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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

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/

An open medical journal, a clipboard and scattered tablets on a desk

Weight Loss Drug Side Effects and How Common They Are

On March 24, 2025September 29, 2026 By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

As more patients start anti-obesity medications, the question that comes up most is about side effects. These drugs are powerful tools for weight loss and metabolic health. They aren’t without risk. Knowing what to expect and how to manage it often decides whether someone stays on treatment or quits in month two.

Gastrointestinal effects are the ones I hear about most. Nausea leads the list. In STEP 1, which studied semaglutide 2.4 mg in adults without diabetes, nausea affected 44.2% of participants against 17.4% on placebo (Wilding et al., NEJM, 2021). In SCALE, the corresponding trial of liraglutide 3.0 mg, nausea affected 40.2% versus 14.7% on placebo (Pi-Sunyer et al., NEJM, 2015). Those two trials are the source of most of the numbers in this post, and they studied different drugs. Smaller meals, avoiding high-fat food, and slow dose titration usually get patients through it.

Constipation and diarrhea both follow the same pattern, common early and improving with time. Hydration, added fiber, and sometimes a stool softener handle most constipation. Diarrhea occasionally warrants a dose adjustment. Rarely, delayed gastric emptying can progress toward obstruction, which presents as bloating, pain, and vomiting and needs prompt evaluation.

Pancreatitis is uncommon and serious. In SCALE, acute pancreatitis occurred in a small number of liraglutide patients and none on placebo, at an incidence around 0.3%. Severe abdominal pain radiating to the back with nausea and vomiting should trigger immediate discontinuation and workup.

Gallbladder disease is a real risk and it is mostly a consequence of the weight loss itself. In SCALE, cholelithiasis occurred in 1.5% of liraglutide patients versus 1.1% on placebo, and acute cholecystitis in 0.8% versus 0.4%. Rapid weight loss and changes in bile concentration are the likely mechanism, which means the risk travels with any effective therapy rather than with this drug class specifically.

Hypoglycemia is uncommon with GLP-1 receptor agonists used alone in patients without diabetes, because these drugs stimulate insulin secretion in a glucose-dependent way. Risk climbs sharply in combination with insulin or a sulfonylurea. That combination is where monitoring and dose adjustment of the background agent become necessary, and it is worth addressing before starting rather than after the first low reading.

Thyroid cancer risk is rare and gets asked about constantly. GLP-1 receptor agonists carry a boxed warning for medullary thyroid carcinoma based on rodent C-cell tumor data, and they are contraindicated in anyone with a personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia type 2. Human data haven’t established a causal link, and a widely publicized French case-control study reporting an association drew substantial methodological criticism in the same journal (Bezin et al., Diabetes Care, 2023). I tell patients the contraindication is firm and the population-level risk remains unproven.

Kidney injury is rare and usually a consequence of dehydration after vomiting or diarrhea rather than a direct drug effect. Pushing fluids during dose escalation is an easy preventive step.

Heart rate increases are reported as well. Resting heart rate can rise by roughly one to four beats per minute on semaglutide or tirzepatide. Palpitations should always be reported.

Pregnancy deserves its own conversation. These medications aren’t recommended during pregnancy, and semaglutide should be stopped at least two months before conception. There is also an interaction with oral contraceptives, since delayed gastric emptying affects absorption. For tirzepatide, patients on oral contraceptives should switch to a non-oral method or add a barrier method for four weeks after starting and for four weeks after each dose increase.

Injection site reactions occur in a small percentage of patients, usually three to five percent. Redness, swelling, and itching are the usual complaints, and rotating sites with good technique resolves most of it.

None of this means patients should avoid these medications. Awareness and early management are what keep people on treatment. I often tell patients to call me if nausea or constipation is interfering with their day-to-day life rather than waiting for the next follow-up. Small changes in dosing or diet usually make the drug tolerable again.

Anti-obesity medications work, and they need thoughtful monitoring. With open communication, most side effects are manageable and most patients stay on track.

New Obesity Drugs Beyond Ozempic and Zepbound Explained

On March 22, 2025September 11, 2026 By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Obesity treatment is shifting fast. For years the standard toolkit was lifestyle counseling plus a handful of older medications. New drug classes now target the actual biology of the disease: hormonal signaling, metabolic rate, body composition. Three groups matter most right now. Nutrient-stimulated hormone-based therapies. Oral small molecule receptor agonists. And activin receptor pathway inhibitors.

NuSHs mimic or amplify the body’s own hormonal response to food. GLP-1 increases satiety, slows gastric emptying, and supports insulin secretion (Wilding et al., N Engl J Med, 2021). GIP regulates fat metabolism and glucose response (Frías et al., N Engl J Med, 2021). Amylin, co-secreted with insulin, works as its own satiety signal (Dehestani et al., J Obes Metab Syndr, 2021). PYY reduces appetite and energy intake (Schmidt et al., Am J Physiol Endocrinol Metab, 2014). Oxyntomodulin reduces intake too, and also raises energy expenditure (Wynne et al., Int J Obes, 2006).

Several drugs in this class are already in trials, and CagriSema pairs an amylin analogue with a GLP-1 receptor agonist, reducing body weight by 17.1 percent in 20 weeks in a Phase 1b trial, not Phase 3 (Enebo et al., Lancet, 2021). Survodutide, a GLP-1 and glucagon receptor agonist, produced weight loss of up to 18.7 percent over 46 weeks (Le Roux et al., Lancet Diabetes Endocrinol, 2024). Retatrutide, which hits GIP, GLP-1, and glucagon receptors together, produced a 24.2 percent reduction over 48 weeks in Phase 2 testing. Women lost about 28.5 percent of body weight, men about 21.9 percent (Jastreboff et al., N Engl J Med, 2023). Oral semaglutide at 50 mg reached 17.4 percent weight loss at 68 weeks, with 37 percent of participants losing more than a fifth of their body weight (Knop et al., Lancet, 2023). Mari-tide is still in Phase 2, with promising early results.

Small molecule receptor agonists are the other track, and their edge is simple: a pill instead of a needle. Orforglipron produced about 14.7 percent weight loss at 36 weeks, in range with the injectables (Wharton et al., N Engl J Med, 2023). Danuglipron is behind it. Early Phase 2 data, in patients with type 2 diabetes rather than obesity specifically, showed reduced appetite alongside improved glucose and weight outcomes (Saxena et al., Diabetes Obes Metab, 2023). Whether that holds up in an obesity-only population is still unclear.

Activin receptor pathway inhibitors take a different approach. They target pathways that preserve muscle while fat comes off, since traditional weight loss burns muscle right along with fat. These drugs try to change that ratio (Heymsfield et al., JAMA Netw Open, 2021).

Bimagrumab, a monoclonal antibody that blocks the activin type II receptor, reduced fat mass by 20.5 percent while increasing lean mass by 3.6 percent over 48 weeks in trials. Combine it with a GLP-1 drug like semaglutide or tirzepatide and the body-composition effect gets stronger still. Taldefgrobep, a myostatin inhibitor originally developed for Duchenne muscular dystrophy, is now being tested for obesity. SRK-439 is another myostatin-targeting antibody in development, aimed at fat loss without the lean-mass cost.

What sets these treatments apart is what the weight loss is made of: more muscle retained, metabolic markers that move too, alongside the pounds lost. That’s a real shift, for patients who may get more durable results and fewer complications, and for clinicians who get more tools to match therapy to the person in front of them.

Weight Loss Medications for Kids and Adults Explained

On March 21, 2025September 11, 2026 By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

As a physician, I know that treating obesity can be tough. Many families put in real effort with diet and exercise and still don’t see enough progress. When that happens, medication becomes worth discussing. Not for everyone. For the right patient, though, it can make a real difference.

Every price below reflects March 2025, when this was first written, and drug pricing in this class moves constantly, list price, cash price, and whatever a given insurer decides to cover can all diverge sharply, so treat every figure below as a historical marker rather than a current quote.

For children ages 12 and older, there are a few choices. Orlistat, brand name Xenical, blocks fat absorption in the gut. Because it stays in the digestive tract, it doesn’t touch appetite or the brain. The catch is side effects. Eat too much fat on this drug and a kid can get oily stools, gas, frequent bowel movements. A low-fat diet helps. It can still be uncomfortable. The price ran about $50 to $200 a month. The FDA cleared it for ages 12 and up.

Liraglutide, brand name Saxenda, is another option. It mimics a gut hormone called GLP-1, helping with appetite control and slowing stomach emptying. It’s effective, and it also helps blood sugar control, which matters if a patient has insulin resistance. But it requires daily injections, and nausea is common. Vomiting and diarrhea can happen too. Monthly cost usually fell between $1,200 and $1,500 a month. The FDA approved it for kids starting at age 12.

Phentermine combined with topiramate, sold as Qsymia, is approved for adolescents 12 and up who meet obesity criteria. Phentermine reduces appetite. Topiramate curbs cravings. Together they can produce substantial weight loss, especially in patients who struggle with binge eating. Side effects include dry mouth, dizziness, insomnia, and mood changes, and blood pressure and heart rate need regular checks. Cost averaged $200 to $300 a month.

Semaglutide, brand name Wegovy, is another GLP-1 receptor agonist, injected once weekly instead of daily. Clinical studies show it produces impressive weight loss. Side effects mirror other GLP-1 drugs: nausea, vomiting, diarrhea, abdominal pain, constipation. Out-of-pocket cost usually ran $1,300 to $1,600 a month. The FDA approved it for adolescents age 12 and up.

Setmelanotide, or Imcivree, is different from everything above. It targets rare genetic conditions that cause obesity, POMC, PCSK1, or LEPR deficiencies, by restoring hormonal signals that regulate hunger. It’s not meant for most patients, only those with a specific genetic diagnosis. For those who qualify, it can work well. The price tag was steep, though: about $16,000 a month.

For adults, the options broaden, and the prices below are again what things cost in March 2025, not today. Phentermine has been used for decades. It works on the central nervous system to suppress appetite, usually prescribed short-term and paired with diet and exercise. It can be effective, but it may cause insomnia, dry mouth, and a faster heart rate, and it isn’t safe for people with heart disease. The cost was low, around $30 to $60 a month.

Bupropion combined with naltrexone, sold as Contrave, takes a different approach. Bupropion affects brain chemistry to help with appetite and mood. Naltrexone reduces cravings. Some patients feel more energetic on it. Side effects can include nausea, dizziness, and insomnia. Mood changes are possible, so follow-up matters. Cost averaged $200 to $300 a month.

Tirzepatide, marketed as Mounjaro, is one of the newest medications. It activates both GLP-1 and GIP receptors, improving satiety and insulin sensitivity. Given as a weekly injection, it has shown striking results for weight loss. Nausea and diarrhea are the most common side effects, as with other drugs in this class. Costs ran high, around $1,000 to $1,500 a month. At publication it was FDA-approved for type 2 diabetes, not obesity, though already used off-label for weight loss.

A few points cut across all of these. Insurance coverage is unpredictable: some insurers won’t cover these drugs at all, others demand proof that lifestyle efforts were tried first. Close monitoring is essential, because side effects vary. None of these drugs replace healthy habits. They work best stacked on top of diet, activity, and behavior change.

For patients and families, the choices can feel like a lot. Knowing what’s actually available, and what each option costs and asks of you, helps match the right treatment to the right person.

Which Medications Can Make Weight Loss Harder?

On March 21, 2025September 11, 2026 By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

As a physician, I often meet patients who are discouraged by weight gain that doesn’t seem to make sense. They may be eating well, exercising regularly, and still the scale keeps moving up. Lifestyle choices matter a great deal. Medications and supplements can matter just as much, and knowing which ones affect weight is worth raising with your own doctor, because the cause can be hiding in plain sight.

Certain prescriptions are known to promote weight gain. Diabetes medications are a good example: insulin, sulfonylureas like glipizide, and thiazolidinediones like pioglitazone often push weight up. Metformin, GLP-1 receptor agonists like semaglutide, and SGLT-2 inhibitors tend to do the opposite and help with weight control.

I’ve also seen this pattern with antidepressants. Drugs like escitalopram, citalopram, or paroxetine can add pounds, as can tricyclics such as amitriptyline. Even trazodone or mirtazapine carry this risk. For some patients, switching to bupropion, fluoxetine, or sertraline makes a noticeable difference.

Atypical antipsychotics are another tricky class. Olanzapine, risperidone, and quetiapine are all associated with weight gain, while ziprasidone tends to have less impact. Anti-epileptic drugs split the same way. Same pattern, different receptors. Valproic acid and gabapentin tend to increase weight; topiramate and lamotrigine usually don’t.

Even medications outside psychiatry and neurology come up in this discussion. Lithium, commonly used as a mood stabilizer, often causes weight gain, and so do glucocorticoids like prednisone, especially with longer courses. Beta blockers such as metoprolol and propranolol carry the same issue, carvedilol usually has less effect, and antihistamines like diphenhydramine or cetirizine can shift weight too, though loratadine tends not to, which is worth remembering the next time an allergy prescription gets refilled without a second thought. Hormonal contraception adds another layer: depo-medroxyprogesterone is linked to weight gain, which can be genuinely frustrating for patients who are otherwise doing everything right. Non-hormonal methods are an option worth raising.

Over-the-counter medications and supplements belong in this conversation too, right alongside anything prescribed. Chronic antihistamine use may interfere with appetite regulation. Proton pump inhibitors, like omeprazole, can indirectly affect weight through changes in gut microbiota. Long-term NSAID use may lead to water retention. Some “energy” or “muscle gain” supplements hide hormones or steroids that work against weight control entirely.

This is why reviewing medications matters so much in a weight conversation. Weight gain gets blamed entirely on diet or activity when the real trigger may be sitting in the pillbox. Of course, no one should stop a medication on their own. Sometimes the benefit outweighs the side effect. Sometimes there’s a safer alternative that gets the same result without the tradeoff.

Bringing medications into the conversation gives us a fuller picture. It lets us make thoughtful adjustments while still focusing on lifestyle. It’s about tailoring a plan that actually supports long-term health, one a patient can live inside for years.

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