Flagship — January 2026

Bariatric surgery — and Roux-en-Y gastric bypass in particular — is still the most durable treatment we have for severe obesity. But "durable" is not "permanent." Most people regain at least some weight from their post-surgery low, and a meaningful minority regain enough to undo a chunk of the metabolic benefits. Until now, the question of what to do next has been answered mostly by extrapolation: GLP-1 drugs work in people who haven't had surgery, so they should probably work in people who have. Probably is not the same as proven.

The new study, led by a team at NYU Langone, enrolled adults who were 18 to 120 months out from gastric bypass, had originally lost at least 25% of their total body weight, and had since regained at least 10% of total body weight from their lowest post-op point. In other words: the exact patient sitting in the clinic asking, "is it worth trying Saxenda?" They were randomized 2:1 to liraglutide 3.0 mg daily or placebo, both with regular lifestyle counseling, for 56 weeks.

The headline result: at 56 weeks, the liraglutide group had lost an average of 8.8% of their total body weight, while the placebo group had gained 1.1%. That gap — roughly ten percentage points of body weight, in people who had already maxed out the most powerful obesity intervention we have — is the kind of separation that makes statisticians sit up.

The responder data is even more telling. 76% of liraglutide patients lost at least 5% of total body weight, compared with 17% of placebo patients. 51% of the liraglutide group cleared the 10% threshold; 26% cleared 15%. None of the placebo group crossed 10%. And perhaps the most clinically meaningful number: 21% of patients on liraglutide ended the trial weighing less than their lowest post-surgery weight — they didn't just claw back regain, they went past it.

Gastric bypass works partly by restricting how much you can eat at once, and partly by rewiring gut hormone signaling — including a big bump in endogenous GLP-1 after meals. Over time, some of that hormonal advantage attenuates. Appetite ticks up. Portion tolerance grows. The post-surgery quiet of the food-noise brain gets louder again.

Liraglutide is, essentially, a pharmacologic version of the same hormone the surgery was leveraging. Adding it back when regain begins isn't a workaround — it's mechanistically coherent. The new trial is the first rigorous confirmation that the mechanism translates into measurable, sustained weight loss in this specific population.

A few honest caveats. The trial ran during the COVID-19 pandemic, which dragged completion rates down — 65% of liraglutide patients and 53.4% of placebo patients finished the 56 weeks. That's a real limitation, even though the analysis still showed a robust effect. The drug studied was liraglutide, not the newer, more powerful semaglutide or tirzepatide that dominate the cultural conversation; whether those agents do even more in this population is a reasonable hypothesis but not yet a trial result. And 56 weeks is a meaningful slice of time but not a lifetime — what happens when patients eventually stop the drug is, as in the broader GLP-1 literature, the open question.

There's also the eligibility framing. This trial wasn't testing GLP-1s as a way to amplify a surgery that's still working; it was testing them as a rescue for one that's started to slip. That nuance matters when you read the social-media version of the story.

Obesity medicine has spent the last few years catching up to a reality patients already lived: weight regulation is biology, not willpower, and the tools that work for it are tools, not character tests. The post-bypass population has been a quiet exception to the GLP-1 boom — people who already did the hardest thing medicine asks of them, and then found themselves back in the same conversation. This trial doesn't make the regret of regain go away. It does, finally, give clinicians a real piece of evidence to hand them instead of a shrug.

The stakes are demographic. The review notes that roughly 30% of Europeans over 65 are already dependent on the care of others, and projects that share could climb to 50% by 2050 as the population ages. For executives planning long careers, aging parents, or their own second acts, that trajectory reframes frailty as an infrastructure problem — one whose solution begins decades before a walker enters the picture. The encouraging counterpoint, the authors write, is that frailty responds to intervention in a way that chronological age does not (Millan-Domingo & Viña, 2025).

The review's first prescription is dietary — but not in the form of a single recommended regimen. The authors emphasize that nutritional interventions for frailty must be personalized, taking into account the individual's baseline status, deficits, and goals (Millan-Domingo & Viña, 2025). That framing is significant. A great deal of consumer nutrition advice still treats older adults as a homogenous group; the review's argument is closer to the logic of precision oncology, where the protocol is built around the patient rather than the diagnosis.

What the chapter does not do is hand readers a universal dosing chart, and we will not invent one. The takeaway for a busy professional is structural: an aging-focused nutrition plan worth its name should be built with a clinician or registered dietitian who can assess actual intake, body composition, and bloodwork — not assembled from supplement-aisle guesswork.

The second lever is exercise, and again the emphasis is on structure and specificity. The authors identify physical training as one of the two major lifestyle changes useful in treating age-associated frailty, and apply the same personalization principle: programs must be tailored to the individual's capacity and trajectory (Millan-Domingo & Viña, 2025). For readers already running on packed calendars, the operational implication is that incidental movement — steps logged between meetings — is not the same intervention as a programmed regimen designed by someone who understands geriatric physiology.

The review treats nutrition and exercise as complementary rather than interchangeable. Eating well without training, or training without adequate fuel, leaves the other half of the equation unaddressed. That pairing — fuel plus stimulus — is the through-line of the chapter's argument.

Perhaps the chapter's most useful contribution is conceptual. The authors explicitly draw the parallel to oncology, where precision interventions are now routine, and argue geriatrics has been slower to adopt the same mindset (Millan-Domingo & Viña, 2025). For the reader, that reframing matters: it suggests the right question to bring to a clinician is not what should someone my age do? but what should I, specifically, do given my labs, my training history, my diet, and my goals?

It is worth being clear about the evidence rating here. This is a narrative review distilling a body of work, not a single randomized trial with a headline effect size. The direction of the evidence is consistent and the mechanistic logic is well established, but the strongest claim the chapter makes — and the strongest claim we will repeat — is that personalized nutrition and structured exercise are the most reliable levers currently available for prevention and reversal of frailty. Magnitude, timeline, and durability will vary by individual.

The pragmatic read for a healthspan-minded reader is straightforward. First, treat frailty as a category worth thinking about now, in your fifties and sixties, rather than as a problem of your eighties. Second, resist the temptation to self-prescribe a protocol from a magazine — including this one — and instead use the review's framing to ask better questions of a qualified clinician. Third, recognize that nutrition and training are paired interventions: each makes the other more effective, and skipping one undercuts the other.

The most quietly radical line in the chapter is its premise: that the trajectory toward dependency is not fixed. For a population whose calendars are full and whose runways are long, that is the part worth holding onto.

The authors — a multidisciplinary panel writing in the journal of the International Association for the Study of Obesity — describe a clinical reality that has outpaced its own playbook. Incretin-mimetic drugs are working as advertised on body weight. But in trial participants treated for 68 to 72 weeks, roughly 10% or more of skeletal muscle mass went with the fat. The review's striking framing: that is approximately equivalent to two decades of age-related muscle loss, compressed into a little over a year.

For a looksmaxing readership, this is the part worth slowing down on. Muscle is the tissue that gives a lean physique its shape — the shoulder cap, the glute shelf, the quad sweep, the visible forearm. It is also the tissue that drives resting metabolism, glucose disposal, and the functional capacity that keeps a body looking athletic in motion rather than merely thin in photos. Losing a meaningful share of it during rapid weight reduction is not a cosmetic footnote. The review warns it can translate into reduced functional and metabolic health, weight cycling, and compromised quality of life.

The evidence here is rated moderate, and the language should match. This is a review synthesizing trial data, not a head-to-head protocol study proving a specific muscle-sparing regimen wins. What the authors do establish is a mechanism and a direction. Caloric restriction of any kind — pharmacological or otherwise — pulls from both fat and lean tissue. Incretin mimetics accelerate the restriction, which appears to accelerate the lean-tissue cost unless something is actively defending against it.

The review identifies two defenses with the strongest support: nutrition and physical activity, especially resistance training. Neither is novel. Both are routinely underdosed by people whose appetite has been pharmacologically muted and whose energy for the gym has dropped along with the hunger signal.

One of the more practical points in the synthesis is also the most counterintuitive: the drugs that make weight loss easy can make the muscle-sparing inputs harder. Appetite suppression is the mechanism, but it doesn't suppress selectively. Protein — the macronutrient most associated with satiety and most needed to defend lean mass during a deficit — is often the first thing that gets crowded out of a shrinking daily intake.

The review's nutrition guidance is direct in spirit if cautious in tone: ensure adequate intake and absorption of high-quality protein and micronutrients, and consider oral nutritional supplements when whole-food intake falls short. The authors do not prescribe a universal gram target, and neither should anyone reading a magazine. The shape of the recommendation, though, is clear: protein adequacy is not optional on these drugs, and many users are quietly under it.

Cardio is not the lever here. The review specifically names resistance training as the modality shown to minimize loss of muscle mass and function during weight-reduction therapy. The mechanism is intuitive: a tissue exposed to a meaningful mechanical signal is a tissue the body is reluctant to break down for fuel, even in a deficit. Subtract that signal during rapid loss and the body takes the path of least resistance.

For the appearance-focused reader, the implication is that the gym session is not an aesthetic add-on during a GLP-1 protocol — it is the protocol's structural counterweight. Without it, the drug is essentially deciding the body-composition split on its own.

The honest read on the current evidence is this: incretin mimetics are a legitimately powerful tool, and the muscle question is not a reason to dismiss them. It is a reason to use them with a body-composition strategy rather than a weight-loss strategy. The Obesity Reviews synthesis does not promise that a protein-forward diet and a serious lifting program will fully neutralize the lean-tissue cost. It argues, with the caution the data warrants, that they are the most credible defenses currently on the table — and that patients on these drugs should be in comprehensive treatment programs built around them.

The glow-up version of that idea is simpler. The drug will lower the number. Whether the body underneath looks — and functions — like the one you wanted is a separate project, and it starts the day the first dose does.

The CAIDE score was built to look forward from middle age. You add up points for the familiar variables — older age, fewer years of formal schooling, higher systolic blood pressure, higher cholesterol, higher BMI, physical inactivity, being male — and the total gives a rough probability of dementia twenty years on. Useful at 50. Less obviously useful at 70, when the twenty-year horizon is a different proposition and many of the inputs have already done their work.

So a group of Hungarian researchers, writing in GeroScience, took 101 healthy adults over 55, sorted them into lower- and higher-CAIDE groups, and ran them through neuropsychological testing and MRI. The higher-risk group performed measurably worse on the Trail-Making Test, a standard probe of executive function and processing speed. They also had smaller global brain volumes and smaller regional volumes, including in the nucleus accumbens, with a trend toward reduced functional connectivity in the default mode, salience, and central attention networks.

None of that is a diagnosis. It is a signal — and a modest-sized one, in a single cohort of healthy volunteers — that the same arithmetic clinicians have used to flag midlife risk still tracks something real in the brains of older adults. The authors put it carefully, and so should we: the score might help identify cognitively higher-risk individuals later in life. That is the appropriate temperature for this finding.

The second study is a different animal: bigger, broader, and observational. Researchers drew on the Chinese Longitudinal Healthy Longevity Survey — 64,872 older adults across multiple waves from 2002 to 2022 — and measured cognitive impairment with a Chinese version of the Mini-Mental State Examination. Through 2018, across four survey waves, prevalence sat at an average of 4.3%. In the 2022 wave, post-COVID, it rose to 6.8%, and the trend held independently of gender, age band, and rural-versus-urban residence.

That is a meaningful step up, and it is the first published look at this question extending through the pandemic. It is also worth reading the same paper's quieter findings. The 2022 wave recorded a decrease in mean calf circumference — a rough proxy for muscle mass, and one worth its own column — alongside an increase in the proportion of overweight participants and, oddly, increases in daily fruit and vegetable intake and regular physical activity. The lifestyle inputs moved in a mixed direction. The cognitive output moved in one.

What does that suggest? Not, on its own, that COVID infection caused the rise. An observational study of this kind cannot make that case, and the authors do not. What it does suggest is that the pandemic era — illness, isolation, disrupted care, deconditioning, the whole package — landed on older brains in a way that shows up at the population level. Whether that bend in the curve straightens out in the next wave of data is, frankly, the question worth watching.

Read together, these two studies do not announce a breakthrough. They do something more useful: they sharpen the focus. The CAIDE work suggests the same modifiable risks that mattered at 50 are still leaving fingerprints on brain structure and function at 60-plus. The CLHLS work suggests the population-level picture got worse in the pandemic years, and that recovery is not automatic.

The practical implications are unglamorous, and they should be. Blood pressure remains the single most consequential number on the CAIDE sheet that you and a clinician can actually move. Lipids, weight, and regular movement are the other three. Education is not retroactively adjustable, but cognitive engagement in the years you have is — reading, conversation, problem-solving, novelty. None of that is a cure, and nobody serious is selling it as one. It is risk reduction, which is the only game on the table.

One caution worth naming: a risk score is a probability tool, not a diagnosis or a prognosis. A high CAIDE number is a reason to have a careful conversation with your doctor about the inputs you can change. A low one is not a permission slip. And neither study tells you anything about what to do about a specific symptom you are noticing this week — that is what an appointment is for.

The evidence here is moderate. One cohort is small. The other is large but observational. Both are pointing, with reasonable confidence, in the same general direction: the levers we already knew about still work, and the last few years have made pulling them more important, not less.

The headlines will keep moving — new biomarkers, new drugs, new scoring systems. The unchanged part is that the brain rewards the same boring habits the heart does, and that the years immediately around a major public-health shock appear to have cost something that the long-running data is now starting to measure. Worth knowing. Worth acting on, at whatever age you are reading this. And worth, as ever, a conversation with someone who knows your chart.

If you are somewhere in the perimenopausal stretch and starting to notice that your cholesterol panel reads differently than it did a decade ago, this is the kind of news worth a minute of your attention. Not because vaccines are a heart-disease cure — they are not — but because the framing has shifted. The new consensus treats immunization as a routine piece of cardiovascular care for adults at high CV risk, and it lays out which shots have the strongest case behind them.

The mechanism, at least the version that fits on a cocktail napkin, goes like this: infections — particularly respiratory ones — light up the body's inflammatory response. That systemic inflammation is not friendly to existing arterial plaque. It can destabilize it, raising the odds of the cascade that ends in a heart attack or stroke. Prevent the infection, the thinking goes, and you blunt the inflammatory hit that might have tipped a vulnerable patient over the edge. The Taiwanese task force frames vaccination as a way to reduce viral and bacterial infections, minimize systemic inflammatory responses, support plaque stability, and reduce the likelihood of CV events in high-risk patients.

The document focuses on a familiar quartet: influenza, pneumococcal disease, herpes zoster (shingles), and COVID-19. None of these are new vaccines. What is new is a formal cardiology-endorsed argument that they belong in the prevention toolkit for people with — or at high risk of — cardiovascular disease.

Take shingles, which most of us file under "painful rash, deal with it later." The consensus authors point out that herpes zoster is associated with an increased risk of stroke and myocardial infarction — a connection that has been building in the literature for years but rarely makes it into the conversation at your annual physical. Influenza and pneumococcal infections, similarly, are flagged as important causes of high morbidity and mortality in older adults, and the downstream cardiovascular complications are part of why.

This is where I have to put on my honest-friend hat. The consensus is exactly that — a consensus, an expert-graded synthesis of the existing literature, not a single blockbuster randomized trial proving that a flu shot prevents your next heart attack. The authors describe it as a set of evidence-based recommendations drawn from the most current information, formulated specifically because vaccination rates in high-CV-risk adults remain sub-optimal despite years of supportive data.

Translation: the signal is real and the recommending bodies are credible, but the strength of the claim is "this is worth doing as part of cardiovascular prevention," not "this replaces anything you are already doing for your heart." That distinction matters. Anyone selling you a vaccine as a miracle cardiovascular intervention is overselling. Anyone telling you it has nothing to do with your heart is behind on the literature.

The other honest caveat: this is a Taiwanese consensus written for a Taiwanese clinical context, drawing on a global evidence base. The infection biology is universal, but the specific schedules, products available, and reimbursement realities are not. If you take one thing into your next appointment, take the question — not the prescription.

Most of the women I write for are not yet in the "high cardiovascular risk" bucket that the consensus is explicitly aimed at. But midlife is exactly when that bucket starts filling up — quietly, without drama, often without symptoms. The years between 35 and 55 are when the risk calculus changes, and they are also the years when a lot of us start dropping the routine preventive stuff because life gets loud.

The useful read on this consensus is not "go demand every vaccine on the list." It is that the wall between "infection prevention" and "heart prevention" is thinner than the way we usually talk about health makes it sound. The body does not file inflammation in tidy categories. A respiratory infection at 52, with a few cardiovascular risk factors already in play, is not just a rough two weeks — it is a stressor on a system that may already be working harder than it should.

None of this is a reason to panic, and none of it replaces the unglamorous basics: sleep, movement, blood pressure, cholesterol, the conversation with your clinician about what your specific risk picture looks like. But the next time the pharmacy sends you a reminder about a shot you have been putting off, it might be worth treating it as a cardiology appointment, too.

The condition now goes by an unlovely acronym: MASLD, for metabolic dysfunction-associated steatotic liver disease. (You may remember it by its older name, NAFLD — non-alcoholic fatty liver disease.) A 2025 review in Clinical and Experimental Hepatology describes it as the most common chronic liver disease in the world, affecting about 30% of adults and roughly 10% of children. Those numbers may be undercounts — MASLD is famously quiet, often producing no symptoms until something else, like a routine blood panel or an ultrasound for a different complaint, flags it.

What's changing is not the prevalence of fatty liver but the company it keeps. The same review names MASLD outright as an important cardiovascular risk factor, and frames it inside a familiar cluster of weight-dependent problems: insulin resistance, prediabetes, type 2 diabetes, lipid disorders, hypertension. If you've ever seen the words "metabolic syndrome" on a lab printout, MASLD lives in that neighborhood.

Here is the part that reframes the whole conversation. A 2025 cross-sectional study in the Middle East Journal of Digestive Diseases looked at 200 patients with coronary artery disease who were headed for angiography, then measured both their fatty-liver severity (by ultrasound) and their carotid arteries (by Doppler). The carotids are the big vessels in your neck that feed the brain; narrowing there is one of the markers cardiologists watch closely.

The pattern was striking. Among patients with carotid stenosis, 44% had grade 2–3 fatty liver, compared with 19% of patients without stenosis. Higher scores on the FIB-4 index — a simple blood-test-based estimate of liver scarring — tracked with more severe coronary involvement and a higher prevalence of carotid narrowing. This is a single cross-sectional study, not proof of cause and effect, and the patients were already known to have heart disease. But it adds to a body of work suggesting that the inflamed, fibrotic liver is not minding its own business — it appears to be part of the same vascular story.

If you're reading this between feedings, here is the version that fits on a sticky note: the drivers of fatty liver are the drivers of heart disease. The review authors are direct about this — the foundation of prevention and treatment is weight reduction through diet and regular physical activity, plus management of the cardiometabolic factors: diabetes, lipid disorders and hypertension. Drug therapy aimed at the liver itself, they note, remains limited; many candidates are still in clinical trials.

That's not a thrilling headline, but it is a kind one. It means the small, ordinary things — a 20-minute walk with the stroller, swapping one ultra-processed snack for something with fiber, not skipping the boring annual check-in with your GP — are doing real work on more than one organ at once. You are not behind because you haven't optimized a supplement stack. The evidence base is moderate, not miraculous; the levers are familiar.

There's a related strand of this story for anyone who has been treated for hepatitis C. Modern antivirals clear the virus in the great majority of cases, but a 2025 expert position statement in Clinical and Experimental Hepatology argues that the cardiometabolic aftermath needs its own care plan. The authors note that HCV is now considered a new, non-classical cardiovascular risk factor, and that the constellation of obesity, insulin resistance, diabetes, lipid problems and fatty liver that follows infection is significant enough to have its own name: metabolic-viral syndrome. Their recommendations focus on hypolipidemic and antithrombotic therapy in patients treated with direct-acting antivirals, with attention to drug interactions. It's a specialist document, but the takeaway for the rest of us is the same: clearing the virus is the start of the conversation, not the end.

None of this is a verdict. The evidence connecting fatty liver to cardiovascular disease is growing and increasingly hard to ignore, but much of it — including the carotid study above — is observational, and the disease-modifying drug story is still being written. What has shifted is the framing. A generation ago, fatty liver was the thing your doctor mentioned in passing on the way out of the room. Today, the people who study it are asking whether it belongs on the same page as your blood pressure and your cholesterol.

For a tired parent, that reframing is, oddly, good news. It means the work you might already be trying to do — sleep when you can, move when you can, eat something that didn't come out of a foil pouch — counts toward more than one ledger. Pour the second coffee. Text your friend back. Tell her it's worth a conversation with her doctor, not a spiral at 2 a.m.

The study, published in Psychology and Aging, leans on something researchers rarely get: three separate "measurement bursts" spread across 18 years, each capturing eight consecutive days of stressors and moods. That's 33,942 days of real life — Mondays, birthdays, bad-news Wednesdays — stacked against Big Five personality scores taken at every wave. The result is a rare, rigorous look at whether daily stress and personality drift together over the long haul. The short answer, according to the researchers: yes, they do.

Quick gloss, because the word does a lot of work here. Stressor exposure is whether something annoying happened — argument, deadline, traffic. Stress reactivity is the size of the emotional bump that follows. Two people can have the same kind of day; one shrugs, the other simmers until dinner. The simmer is reactivity.

Why does that matter for who you are? Personality researchers increasingly think of traits less as fixed furniture and more as patterns that get rehearsed. Every day you respond to friction in a certain way, you're sort of practicing being a person who responds that way. Do it for two decades, and the practice may start to show up on the trait questionnaire.

Here's where it gets interesting. At the starting line, people who reacted more strongly to daily hassles also tended to score lower on extraversion and conscientiousness, and higher on neuroticism, the authors report. That part isn't shocking — those links show up in shorter studies too.

The longitudinal piece is the headline. People whose reactivity climbed across 18 years also tended to see declines in extraversion, agreeableness, and openness. Translation, roughly: more emotionally bumpy days seemed to travel alongside becoming a little less outgoing, a little less easygoing, a little less curious about new things. None of those shifts are catastrophic on their own, but compounded over a couple of decades, they hint at a slow rewiring of social and exploratory life.

The non-findings are just as worth noting. Changes in reactivity were not linked to changes in neuroticism or conscientiousness over time. That's a useful surprise: the trait we'd most expect to budge — neuroticism, basically the dial for negative emotionality — didn't move in step with reactivity at the change level. The authors don't claim to know why, and neither will I.

Honestly? Seriously, but not breathlessly. PinnacleLife rates the evidence here Moderate, and that feels right. The design is unusually strong for personality science: a big sample, repeated daily diaries (not just one-off surveys), and a multilevel model built to separate "how you usually are" from "how you're changing." That's miles beyond a single-wave correlation.

But — and it's a real but — this is still observational. Nobody randomly assigned anyone to a more reactive life. Genetics, health events, relationships, income, even sleep could be quietly steering both reactivity and personality. The study can show the two drift together; it can't prove one tugs the other.

It also doesn't tell us what to do. The data don't show that lowering your reactivity will pull extraversion back up, or preserve openness into your seventies. That's a hopeful hypothesis, not a finding. Anyone selling you a "reactivity protocol" off the back of this paper is getting ahead of the science.

I'll be honest, the thing that stuck with me wasn't the trait list. It was the reframe. We tend to think of "who we are" as the big stuff — career, relationships, the story we tell at parties. This study is a quiet argument that the small stuff might matter just as much. The 4 p.m. inbox flare. The grocery line. The eight-day stretch where nothing went right.

None of that proves anything about your future self. But the next time a tiny stressor hits and you feel the simmer start, it might be worth a second of curiosity instead of self-judgment. Not because one bad reaction will define you — it won't — but because, over a long enough timeline, the pattern might be doing more work than we ever gave it credit for.

For years, the perioperative debate around GLP-1 receptor agonists has centered on a single anesthesia concern: delayed gastric emptying and the aspiration risk it creates on induction. That conversation isn't over. But the newer data look further down the timeline — at 90-day complications, readmissions, revisions — and they suggest the risk profile is not uniform across the body. It's joint-specific, and probably tissue-specific.

Start with the good news. A retrospective national-database analysis of 14,065 patients with type 2 diabetes undergoing primary total hip arthroplasty between 2016 and 2021 used propensity score matching to compare 812 GLP-1 users against 3,248 non-users. The headline: no significant differences in 90-day surgical or medical complication rates, and no difference in one-year revision or periprosthetic joint infection rates. If anything, the non-GLP-1 group was more likely to have extended hospital stays of three days or longer (odds ratio 1.25).

That's a clean signal for the hip. For a 45-year-old diabetic patient staring down a THA, the current best evidence does not flag the GLP-1 as a reason to pause or panic.

Now the part that should make you slow down. A separate 2025 analysis using the TriNetX database looked at total shoulder arthroplasty — anatomic and reverse — from 2010 to 2023. After 1:1 propensity matching, 1,259 GLP-1 users were compared to 1,259 controls. In the 90 days after surgery, GLP-1 users showed significantly higher rates of deep vein thrombosis (1.6% vs. 0.9%, OR 3.0), myocardial infarction (1.6% vs. 0.9%, OR 2.84), pneumonia (3.34% vs. 1.50%, OR 2.25), transfusion (7.1% vs. 4.3%, OR 1.7), and readmission (8.1% vs. 5.2%, OR 1.6). These held up after Bonferroni correction at a strict P<.005 threshold.

Why the shoulder and not the hip? The authors don't fully explain it, and neither will I — that's the honest answer at this stage. Possibilities range from differences in patient positioning and pulmonary mechanics during shoulder surgery, to the underlying populations selecting into each procedure, to residual confounding the propensity model couldn't catch. What's clear is that the assumption "GLP-1s look fine in knees and hips, so they're fine everywhere" doesn't hold.

There's a third piece of 2025 data that doesn't fit neatly into a surgical checklist but matters enormously for anyone making a perioperative plan. A cohort study of 69 individuals with type 2 diabetes tracked what happened when patients had to stop dulaglutide during a global supply shortage. Within three months of discontinuation, average HbA1c rose from 7.0% ± 0.9% to 8.1% ± 1.4%, and fasting glucose climbed from 129 ± 31 to 156 ± 50 mg/dL. Switching to DPP-4 inhibitors or SGLT2 inhibitors did not fully compensate.

For a surgical patient, that's a real problem. Elevated perioperative glucose is itself an independent risk factor for wound complications and infection. If your surgeon asks you to hold your GLP-1 in the days before a procedure — a reasonable request given the aspiration question — and you can't easily restart it afterward because of a supply gap, you may be trading one risk for another. This is a conversation to have on the front end, not the day before.

None of these studies are randomized trials. They are retrospective, propensity-matched cohort analyses — strong enough to flag patterns, not strong enough to dictate a protocol. The evidence here is moderate, not settled. Mechanism is largely inferred, not demonstrated. And the shoulder data, in particular, will need replication and prospective work before anyone can say with confidence whether the drug, the population, or the procedure is doing the driving.

What does change today is the quality of the conversation you can have with your own clinician. If you're on a GLP-1 and you have elective surgery on the calendar, the procedure type matters. The continuity of your therapy on the back end matters. And the default assumption that "these drugs are universally safe around surgery" is no longer adequate — not because the drugs are dangerous, but because the picture is more granular than the marketing.