be more severe and more persistent (6).

So the group most likely to get shingles, and most likely to be left with lasting nerve pain afterward, overlaps heavily with the group I see for weight and glucose.

There is a second reason this matters in diabetes that has nothing to do with the vaccine. Postherpetic neuralgia and diabetic peripheral neuropathy feel similar, they get treated with the same drugs, and I have seen the second diagnosis absorb the first. If burning pain shows up in a band, on one side, in a person who also has stocking-glove neuropathy, that is shingles until proven otherwise, whatever the chart already says.

Age 50 is also, not coincidentally, right in the middle of the menopause transition, which is the other half of what I do. If a woman is already in front of me talking about hormone therapy and bone density, the shingles vaccine is a reasonable thing to raise in the same visit, and often nobody has.

If you already have it, the clock is the thing

Antivirals for shingles work best started within 72 hours of the rash appearing. After that the benefit falls off steeply.

That single fact is the strongest argument I know for handling suspected shingles by video. A one-sided painful band of blistering rash with a burning prodrome is one of the more recognizable things in medicine, and a decent photograph plus a history usually settles it. The bottleneck has never been diagnostic difficulty. It has been how long it takes to be seen, and a visit you can get this afternoon beats a better visit on Thursday.

Two exceptions I do not manage remotely. A rash near or in the eye, particularly on the tip of the nose, needs same-day ophthalmology because of the risk to the cornea. Shingles in someone significantly immunocompromised, or a disseminated rash crossing the midline, goes in person.

For patients

If you are 50 or over, you are eligible for Shingrix regardless of whether you remember having chickenpox, and regardless of whether you had the old vaccine years ago.

If you are immunocompromised, the recommendation starts at 19 (7).

Expect to feel rough for a day after each dose, and get the second one anyway. One dose is not the regimen.

If a painful one-sided rash appears, get seen inside three days. Do not wait to see whether it spreads.

For colleagues

The dementia data is worth knowing and worth describing accurately. The strongest causal design was done on a product no longer sold in the United States, and patients who have read a headline usually have not been told that.

Diabetes belongs on the list of reasons to push the vaccine actively rather than mention it in passing.

And check the vaccine history of the metabolic patients. Nobody owns this conversation, so it tends not to happen. I have started treating it as part of the same visit rather than something to refer out, and it costs about ninety seconds.

The Bottom Line

Shingrix prevents shingles about 97 percent of the time in adults over 50, and it prevents postherpetic neuralgia, which is the thing actually worth avoiding. A natural experiment in Wales found 20 percent less dementia over seven years in vaccinated adults, and a second study suggests the current recombinant vaccine carries a similar signal, but the strongest of that evidence came from a live vaccine the United States no longer uses. Get the vaccine for the nerve pain it reliably prevents rather than the dementia it might. If you have diabetes, your risk of both shingles and lasting nerve pain afterward is meaningfully higher, which moves this up the list. And if a one-sided painful rash turns up, the antiviral window is 72 hours.

Sources

1. Lal H, Cunningham AL, Godeaux O, et al. Efficacy of an adjuvanted herpes zoster subunit vaccine in older adults. N Engl J Med. 2015;372(22):2087-2096. PMID 25916341. https://pubmed.ncbi.nlm.nih.gov/25916341/

2. Cunningham AL, Lal H, Kovac M, et al. Efficacy of the herpes zoster subunit vaccine in adults 70 years of age or older. N Engl J Med. 2016;375(11):1019-1032. PMID 27626517. https://pubmed.ncbi.nlm.nih.gov/27626517/

3. Eyting M, Xie M, Michalik F, et al. A natural experiment on the effect of herpes zoster vaccination on dementia. Nature. 2025;641(8062):438-446. PMID 40175543. https://pubmed.ncbi.nlm.nih.gov/40175543/

4. Taquet M, Dercon Q, Todd JA, Harrison PJ. The recombinant shingles vaccine is associated with lower risk of dementia. Nat Med. 2024;30(10):2777-2781. PMID 39053634. https://pubmed.ncbi.nlm.nih.gov/39053634/

5. Huang CT, Lee CY, Sung HY, et al. Association between diabetes mellitus and the risk of herpes zoster: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2022;107(2):586-597. PMID 34536279. https://pubmed.ncbi.nlm.nih.gov/34536279/

6. Wen SY, Ou-Yang C, Hsu CY, et al. Impact of type 1 versus type 2 diabetes on developing herpes zoster and post-herpetic neuralgia: a population-based cohort study. Acta Derm Venereol. 2023;103:adv9400. PMID 37787418. https://pubmed.ncbi.nlm.nih.gov/37787418/

7. Anderson TC, Masters NB, Guo A, et al. Use of recombinant zoster vaccine in immunocompromised adults aged 19 years and older: recommendations of the Advisory Committee on Immunization Practices. MMWR Morb Mortal Wkly Rep. 2022;71(3):80-84. PMID 35051134. https://pubmed.ncbi.nlm.nih.gov/35051134/

A folded white towel beside a plain bar of soap in a ceramic dish and a safety razor on a sunlit wooden bathroom shelf

Why Do I Keep Getting Boils?

On August 29, 2026August 30, 2026 By Dr. Scott RennieIn Skin & Wound CareLeave a comment

“Boil” is not a diagnosis. It is a word patients use for a painful lump that came up, hurt, and either drained or had to be opened. Underneath that one word sit at least four different problems with four different answers, and the reason people keep getting them is usually that nobody has said which one they have.

So the useful question is not what to put on it. It is where they keep happening.

Location does most of the diagnostic work

A furuncle is an infected hair follicle. It can turn up anywhere hair grows, it is usually staph, and a person who gets one is not necessarily a person who will get another.

Hidradenitis suppurativa lives in specific places. Armpits, groin, under the breasts, inner thighs, buttocks, around the anus. The same sites, over and over, often on both sides.

A pilonidal sinus sits in the cleft at the top of the buttocks and essentially nowhere else.

An inflamed epidermoid cyst comes back in exactly the same spot every time, because the sac is still there.

Four sites, four answers. If your lumps keep appearing in your armpits and groin, the working diagnosis is not recurrent boils.

The one that gets missed for years

Hidradenitis suppurativa is the diagnosis I most want people to know the name of, because the delay in getting it is measured in years rather than visits, and misdiagnosis is one of the biggest drivers of that delay (1).

What separates it from recurrent furuncles:

The same locations, repeatedly. Tunnels under the skin connecting one lesion to the next, which patients often describe as the drainage coming out somewhere other than where it went in. Rope-like scarring that builds up over years. Blackheads appearing in pairs, which is a small finding and quite specific. A family history, which is present often enough to be worth asking about.

Cultures from HS lesions frequently grow something, which is how it keeps getting called an infection. It is an inflammatory disease of the follicle, and antibiotics in it are working as anti-inflammatories more than as antimicrobials.

If you have been given six courses of antibiotics for boils in the same two places, you probably have HS and nobody has said so.

What actually treats an abscess

Drainage. Not antibiotics.

The IDSA guideline on skin and soft tissue infection puts incision and drainage as the treatment for a drainable abscess, with antibiotics as an adjunct in defined situations rather than a substitute (2). An abscess that is not opened does not resolve because someone took cephalexin.

This is why, practising by video, my rule is that a suspected abscess goes out to be drained rather than getting a prescription from me. I am firmer about that than some colleagues are, and I have not regretted it. A camera cannot tell me whether something is fluctuant, and a prescription that delays drainage by four days makes the eventual procedure bigger.

Why they keep coming back

For genuine recurrent furunculosis, the usual driver is staph colonization. The organism lives in the nose, the axillae, the groin, and it seeds new follicles.

Decolonization is the standard answer: intranasal mupirocin, chlorhexidine washes, attention to towels and razors. What is worth knowing is that treating the whole household beats treating the individual. Fritz and colleagues randomized exactly that comparison in children with community-associated staph infection and found household-wide decolonization more effective at eradication than treating the index patient alone (3).

That matters practically, because the patient who keeps recurring is often the one person in a house of four getting treated.

The part that belongs to my day job

Obesity, smoking and diabetes all sit behind recurrent skin infection, and they sit behind HS particularly hard.

Friction and skin folds are part of it, and plenty else is going on besides. Higher glucose impairs neutrophil function. Adipose tissue is metabolically active and inflammatory. Skin folds hold moisture and macerate. And the inflammatory biology of HS overlaps with metabolic disease in a way that is more than coincidence of body habitus.

What has changed recently is that we have a drug class that moves several of those levers at once. Multiple cohorts and case series now report reduced HS disease activity, fewer flares and less pain in patients treated with GLP-1 receptor agonists (4), and a cross-sectional survey found roughly two thirds of respondents reporting improvement in HS-specific measures (5).

I want to be careful here, because the enthusiasm is ahead of the evidence. These are retrospective cohorts and patient-reported surveys, not randomized trials with standardized background therapy. I take the signal seriously in a patient who has both conditions and would be a candidate for the drug anyway. I would not start an incretin in someone whose only indication is their skin.

Smoking is the other lever, and in HS it is a big one. If someone with HS smokes, that is the highest-yield conversation available, and it is not close.

For patients

Notice where they happen. If it is armpits, groin, under the breasts or the buttocks, and it is the same places repeatedly, ask your clinician about hidradenitis suppurativa by name. Naming it is often what gets the diagnosis moving.

If you have a painful lump with a pocket of pus in it, it needs draining. An antibiotic on its own will not finish the job.

If you get recurrent boils and there are other people in your house, ask whether the whole household should be treated rather than just you.

For colleagues

Ask where, not what. Location sorts furuncle from HS from pilonidal faster than any other question, and it is the question that shortens the diagnostic delay.

Household decolonization outperforms individual decolonization, and we mostly still prescribe the individual version.

The GLP-1 and HS literature is worth knowing and worth being careful with. When a patient with both asks whether the drug will help their skin, name the study designs and stop short of promising.

The Bottom Line

Recurrent boils in the armpits, groin, under the breasts or the buttocks are usually hidradenitis suppurativa, and the average person with it waits years for someone to say the word. A true abscess is treated by drainage, with antibiotics as an adjunct rather than a substitute. Recurrent furunculosis is usually a colonization problem, and treating the whole household beats treating the patient. And if the same person has recurrent skin infection, obesity and smoking, the skin is the symptom being presented and the other two are what is driving it.

Sources

1. Murray N, et al. Equity and Outcome Events in Hidradenitis Suppurativa: Exploring Effect Modifiers Associated with Diagnostic Delay in the Real World. Dermatol Ther (Heidelb). 2024;14(12):3211-3227. PMID 39487935. https://pubmed.ncbi.nlm.nih.gov/39487935/

2. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-52. PMID 24973422. https://pubmed.ncbi.nlm.nih.gov/24973422/

3. Fritz SA, Hogan PG, Hayek G, et al. Household versus individual approaches to eradication of community-associated Staphylococcus aureus in children: a randomized trial. Clin Infect Dis. 2012;54(6):743-751. PMID 22198793. https://pubmed.ncbi.nlm.nih.gov/22198793/

4. Rao S, et al. Skin Impacts and Tradeoffs of GLP-1 Therapy: Improved Patient-Reported Outcomes of Inflammatory Skin Disease. Dermatol Ther (Heidelb). 2026. PMID 42579223. https://pubmed.ncbi.nlm.nih.gov/42579223/

5. Javaheri ED, et al. Impact of GLP-1 Receptor Agonists on Hidradenitis Suppurativa: A Cross-Sectional Survey. Int J Dermatol. 2026 Jul 16. PMID 42461155. https://pubmed.ncbi.nlm.nih.gov/42461155/

6. DermNet. Hidradenitis suppurativa. https://dermnetnz.org/topics/hidradenitis-suppurativa

A stack of folded white cotton bed linens beside a plain tube of cream and a glass of water on a sunlit wooden nightstand

Why Am I Still Itching After Scabies Treatment?

On August 29, 2026September 11, 2026 By Dr. Scott RennieIn Infectious DiseaseLeave a comment

The scabies post I wrote in 2012 gets read more than anything else on this site, which still surprises me. And the question that comes back from it is almost always the same one. I did the treatment. Why am I still itching?

There are two very different answers, and telling them apart is the whole job.

Itching is not the same as infestation

Scabies itch is an allergic response. The mite burrows, and your immune system reacts to the mite, its eggs and its waste. Kill every mite tonight and all of that material is still sitting in your skin tomorrow, and your immune system is still reacting to it.

So the itch outlasts the infestation. Reliably. Two to four weeks is ordinary and six is not rare, and during that time you can be completely mite-free and completely miserable.

This is the single most useful thing to know about scabies, and almost nobody is told it at the pharmacy counter. People finish the cream, itch for another two weeks, conclude it failed, and go looking for a second prescription they may not need.

How to tell persistent itch from actual failure

The direction of travel matters more than the intensity.

Post-treatment itch gets slowly better. Some days are worse, but the trend over a fortnight runs downward, no new spots appear, and the places that itched worst at the start are the places that quiet down first, which is what you would expect if what is happening is an immune reaction winding itself down rather than an infestation carrying on.

Failure looks different. New burrows, fresh papules in places that were clear, itch that is escalating rather than settling, and household contacts starting to scratch two weeks after you did.

Burrows settle it. Thin, slightly raised, greyish lines a few millimetres long, most often in the finger webs, the wrists, the belt line, around the nipples, and on the genitals. New burrows mean live mites.

Timing helps too. An itch that was improving and then turned around at week three is reinfestation or failure. The tail of the original reaction does not do that.

Failure is more common than people think

A systematic review and meta-analysis in the British Journal of Dermatology pooled 147 studies and put the overall treatment failure rate at 15.2 percent (1). Not a rounding error. Roughly one in seven.

By drug, permethrin failed 10.8 percent of the time, oral ivermectin 11.8 percent and topical ivermectin 9.3 percent (1).

Two numbers from that paper changed how I think about this. The first is dosing: a single dose of oral ivermectin failed 15.2 percent of the time against 7.1 percent for two doses (1). Ivermectin does not kill eggs. One dose leaves the next generation to hatch, which is why the second dose at day eight to fourteen is not optional.

The second is the trend. Across studies from 1983 to 2021, overall failure rose by 0.27 percent per year, and permethrin failure by 0.58 percent per year (1). The authors are careful to say that no study in the review actually assessed resistance, so this is a signal and not a finding. But permethrin is working less well than it used to, and if your treatment failed, that is a real possibility rather than a personal failing.

The boring reasons treatment fails

Usually the reason is application.

Neck down, every square inch. People miss the same places every time: between the toes, under the fingernails and toenails, the navel, the buttock crease, behind the ears. In infants, the elderly and anyone immunosuppressed, the scalp and face need treating too, which contradicts the neck-down instruction most people are given.

Leave it on eight to fourteen hours. Wash hands after applying and it comes straight back off, so reapply to the hands after any handwashing.

Treat everyone in the household on the same day, symptoms or not. Someone incubating quietly will hand it back to you in three weeks.

Repeat at day seven. The cream does not reliably kill eggs either, which is the same problem ivermectin has and the same reason the second application exists.

On the laundry, I am less strict than most instructions you will read. Classic scabies transmits by prolonged skin-to-skin contact, and fomite transmission is minor outside crusted scabies. Bedding, towels and clothing from the last three days, hot wash or bagged for three days, is enough. Nobody needs to shampoo a mattress.

The lumps that stay for months

Nodular scabies is worth naming because it frightens people. Firm, itchy, reddish-brown nodules on the scrotum, groin or armpits. They can persist for weeks to months after successful treatment. They are a granulomatous immune response, not live infestation, and treating them again with a scabicide does nothing. They respond to a topical steroid and to time.

When the itch is not scabies at all

Here is where I want to be direct, because this is the failure mode I care most about.

If you were treated for scabies, you never had burrows, no household contact ever itched, and you are still itching at eight weeks, the working diagnosis was probably wrong.

Generalized itch with no primary rash is its own clinical problem, and the list behind it is largely internal. Dry skin and eczema account for most of it. But persistent itch without a rash is also how uncontrolled diabetes, chronic kidney disease, cholestatic liver disease, thyroid disease, iron deficiency and some blood disorders present. In a patient with unexplained itch and no burrows, I would rather check an A1c, a metabolic panel, liver function, thyroid and a CBC than write a third prescription for permethrin.

That scenario is not rare. It is the one that gets missed while everyone concentrates on the mite.

What I ask for on a video visit

Two photographs. One from a distance showing the distribution, which is diagnostic in itself, and one macro shot as close as the phone will focus, aimed at a finger web or a wrist. Back up six inches if it will not focus, which fixes it nearly every time.

I ask when the itch is worst, because scabies is classically worse at night, and I ask who else in the house is scratching. The household answer is often better evidence than the photographs.

For patients

Itching for two to four weeks after correct treatment is expected and does not mean it failed. Watch the direction, not the intensity.

If you were given a single dose of oral ivermectin and nothing else, ask about the second dose. If new spots or new burrows appear, go back. And if you have been itching for two months with nothing to see on the skin, ask for blood work rather than another cream.

For colleagues

The two-dose ivermectin regimen has the evidence behind it and single-dose prescriptions are still going out. That is the cheapest fix available in this whole area.

Tell people at the point of prescribing that the itch will outlast the mite. It prevents a second visit, a second prescription and a great deal of anxiety, and it takes about ten seconds.

And keep systemic pruritus on the list. A patient on their third scabicide with no burrows and no contacts deserves labs, not a refill.

The Bottom Line

Itch that is slowly improving two to four weeks after treatment is the immune system finishing its argument with a mite that is already dead. Itch that is escalating, or that comes with new burrows or newly scratching housemates, is failure or reinfestation, and failure runs around one in seven. If you got one dose of ivermectin, you got half a treatment. And if the itch has gone on for months with nothing visible on the skin, the problem may never have been on your skin at all.

Sources

1. Mbuagbaw L, Sadeghirad B, Morgan RL, et al. Failure of scabies treatment: a systematic review and meta-analysis. Br J Dermatol. 2024;190(2):163-173. PMID 37625798. https://pubmed.ncbi.nlm.nih.gov/37625798/

2. DermNet. Scabies. https://dermnetnz.org/topics/scabies

A plate of boiled eggs and cottage cheese beside a rolled gauze bandage and a glass of water on a sunlit wooden table

Why Won’t My Wound Heal?

On August 29, 2026August 30, 2026 By Dr. Scott RennieIn Skin & Wound CareLeave a comment

The question comes up on almost every wound follow-up, and it is nearly always phrased the same way. What should I be eating to make this heal faster?

It is a good question. The answer patients get is usually a list of vitamins, which is mostly wrong, or a shrug, which is worse. There is real evidence here. It just does not point where the supplement aisle points.

A healing wound is a construction project

Closing a wound means building tissue. Collagen synthesis, angiogenesis, epithelial migration, immune cell proliferation. All of that runs on amino acids and calories, and the demand is above baseline for as long as the wound is open. A large or chronic wound raises resting energy expenditure meaningfully.

Which means the first question is not which supplement. It is whether the person is eating enough of anything at all. In older adults with a chronic wound, the answer is frequently no, and no capsule fixes an 1,100 calorie a day intake.

What glucose does to the machinery

Hyperglycemia interferes with wound healing at several points at once. Glycosylation impairs neutrophil and macrophage function, which stretches out the inflammatory phase instead of letting the wound progress to proliferation. Fibroblast activity falls. VEGF expression falls, so new vessels are slower to arrive. Matrix metalloproteinase activity rises, which means the collagen that does get laid down is broken down faster than it should be. Collagen density ends up lower.

Put underlying peripheral arterial disease on top and the wound has a supply problem as well as a manufacturing problem.

This is why I care about the A1c on a wound visit and not only on a diabetes visit. The same laceration on a person running an A1c of 11 and a person running a 6 is two different clinical situations, and only one of them is going to close on schedule.

An aside that patients find more persuasive than any of the biochemistry: the glucose control that matters for a wound is the control over the next several weeks, not the number on the day of the injury. That is actionable. It gives someone something to do about a wound that is already there.

The protein number

For adults with a pressure injury who are malnourished or at risk of it, the 2019 international guideline from EPUAP, NPIAP and the Pan Pacific alliance recommends 1.25 to 1.5 grams of protein per kilogram of body weight per day, with 30 to 35 kilocalories per kilogram per day for energy (1).

Those are the best-supported numbers in wound nutrition, and I use them as the floor for any significant open wound, not only pressure injuries. Most people are nowhere near them. A 70 kilogram adult needs roughly 88 to 105 grams of protein a day on that recommendation, and the typical intake I hear described on a video visit is half that.

Worth noting the overlap with the rest of my practice. When I start a patient on an incretin I ask for 1.6 grams per kilogram per day and strength training two to three times a week, because the risk on those drugs is lean mass loss. A patient on an incretin who also has a wound is being asked for the same thing for two different reasons, which makes the conversation easier rather than harder.

Arginine, and how good the evidence actually is

Arginine gets singled out because it is a substrate for nitric oxide and for proline, and proline goes into collagen. The 2019 guideline recommends a high-calorie, high-protein oral nutrition supplement fortified with arginine, zinc and antioxidants for adults with a stage 2 or greater pressure injury who are malnourished or at risk of malnutrition (1).

Read that recommendation carefully, because it is narrower than how it gets quoted. It is for a specific wound severity, in a specific nutritional context, and the arginine comes inside a fortified supplement rather than as arginine on its own (2). The trials behind it tested the whole formulation. Nobody has shown that arginine by itself, added to an adequate diet in a well-nourished person, does anything for a wound.

I have no objection to those supplements in the patients the guideline describes. I do object to a well-fed person with a healing surgical incision spending money on arginine capsules.

Vitamin C and zinc

Both are genuinely required for wound healing. Vitamin C is a cofactor for the hydroxylation steps in collagen synthesis, and frank scurvy produces wounds that will not close. Zinc deficiency impairs epithelialization.

None of that means supplementing someone who is not deficient helps. Reviews of vitamin and mineral supplementation in wound care keep landing in the same place: unclear benefit unless there is a confirmed or suspected deficiency, and no well-powered randomized trial showing that routine vitamin C or zinc speeds healing in replete patients (3).

So I correct documented deficiencies and I do not supplement reflexively. High-dose zinc in particular is not harmless; it interferes with copper absorption over time.

This is the part of the conversation patients like least, and I say it anyway.

What matters more than any of it

Smoking. Sørensen’s meta-analysis of surgical patients found substantially higher rates of wound complications and infection in smokers, and improvement with cessation before surgery (4). If a patient with a slow wound smokes, that is the highest-yield thing on the list, and it is not close.

Then perfusion. A wound on a limb without a decent pulse is a vascular problem wearing a dressing, and no amount of protein fixes it.

Then offloading and moisture balance, which are mechanical rather than nutritional and are where most home wound care goes wrong.

Nutrition belongs on the list. It belongs below those.

For patients

Eat more protein than you think you need while a wound is open. Aim for something in the range of 1.25 to 1.5 grams per kilogram of your body weight per day, which for most adults means adding a protein source to every meal rather than eating one large dinner. If you are diabetic, the wound is a reason to tighten control now, not later.

Skip the wound-healing supplement stack unless your clinician has found an actual deficiency. If you smoke, stopping will do more for that wound than everything else on this page combined.

For colleagues

Ask what people are eating before you reach for a supplement, and ask in grams rather than in general terms. The 1.25 to 1.5 g/kg recommendation is easy to quote and rarely translated into food for the patient, which is where it fails.

Check a zinc or vitamin C level if the history suggests deficiency, then treat what you find. Do not treat the wound with a multivitamin on principle.

And put smoking cessation at the top of the plan for any wound that is behind schedule, ahead of the dressing change conversation.

The Bottom Line

Wounds heal on protein, calories and blood flow, in something like that order, and they stall on high glucose and tobacco. The guideline numbers worth remembering are 1.25 to 1.5 grams of protein per kilogram per day and 30 to 35 kilocalories per kilogram per day. Arginine and antioxidant supplements have a real place, in malnourished patients with stage 2 or worse pressure injuries, and almost nowhere else. Vitamin C and zinc are worth correcting when they are low and worth skipping when they are not. If you fix only one thing on this list, fix the smoking.

Sources

1. European Pressure Ulcer Advisory Panel, National Pressure Injury Advisory Panel and Pan Pacific Pressure Injury Alliance. The Role of Nutrition for Pressure Injury Prevention and Healing: 2019 International Clinical Practice Guideline recommendations. https://cdn.ymaws.com/npiap.com/resource/resmgr/The_Role_of_Nutrition_for_Pr.pdf

2. Chu AS, Delmore B. Arginine: What You Need to Know for Pressure Injury Healing. Adv Skin Wound Care. 2021;34(12):630-636. PMID 34807894. https://pubmed.ncbi.nlm.nih.gov/34807894/

3. Indian Health Service National Pharmacy and Therapeutics Committee. Formulary Brief: Nutritional Supplements in Wound Healing. https://www.ihs.gov/sites/nptc/themes/responsive2017/display_objects/documents/guidance/NPTC-Formulary-Brief-NutritionalSupplementsinWoundHealing.pdf

4. Sørensen LT. Wound healing and infection in surgery. The clinical impact of smoking and smoking cessation: a systematic review and meta-analysis. Arch Surg. 2012;147(4):373-383. PMID 22508785. https://pubmed.ncbi.nlm.nih.gov/22508785/

5. Armstrong DG, Boulton AJM, Bus SA. Diabetic Foot Ulcers and Their Recurrence. N Engl J Med. 2017;376(24):2367-2375. PMID 28614678. https://www.nejm.org/doi/10.1056/NEJMra1615439

A hand mirror, a pair of folded cotton socks and a home glucose meter with a lancet on a sunlit wooden table

What Does Diabetes Do to Your Skin?

On August 29, 2026August 30, 2026 By Dr. Scott RennieIn Skin & Wound CareLeave a comment

Skin is the one organ I can actually see on a video visit. No stethoscope, no palpation, no reaching across the desk. Just a camera, whatever light the patient happens to have, and a screen. That limitation has made me pay closer attention to skin than I did when I worked in urgent care, because on video it is often the first physical evidence that something metabolic is going on.

Between 30 and 70 percent of people with diabetes develop a skin problem attributable to the disease at some point (1). That is an enormous range, which tells you the studies are measuring different populations and different definitions rather than anything precise. Take the range as what it is, a signal that this is common, not a statistic to quote back to anyone.

What follows is what I look for, why it matters, and where I think the usual advice is weaker than it sounds.

The velvet patch on the back of the neck

Acanthosis nigricans is the one I care about most, because it is visible, it is early, and patients almost never bring it up. Dark, thickened, velvety skin in the folds. Back of the neck, armpits, groin, under the breasts. Patients describe it as dirt that will not wash off, and some have been scrubbing at it for years.

The mechanism is insulin. Hyperinsulinemia drives IGF-1 receptor activation on keratinocytes and fibroblasts, which proliferate (2). So the plaque is a rough readout of how much insulin the pancreas has been pushing out to keep glucose in range. It shows up before the fasting glucose does. Sometimes years before.

Skin tags travel with it and share the same driver (2). A patient with acanthosis nigricans and a crop of acrochordons on the neck and axillae is telling you about their insulin resistance without a single lab drawn.

Here is where I differ from what patients are usually told. Dermatology handles acanthosis nigricans as a cosmetic complaint and offers topical retinoids, urea, sometimes laser. Those do something to the appearance. None of them touch the reason it is there. I follow the ADA rule and screen every adult from 35 regardless of BMI, and when I see that patch I do not wait for the birthday. I check an A1c.

It also improves. Not overnight, and not completely in everyone, but weight loss and improved insulin sensitivity soften the plaques over months. That is worth telling someone who has been scrubbing their neck since high school.

Skin tags carry information

I have a whole post on what skin tags are and what they look like, and it gets steady traffic from people worried about a lesion. What that post does not do is explain why someone in their thirties suddenly has fifteen of them.

Friction is part of it. Insulin is the rest.

What high glucose actually does to a wound

This one deserves its own post and is getting one. The short version: glycosylation impairs neutrophil and macrophage function, which prolongs the inflammatory phase instead of letting the wound move on to proliferation. Fibroblast activity drops, VEGF expression drops, matrix metalloproteinases go up, collagen density falls. Layer underlying vascular disease on top of that and you have a wound that stalls.

The practical consequence is that a cut on someone with an A1c of 11 is a different clinical problem than the same cut on someone with an A1c of 6, even though it looks identical on camera.

The infections that come with the territory

Candidal intertrigo lives in the skin folds, and the bigger the fold the more reliably it shows up. Beefy red, satellite lesions at the edge, itching or burning rather than pain. Patients treat it with hydrocortisone from the drugstore, which makes it worse, and then arrive convinced they have an allergy.

Tinea in all its addresses, feet, groin, nails. Onychomycosis in particular is stubborn and, in a diabetic foot, is not merely a nuisance: a thickened dystrophic nail is a pressure point and a portal.

Then cellulitis. Elevated glucose, impaired barrier, and a break in the skin from a fissure or a fungal infection between the toes. My rule for an abscess is that it goes out for drainage rather than getting empiric antibiotics from me over video, and I am firmer about that than some colleagues are.

Hidradenitis suppurativa, and what changed

HS has been badly served for a long time. Painful nodules and sinus tracts in the axillae, groin and under the breasts, frequently mistaken for recurrent boils for years before anyone names it. The association with obesity is strong and it is not a coincidence of body habitus alone; the inflammatory biology overlaps.

What has changed recently is incretin therapy. Multiple cohorts and case series now report reduced disease activity, fewer flares and less pain in HS patients treated with GLP-1 receptor agonists, alongside the expected BMI reduction (3). A cross-sectional survey found roughly two thirds of respondents reporting improvement in HS-specific measures (4).

I want to be honest about the strength of that evidence, because the enthusiasm is running ahead of it. These are retrospective cohorts, case series and patient-reported surveys. There is no adequately powered randomized trial with standardized background therapy. The signal is consistent enough that I take it seriously in a patient who has both conditions and would be a candidate for the drug anyway. It is not a reason to start an incretin in someone whose only indication is HS.

The foot

Somewhere between 19 and 34 percent of people with diabetes will develop a foot ulcer in their lifetime (5). The number that changed how I talk to patients is not that one, though. It is what happens after the ulcer closes: roughly 40 percent recur within one year, close to 60 percent within three years, and 65 percent within five (5).

Armstrong and colleagues argued from that data that a patient whose wound has closed should be thought of as in remission rather than healed (5). I use that word deliberately with patients now, because a person who believes they are healed puts the mirror away and stops looking at the bottom of their feet, while a person who believes they are in remission keeps checking, keeps wearing the shoes that were fitted for them, and calls about a blister on the day it appears rather than three weeks later when it has become something else. Remission gets you daily foot checks. Healed gets you a pair of sandals and a summer of walking on hot pavement with neuropathy.

That framing does more work in a fifteen-minute visit than any amount of education about glycemic targets.

What I ask for on video

Skin over a camera is genuinely hard. Autofocus hunts, phone processing smooths texture, and the color balance depends on whether someone is under a kitchen light or a window.

So I ask for two photographs of anything I need to actually assess. One from a distance, far enough back to show where the lesion sits and what the surrounding skin looks like, and one macro, as close as the phone will focus without blurring. Multiple angles if there is any elevation to it. The blur problem is the single most common reason I have to ask twice, and it is almost always because the patient is closer than the lens can handle. Backing up six inches fixes it.

For anything in a fold, I want the fold held open in the shot. For feet, I want the sole and between the toes, which usually means someone else holds the camera.

For patients

If the skin on the back of your neck or in your armpits has gone dark and thick and will not scrub off, that is not hygiene, and it is worth an A1c. If you are getting skin tags in bunches, same. If you have painful recurring lumps in your armpits or groin that have been called boils for years, ask specifically about hidradenitis suppurativa by name, because that is often what gets the diagnosis moving.

And if you have diabetes, look at your feet every day. Every day, including between the toes, including the bottom, using a mirror or a family member if you cannot see them.

For colleagues

Acanthosis nigricans in an adult is a screening prompt, not a dermatology referral. Check the A1c and the lipids before you send them for cosmetic treatment of the plaque.

The GLP-1 and HS literature is worth knowing about and worth being careful with. When a patient with both conditions asks whether the drug will help their skin, the honest answer names the cohorts, names their design, and stops short of promising anything.

On the foot, adopt the remission language. It changes adherence in a way that repeating ulcer statistics does not.

The Bottom Line

Skin is where metabolic disease announces itself, often years before a lab does. A velvety patch behind the neck, a crop of skin tags, a yeast infection in a fold that keeps coming back, a nail that will not clear. None of those are dermatologic curiosities to be treated in isolation. They are all the same disease showing up at the surface, and treating the surface without asking why it is there wastes the information. Check the A1c. Look at the feet. And when a wound closes on a diabetic foot, say remission, not healed.

Sources

1. Vâță D, et al. Cutaneous Manifestations Associated with Diabetes Mellitus: A Retrospective Study. Diseases. 2023;11(3). PMID 37606477. https://pubmed.ncbi.nlm.nih.gov/37606477/

2. Marchand L, et al. All about skin manifestations of insulin resistance and type 2 diabetes: acanthosis nigricans and acrochordons. Postgrad Med J. 2020;96(1134):237. PMID 31611265. https://pubmed.ncbi.nlm.nih.gov/31611265/

3. Rao S, et al. Skin Impacts and Tradeoffs of GLP-1 Therapy: Improved Patient-Reported Outcomes of Inflammatory Skin Disease. Dermatol Ther (Heidelb). 2026. PMID 42579223. https://pubmed.ncbi.nlm.nih.gov/42579223/

4. Javaheri ED, et al. Impact of GLP-1 Receptor Agonists on Hidradenitis Suppurativa: A Cross-Sectional Survey. Int J Dermatol. 2026 Jul 16. PMID 42461155. https://pubmed.ncbi.nlm.nih.gov/42461155/

5. Armstrong DG, Boulton AJM, Bus SA. Diabetic Foot Ulcers and Their Recurrence. N Engl J Med. 2017;376(24):2367-2375. PMID 28614678. https://www.nejm.org/doi/10.1056/NEJMra1615439

6. International Working Group on the Diabetic Foot. IWGDF Guidelines on the prevention and management of diabetes-related foot disease, 2023. https://iwgdfguidelines.org/guidelines-2023/

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

What the Label Now Says

The Trial Behind It

Where This Leaves Ozempic, Wegovy, and Zepbound

For Patients

The Practical Question for Prescribers

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

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Sources

Where the label usually comes from

The label is not free

There is a score for this, and it runs on history alone

What I actually do with this on a video visit

What a real reaction looks like, and what has changed about treating it

For patients

For colleagues

The Bottom Line

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Start with the boring part, because it is the part that matters

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What I actually think about it

The part that belongs to my day job

If you already have it, the clock is the thing

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For colleagues

The Bottom Line

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Location does most of the diagnostic work

The one that gets missed for years

What actually treats an abscess

Why they keep coming back

The part that belongs to my day job

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Itching is not the same as infestation

How to tell persistent itch from actual failure

Failure is more common than people think

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The lumps that stay for months

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What I ask for on a video visit

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The Bottom Line

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A healing wound is a construction project

What glucose does to the machinery

The protein number

Arginine, and how good the evidence actually is

Vitamin C and zinc

What matters more than any of it

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The velvet patch on the back of the neck

Skin tags carry information

What high glucose actually does to a wound

The infections that come with the territory

Hidradenitis suppurativa, and what changed

The foot

What I ask for on video