Tag: Obesity Medicine

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Longevity Medicine: What Actually Works, and What Doesn’t

On By Dr. Scott RennieIn Longevity & Healthy AgingLeave a comment

Longevity medicine is a wide field, and most of it is not what gets marketed. This is a review of what the evidence actually supports, from fitness and blood pressure to the drugs and supplements patients ask about by name.

Patients bring me longevity questions on video, which is how every visit I do happens. It usually arrives as a general question about what I recommend for living longer, followed by one specific thing they read about online. Phosphatidylcholine. Rapamycin. GLP-1 medications.

Here is the part that disappoints almost everybody. The things with the largest measured effect on how long you live are cheap, boring, and nobody can patent them, so nobody sells them. The drugs people ask about by name sit lower on the list, and several sit there with no human results at all. That does not make them worthless. I prescribe GLP-1 receptor agonists and think they are the most important thing to happen to metabolic medicine in my working life. The point is ordering.

What actually works, and it is not a close call

Start with cardiorespiratory fitness, which means how well your heart and lungs move oxygen while you work hard. Nothing else here comes close to it.

Mandsager’s team at Cleveland Clinic followed 122,007 patients who had treadmill tests between 1991 and 2014. The fittest group came out at an adjusted hazard ratio of 0.20 against the least fit (1). A hazard ratio compares the risk in one group against another. Anything under 1.00 means less risk, so 0.20 means the fittest people died at roughly a fifth the rate of the least fit. That is an enormous gap.

That paper also produced the line that being unfit is worse than smoking, and here is the correction. It reported hazard ratios of 1.41 for smoking and 1.40 for diabetes sitting next to 1.41 for below-average fitness (1). Those are similar sizes inside one model. Nobody raced them against each other, and a poor treadmill result is partly a measure of disease nobody has found yet. The pattern does hold up elsewhere, at roughly 14 percent lower death rates for each one-MET gain in fitness (2). A MET is a unit of effort, and one MET is about what your body burns sitting still, so gaining one is real training.

Resistance training is the second lever, and the useful finding is where it stops. Momma pooled dozens of studies and found that any muscle-strengthening work was linked to a 10 to 17 percent lower risk of death, heart disease, cancer and diabetes. The benefit peaks at 30 to 60 minutes a week and flattens after 60 (3). Two half-hour sessions. That is the whole prescription, and the flattening is the part fitness content never mentions, because there is no business in telling somebody they are done.

Grip strength comes at it sideways. In PURE, across 139,691 adults in 17 countries, the death rate rose with a hazard ratio of 1.16 for every 5-kg drop in grip (4). Grip stands in for how much muscle you carry. Nobody should go train their hands.

Nobody ever counted to ten thousand

Paluch pooled 15 cohorts and found the benefit of daily steps levels off around 6,000 to 8,000 for adults 60 and older, and 8,000 to 10,000 under 60 (5).

Here is my one digression. The 10,000 figure has no medical origin whatsoever. It came from a pedometer sold in Japan in 1965, the manpo-kei or ten-thousand-step meter, named partly because the Japanese character for ten thousand looks a bit like a person walking. A marketing name became a health target millions of people feel guilty about missing. Nobody ever checked the math.

The interventions with no sales force

SPRINT assigned people at random to a tight blood pressure goal, under 120 on the top number, against the usual goal of under 140. All-cause mortality, meaning death from any cause, came out at a hazard ratio of 0.73, with an NNT of about 90 over a median of 3.26 years (6). NNT is the number needed to treat. Hold 90 people to the tighter goal for a bit over three years and one of them lives who otherwise would not have. Nothing sold as a longevity supplement has an NNT, because none of them has ever been tested against death.

Quitting smoking gives back more life still. From Jha’s 201,248 US adults, quitting between 25 and 34 gets back about ten years, and quitting in your late fifties still returns four (7).

Sleep follows a U-shaped curve, with the lowest risk near seven hours and the risk climbing faster on the long side, up to a relative risk of 1.37 at ten hours (8). What I want people to stop expecting is a heart benefit from CPAP. SAVE assigned 2,717 adults with moderate-to-severe sleep apnea and known heart disease at random, and the main result came back at HR 1.10, flatly null, which means no difference at all (9). None. CPAP treats symptoms. Say that out loud when you prescribe it.

Then the one physicians skip. Holt-Lunstad’s pooled work put the odds of dying at 1.29 for social isolation and 1.26 for loneliness, with living alone at 1.32 (10). The line about loneliness equalling fifteen cigarettes a day restates those same odds rather than adding a calculation, so hold it loosely.

Diet belongs here too, and PREDIMED is where the honest version lives. Its Mediterranean groups cut the main heart outcome by roughly 30 percent, which is a real result, though the trial was never built to measure death from any cause, and it was pulled and republished in 2018 after an audit found problems with how 1,588 of 7,447 people were assigned (11). Eat that way for your heart. It does not follow that it buys you years.

Weight loss, and what SELECT actually settled

For years there was no good answer on whether losing weight on purpose lowers the death rate. Look AHEAD assigned 5,145 adults with type 2 diabetes at random to an intensive diet and exercise program, held weight loss near 6 percent, and returned a heart outcome of HR 0.95 before stopping for futility (12). Well conducted. Well powered. Null.

SELECT changed that without finishing it. 17,604 adults with overweight or obesity and known heart disease, no diabetes; major heart events hit 6.5 percent on semaglutide against 8.0 on placebo, HR 0.80 (13). All-cause mortality came in at HR 0.81, 95% CI 0.71 to 0.93, and gets quoted everywhere as proof. It is not, and the reason is worth knowing. The trial used hierarchical testing, which means the questions were ranked in advance and answered in order, and once one of them fails, nothing below it counts as proof anymore. That chain broke a step earlier, at heart-related death, HR 0.85, CI 0.71 to 1.01, P=0.07. So the rule bit. So the death result is a strong hint. I think the effect is probably real. I will not tell you it has been proven.

The prescriptions people ask me for by name

GLP-1 receptor agonists are the only drugs here I reach for gladly, and I use them for obesity and its complications. FLOW cut its main kidney outcome to HR 0.76 in 3,533 patients with type 2 diabetes and chronic kidney disease, stopped early because the drug was plainly working, and turned up roughly 20 percent lower all-cause mortality among the secondary results, though I could not confirm the exact confidence interval on that one (14). SURMOUNT-MMO is testing tirzepatide against a combined outcome that includes death from any cause, and it has reported nothing (15). Orforglipron, approved April 2026 as the first pill in the class, has no death data either (16). I prescribe it. I do not pretend it has evidence it does not have.

The catch is muscle. Across these trials, lean tissue was about 45 percent of the weight lost with semaglutide in STEP-1 and about 26 percent with high-dose tirzepatide in SURMOUNT-1 (17). Lean tissue is mostly muscle. Losing close to half your weight as muscle matters in a 68-year-old whose grip is already borderline. It matters a lot. Protein at 1.0 to 1.2 g/kg/day is the geriatric target, and in older patients that is the number I use (18). For most other adults the adequate intake sits higher, and I aim for 80 to 120 grams a day, or 1.6 g/kg/day. Resistance training two to three days a week, covering all major muscle groups, is what decides how much of that muscle survives the loss.

Metformin I would not prescribe to a person without diabetes for longevity. The famous claim is Bannister’s 2014 comparison, which adjusted for nothing: 14.4 deaths per 1,000 person-years among metformin-treated diabetics against 15.2 in matched non-diabetic controls (19). A twenty-year reanalysis found the reverse (20). Most of that first result is confounding by indication, meaning the people who stay on metformin alone were healthier to begin with, in better shape before anyone handed them a pill, so the drug quietly takes credit for a head start it never gave them. TAME was meant to settle it, and as of August 2026 AFAR’s own page still describes it as seeking funding, enrollment not begun (21). Two randomized trials meanwhile found metformin blunting the gains older adults get from exercise, cutting improvements in how well muscle cells make energy and in fitness (22), and losing to placebo on lean mass at 1,700 mg/day over 14 weeks of resistance training (23). Fitness and muscle are the two biggest levers in this piece. Dulling both to chase a result nobody has repeated is a bad trade.

Rapamycin. PEARL assigned 114 adults aged 50 to 85 at random to placebo or 5 or 10 mg of weekly compounded rapamycin for 48 weeks and found it tolerable, with side gains in lean tissue and self-reported pain in women at the higher dose (24). The trial was funded and run by AgelessRx, a longevity telehealth company that sells the thing being studied. Human data on living longer does not exist. I would not write it for this. Senolytics have less. A senolytic is a drug built to clear out worn-out cells that have stopped dividing but keep irritating the tissue around them, and no senolytic has produced any human data on health or lifespan. Everything published so far is safety work (25).

Statins I treat as cholesterol drugs, which is what the guidelines say they are; PREVENTABLE reports in December 2026 on adults over 75 without heart disease (26).

Aspirin is the cleanest example of a longevity assumption failing once somebody randomized it. ASPREE tested low-dose aspirin in healthy older adults for primary prevention, meaning people who had never had a heart attack or a stroke. They died at a higher rate on aspirin, HR 1.14, driven mainly by cancer death, with more major hemorrhage, meaning serious bleeding, and no heart benefit (27). The primary endpoint, which is the single question a trial is built to answer, was years lived without disability, and it showed nothing (28). If you take a daily aspirin with no vascular disease because someone suggested it in 2006, raise it at your next visit.

The supplement aisle, and phosphatidylcholine in particular

NAD+ precursors sell on a mechanism and a biomarker. A biomarker is something you can measure in blood that may or may not track with how you feel or how long you live. Nicotinamide riboside raises whole-blood NAD+ up to 142 percent at 1,000 mg over two weeks, in an open-label study with no clinical endpoint (29). A review of ten NMN trials found the same shape: NAD+ rises, a thin signal on physical performance, nothing resembling a disease or death outcome (30). Tested against thinking and memory in people with mild cognitive impairment, it moved the blood chemistry and nothing else (31).

The ones people tell me they are already on are NAD+ precursors, NMN or NR, and resveratrol. Resveratrol has its own long and contested story, which this post is not going to settle, so read its absence from the rest of this as scope rather than a verdict.

NMN’s legal status is a mess. FDA ruled in November 2022 that it does not count as a dietary supplement, and trade reporting says two FDA letters dated September 29, 2025 reversed that. I have not confirmed those letters against FDA’s own text, so treat the status as unsettled.

Taurine is the most interesting fight in the field. Singh’s 2023 Science paper stretched the median mouse lifespan by 10 to 12 percent and reported that taurine in the blood falls with age in humans, monkeys and mice (32). That second claim is what created the product. An NIA-led group then found taurine flat or rising with age across three human groups plus primates and mice (33), and a separate group measuring 137 men aged 20 to 93 found no link between taurine and age, muscle, strength or how well muscle cells make energy (34). The mouse result stands unchallenged. The human claim underneath the marketing failed to repeat. Twice. No trial has tested taurine against a real human outcome. Anyone selling you certainty either way has not read all three papers.

Phosphatidylcholine earns its own answer, because the real story beats the marketing one. It is a fat molecule and one of the main ways we get choline from food, sold in pills for memory and cell health, and injected as a fat-dissolving product. Pill trials of phosphatidylcholine and lecithin have not helped memory in Alzheimer’s disease, the supporting work on lifespan sits in worms and mice, and no human trial measures anything that matters.

The case against it is better built than the case for it. Choline, phosphatidylcholine and carnitine feed gut bacteria that make a compound called trimethylamine, which the liver turns into TMAO. Tang followed 4,007 heart patients and found that high TMAO went with more heart attacks and strokes (35), building on Wang’s 2011 Nature paper showing that gut bacteria breaking down phosphatidylcholine drives artery disease in animals (36). Read that honestly and the research against phosphatidylcholine pills is stronger than the research for them. I would not take it. The injected version is worse. FDA warns about phosphatidylcholine and sodium deoxycholate products sold online as Aqualyx, Lipodissolve and Kabelline, and the only approved injection for fat reduction is deoxycholic acid on its own, for fat under the chin (37).

The money I would rather you did not spend

Injectable peptides bought online are the clearest line I draw. FDA put several, BPC-157 and epitalon among them, into category 2 of its bulk drug substances list in September 2023, which flags a real safety risk and blocks pharmacies from mixing them up for patients (38). There has been plenty of trade reporting that HHS moved to pull most of them back off that list. I have not confirmed any of it against FDA’s own text, so I am not going to tell you the rules changed. Coming off a restricted list would not be approval anyway. It never was.

I have seen videos online of people advocating injecting peptides, and it makes me uneasy.

Stem cell and exosome clinics have a legal record anyone can read. A federal court ruled against US Stem Cell Clinic in 2019, finding its product adulterated and misbranded, which are the legal terms for failing quality standards and being sold under a false label, and the reported harms include blindness. FDA states there is no approved exosome product for any medical use in this country (39). Young plasma got its own February 2019 FDA notice: no convincing evidence of benefit, against risks including fluid overload, TRALI, which is a serious lung injury, and catching an infection from the donor (40).

Growth hormone marketed for aging can put you in criminal court. 21 U.S.C. §333(e) makes it a federal felony to hand out hGH for anything other than an FDA-approved use in a diagnosed disease, and FDA counts writing the prescription as handing it out (41). It is the only drug in the code carrying that rule. The pitch still traces to Rudman’s 1990 NEJM paper: 21 men, six months, no placebo group, an 8.8 percent rise in lean body mass (42). Nobody counted deaths, and nobody was blinded. NEJM said in 2003 that consumers who meet those citations are being misled (43). Still doing sales work.

Consumer epigenetic age tests belong in the entertainment column. A 2025 preprint reports that running one sample twice can give answers as much as nine years apart on some clocks, and the reliability problem shows up in peer-reviewed work too (44). If your number moves three years after you start a supplement, you measured the test.

Full-body MRI in people with no symptoms is the expensive one. Scans turn up a confirmed cancer roughly 1.1 to 1.5 percent of the time, while about 95 percent of healthy adults show an incidental finding, meaning something the scan spots by accident, and around 91 percent of those turn out to mean nothing (45). Nine in ten. Nothing. What it reliably produces is a repeat MRI, a biopsy of something harmless, and months of fear. Skip it.

For patients, and for the clinicians reading over their shoulder

If you are a patient, work the list in the order the effect sizes come in. Blood pressure to target, which on my end means you own a cuff and bring me the readings, since I cannot take them from here. Quit smoking at any age, because the payoff is measured in years rather than percentage points. Build an aerobic base and lift something twice a week. Then, with whatever money and attention is left over, consider a supplement, and ask one question before you buy it: what did the trial actually measure? If the answer is a blood level, a clock or a marker, it did not measure your life. That question alone empties most of the aisle.

If you are a clinician, the awkward part of this field is that our best-evidenced longevity drugs are ones we already prescribe under other names. Blood pressure drugs, statins, GLP-1 receptor agonists, quit-smoking therapy. Patients arrive on video already carrying things they bought from direct-to-consumer platforms, so ask what they are taking without an eyebrow, because a patient who feels judged stops telling you. Get the compounded rapamycin, the peptide vial and the NMN into the chart and screen interactions properly. When you quote SELECT, quote the hierarchical testing failure along with it.

The Bottom Line

The gap between the best-proven ways to live longer and the most heavily marketed ones runs opposite to the ad money. Cardiorespiratory fitness, blood pressure control, and never picking up another cigarette sit at the top, with effects no capsule has come near.

GLP-1 receptor agonists have real outcome data and a real reason to use them. Metformin for longevity in people without diabetes rests on a weak comparison nobody randomized, plus two randomized trials showing it gets in the way of exercise. Rapamycin is interesting and unproven in humans. Senolytics have nothing at all. Aspirin in healthy older adults who had never had a heart attack made things measurably worse. NAD+ precursors move a blood level nobody has shown you should care about, the human claim behind taurine failed to repeat, and phosphatidylcholine has better research against it than for it.

Buy the used bike before you buy the peptide. If you want one thing to do this week, it does not cost anything.

Scott Rennie, D.O.
Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Sources

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Large red EMERGENCY sign on the exterior of a hospital emergency department

Nurse Practitioners vs. Doctors in the ER: What the Research Actually Shows

On By Dr. Scott RennieIn Healthcare System & TechnologyLeave a comment

A paper landed in the American Economic Review this month that is going to get quoted badly by almost everyone who quotes it. Physician groups will pull three numbers out of it. Nursing organizations will pull a different three. Both sets are in there, which is exactly why the paper is worth an hour of your attention instead of a headline.

David Chan and Yiqun Chen looked at 1.1 million emergency department visits across 44 Veterans Health Administration sites, involving 156 nurse practitioners and 1,348 physicians (1)(2). What makes it different from the usual scope-of-practice study is the design. VA provider schedules are set months in advance. Patients show up when they show up. That mismatch means the question of whether you got an NP or a physician on a given night was close to a coin flip rather than a reflection of how sick you looked, and it lets the authors claim causation instead of the correlation that plagues most of this literature.

What the numbers say

Patients seen by NPs had emergency stays 11 percent longer and cost about 7 percent more, roughly 66 dollars per visit (1)(3). Thirty-day preventable hospitalizations ran 20 percent higher. The AMA ran the arithmetic forward and estimated that routing a quarter of VA emergency patients to NPs adds about 129 million dollars a year net, after accounting for the salary difference between the two groups (3).

Thirty-day mortality showed no statistically significant difference (2).

Hold onto both of those. People are going to publish articles this fall that mention one and not the other.

The number everyone is going to skip

Here is the finding I think actually matters, and it is the one I expect to see least in the press coverage. It needs a slow walk, because it is the part that gets garbled every time.

Everything in the section above compares two averages. Add up all 156 NPs and take the mean. Do the same for the 1,348 physicians. Compare the two. Physicians win that comparison, and I am not waving that away.

Now throw the other profession out and look at physicians alone. We are not all the same. Some of us order a great deal of testing and some order very little. Look at length of stay instead, or at thirty-day bouncebacks, and the same wide scatter turns up. The NP group has an equally wide scatter inside it.

What Chan and Chen found is that the spread inside each profession is larger than the distance between the two averages. The gap between a low-resource physician and a high-resource physician is wider than the gap between the typical physician and the typical NP.

Put those two facts together and the distributions overlap most of the way. The strongest NPs sit well inside the physician range. The physicians at the expensive end sit well inside the NP range.

So the authors ran the obvious test. Pull one NP at random. Pull one physician at random. Compare what each of them actually did, and repeat that many times over. The NP is the better performer in 38 out of every 100 draws (1)(2).

That is not a rounding error, and the number is worth calibrating against the two ends it could have landed on. If the professions were genuinely separate tiers, with the weakest physician still ahead of the strongest NP, you would expect something near zero. If they were interchangeable you would expect 50. Thirty-eight sits far closer to interchangeable than to separate.

Two things it does not say. It does not say NPs are 38 percent as good. It does not say that 38 percent of NPs outperform physicians across the board. It describes random one-to-one matchups and nothing wider than that.

And physicians still take 62 of those 100 draws. The average difference did not evaporate. Both of those are true at the same time, and holding both at once is the whole trick with this paper.

The gap also moved around depending on what walked in the door. For the least complicated cases, the extra cost attached to NP care fell by roughly 80 percent compared with the average case (2). It narrowed further as NPs accumulated years, and narrowed again as they accumulated reps with a specific condition. Chan framed the takeaway as a question of “which patients they should see” rather than whether NPs should practice at all, and I think that is the honest reading of his own data.

The mechanism looks like uncertainty, not carelessness. NPs ordered more diagnostic testing and more specialist consults. For sepsis, stroke, and heart failure they were substantially more likely to admit. They wrote fewer opioid prescriptions and more antibiotic prescriptions (2). Read that list as a set and a pattern shows up: when the picture was ambiguous, the threshold to spend a resource dropped. Anyone who has been six months out of residency recognizes that behavior in themselves, because we all did it, and the thing that fixed it was not a different diploma but two thousand more patients.

An aside, because the word keeps getting misused. “Productivity” here is an economics term. It means outputs relative to inputs consumed, not effort expended and not how hard someone works. Nothing in this paper says NPs work less hard. It says a given clinical result cost more to produce.

Where I think it is weakest

One health system. One care setting. One hundred fifty-six NPs, against a national workforce of more than 461,000 licensed NPs (4)(5). The AANP’s objection that you cannot generalize from that sample to every emergency department in the country is fair, and I would make the same objection if the finding had gone the other way.

The VA population is also not America. Older, more male, more comorbidity, and enrolled in an integrated system with a shared record. The VA also grants full practice authority, which means these NPs were working without the collaborative arrangement most of my colleagues in private systems actually have. What the paper cannot see is the physician who glanced at a chart, said one sentence in passing, and quietly changed a plan. That interaction leaves no data trail and it happens constantly.

None of that makes the effect estimates wrong. It makes them local. An 11 percent length-of-stay difference in a VA emergency department is a measurement of that department, and treating it as a national verdict on a profession is a category error.

What this means for a virtual urgent care visit

Most of my work is telemedicine, so this is the setting I thought about first. Virtual urgent care now runs largely on nurse practitioners and physician assistants, and the mechanism Chan and Chen identified does not carry over to a video call cleanly. I cannot order a CBC in the middle of an encounter. I cannot walk anyone down the hall for imaging. When uncertainty rises the levers available are prescribe empirically or send the patient somewhere with hands, which happen to be the same two the study found NPs pulling more often (2).

There turned out to be more to say about that than belongs inside a piece about an economics paper. What the payment and rating structures do to the decision. Why recognizing the sick patient matters more in this setting than almost any other. What happens when the platform cannot order a test at all. I put all of it in its own article: Spotting the Sick One: The Only Decision That Really Matters in Virtual Urgent Care.

Virtual weight management is a different problem, and a more forgiving one.

Weight management is a different animal, and I think the gap mostly closes

Obesity medicine breaks almost every condition that produced the ED result. There is no undifferentiated chest pain arriving at 2 a.m. The diagnosis is usually made before the visit starts. Care is longitudinal, protocol-heavy, and forgiving of a decision revisited in four weeks. The study’s own results predict a smaller gap here, because it found the difference shrinking by about 80 percent on the least complex cases and shrinking again with condition-specific experience (2). An NP who has titrated a thousand patients through semaglutide dose escalation has more relevant pattern recognition than a physician who has titrated forty.

That said, the complexity in this field is real. It just shows up in different places than people expect. Sorting expected GLP-1 nausea from something needing imaging. Recognizing that a patient on 30 units of basal insulin and a sulfonylurea will need those doses coming down as the weight comes off, before the hypoglycemia arrives rather than after. Pancreatitis history. Family history of medullary thyroid carcinoma. Restrictive eating patterns that look like excellent adherence on a video call and are not. Secondary causes, and the long list of psychiatric medications that drive weight gain and never get revisited.

So the risk in virtual weight management is not the credential on the screen. It is the eight-minute refill visit, whoever is running it. A physician doing rushed protocol care and an NP doing thorough protocol care are not close, and I would put my patients with the second one.

The tell is what got asked. Did anyone go back through the medication list once the weight started coming off, or was the box checked and the refill sent? Did anyone ask what the patient is actually eating on the days the nausea is bad, which is the question that separates a tolerable side effect from six weeks of accidental starvation. Nothing on that list has a degree attached to it. It has time attached to it, and time is a scheduling decision made by somebody in an office who has never met the patient.

For patients

You are allowed to ask who you are seeing and what their background is, and no reasonable clinician will be offended. What you should not do is treat the letters after the name as the whole answer. This study says a randomly chosen NP outperforms a randomly chosen physician 38 times out of 100. Experience with your specific problem is the more useful question. If you are starting a GLP-1, ask how many patients they have managed on it. If you are calling a virtual urgent care with chest pain or a severe headache, understand that any competent clinician in that setting is going to send you somewhere with a CT scanner, and that is the correct answer rather than a failure of the visit.

For clinicians

Two things I would take into practice from this paper. First, the within-profession spread being wider than the between-profession spread should change how we think about quality improvement. We spend enormous political energy on scope-of-practice fights and almost none on identifying and coaching the outliers inside our own group, and the data says the second one has more room in it.

Second, the actionable finding for anyone designing care is the complexity gradient rather than the average effect. Straightforward cases should route broadly. Diagnostic ambiguity and high-acuity complaints should route to whoever has the most reps with them, assigned on individual performance data rather than on license class. That is a solvable engineering problem and almost nobody is solving it.

The Bottom Line

This is a serious paper with a genuinely strong design, and its central finding is not the one being headlined. Physicians came out ahead on average in a VA emergency department. NPs came out ahead in 38 percent of head-to-head matchups, the difference nearly disappeared on straightforward cases, and thirty-day mortality was a wash. The spread inside each profession was wider than the gap between them, which is the part worth carrying around.

For virtual weight management I expect the gap to be small, and I care far more about how much time the visit gets and how deep the protocol runs than about which degree is on the screen.

Match the case to the clinician. That is the finding.

Scott Rennie, D.O.
Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Sources

  1. Chan DC Jr, Chen Y. The Productivity of Professions: Evidence from the Emergency Department. American Economic Review, August 2026. https://www.aeaweb.org/articles?id=10.1257/aer.20241007
  2. Berkeley Research. New study upends traditional thinking about doctors versus nurse practitioners. August 22, 2026. https://vcresearch.berkeley.edu/news/new-study-upends-traditional-thinking-about-doctors-versus-nurse-practitioners
  3. American Medical Association. Nurse practitioners’ care linked to 11% longer stays in the ED. https://www.ama-assn.org/practice-management/scope-practice/nurse-practitioners-care-linked-11-longer-stays-ed
  4. Clinician.com. Organizations Take Issue with Data Regarding Nurse Practitioner Care in the ED. https://www.clinician.com/articles/organizations-take-issue-with-data-regarding-nurse-practitioner-care-in-the-ed
  5. American Association of Nurse Practitioners. Nurse Practitioners in Primary Care (2025 NP count). https://www.aanp.org/advocacy/advocacy-resource/position-statements/nurse-practitioners-in-primary-care
  6. Chan DC Jr, Chen Y. The Productivity of Professions: Evidence from the Emergency Department. NBER Working Paper No. 30608, issued October 2022, revised August 2026. https://www.nber.org/papers/w30608
Man holding dumbbell and protein shake on mountain with rising fitness progress chart

Do Ozempic and Zepbound Cause Muscle Loss?

On By Dr. Scott RennieIn Weight Loss & Metabolic Health1 Comment

Every few months a new worry about GLP-1 therapy moves through the news cycle. Lately the one I’m fielding most on video visits is muscle. Patients read a headline about “Ozempic muscle” or see a segment warning that these drugs are quietly turning people frail, and they show up to their visit asking whether the weight they’re losing is actually fat, or whether they’re hollowing out their strength along with it. Most just phrase it in terms of what they saw online: GLP or Ozempic muscle loss. Truth is, most of my patients aren’t that worried about it at first. They’re focused on getting the fat off. But some have seen the scare ads on Facebook and other social media railing against GLP-1 medications in general, touting muscle loss as the reason to avoid them. It’s a fair question, and it deserves a real answer.

What the data actually shows

Here’s the uncomfortable part first: the concern isn’t manufactured. Across GLP-1 and dual-agonist trials, roughly 25 to 40 percent of total weight lost is lean mass rather than fat mass, and that share climbs with higher doses and greater total weight loss. In patients losing more than 15 percent of body weight on high-dose therapy, average lean mass decline runs in the range of 10 to 15 percent. That’s not trivial, and it’s higher than what we’d want to see if the sole measuring stick were “weight coming off.”

Lean mass loss and clinically meaningful muscle loss aren’t the same thing, though, and this is where I think the public conversation gets sloppy. Lean mass includes water, organ tissue, and connective tissue alongside contractile muscle. Some degree of lean mass loss happens with any significant weight reduction, including bariatric surgery and aggressive caloric restriction without any medication at all. The relevant clinical question is whether strength and function held up, and whether frailty risk moved. On that narrower and more important question, the current evidence is reassuring for most patients: there’s no consistent signal that GLP-1-induced weight loss causes outright sarcopenia or functional decline in the general obesity population studied so far.

Where the concern sharpens is in specific subgroups: adults over 65, patients with baseline sarcopenia or frailty, and anyone starting from a lower muscle reserve. That’s the population where I’m paying closer attention now, more than the healthy 40-year-old with obesity and good baseline strength.

What’s changing in how we prescribe

A few practical shifts have made their way into how I approach this with patients this year. When muscle preservation is a priority, I start low and titrate slower. This isn’t new advice for tolerability, but it applies here too: aggressive, fast weight loss appears to pull proportionally more from lean mass than a slower trajectory toward the same endpoint.

Protein intake is no longer an aside I mention on the way out the door. Current guidance points to 1.2 to 1.6 g/kg of body weight per day for patients on GLP-1 therapy, meaningfully higher than general population recommendations, and given how much these medications suppress appetite, hitting that number takes real intention. I’ve started asking patients to walk me through a typical day’s protein intake rather than assuming they’re getting enough just because they’re eating less overall.

Resistance training is now part of the treatment plan itself, prescribed with the same specificity as the medication. Two or more sessions a week of resistance work is the most consistent lever we have for preserving lean mass during GLP-1-driven weight loss. For patients who’ve never lifted weights, even bodyweight or band-based resistance work at home is a reasonable starting point, and it’s worth a specific referral to physical therapy or a trainer rather than a general nudge.

And I’m tracking more than the scale. For patients on higher doses, losing significant weight, or starting from a place of reduced muscle reserve, I’m now discussing body composition tracking, whether that’s a DEXA scan, bioelectrical impedance, or simply following functional measures like grip strength and chair-stand time, rather than relying on weight alone to judge how treatment is going. I’ll say plainly: I don’t yet fully trust the consumer-grade body composition numbers patients bring me on their phones. Grip strength and chair-stand time are the measures I put the most weight on. Over video I’m relying on what a patient can demonstrate on camera and tell me, rather than testing it myself, which is a real limitation of doing this work remotely.

Muscle is not the only tissue worth watching on these drugs. Nerve complaints turn up too, from skin that hurts to the touch through to the more serious neuropathies, and the risk of both rises with dose and with how fast the weight comes off. I cover that separately in GLP-1 skin and nerve pain.

What’s coming that may change this conversation further

Drug development is moving on this too, well past prescribing technique. At the American Diabetes Association’s 85th Scientific Sessions this year, early data from the BELIEVE study looked at bimagrumab, an antibody that blocks activin receptor signaling, paired with semaglutide, specifically to see whether it could preserve lean mass during GLP-1 weight loss without blunting fat loss. Separately, researchers at Stanford published mouse data in June showing that a muscle-repair-targeted compound improved muscle regeneration and strength recovery alongside GLP-1 treatment, again without compromising fat loss. Neither approach is available for patients today, but they reflect where the field is heading: toward combination approaches that decouple fat loss from lean mass loss more deliberately.

Where the newer agents in the pipeline land on this question is also worth watching. Retatrutide, the triple GIP/GLP-1/glucagon agonist from Lilly, posted strong topline results across its TRIUMPH program this year, with weight loss in the 20 to 28 percent range depending on the trial population, and a BLA submission is planned for early 2027. Amgen’s MariTide, a monthly injectable combining a GLP-1 agonist with an amylin antibody, showed roughly 20 percent weight loss in Phase 2 with a safety profile consistent with the existing GLP-1 class. Body composition data from both programs will matter as much as the topline weight-loss numbers once they mature.

The bottom line

Muscle loss with GLP-1 therapy is real, but it’s manageable, not a reason to avoid treatment or panic mid-course. Older adults and anyone with baseline frailty need the closest attention, and so does anyone pursuing rapid, high-percentage weight loss on a higher dose. I order a DEXA when I actually need an answer to how much of that weight is fat, and it’s an easier call in a patient who might also have osteoporosis, since the same scan answers both questions. Insurance makes this harder than it should be, and plenty of patients who already know they’re overweight don’t want to pay out of pocket just to confirm it. Protein intake and resistance training aren’t optional add-ons anymore. They’re as much a part of the standard prescription as the injection itself.

Scott Rennie, D.O.
Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Sources:

GLP-1 Therapies in 2026: Beyond Blood Sugar and the Scale, AJMC: https://www.ajmc.com/view/glp-1-therapies-in-2026-beyond-blood-sugar-and-the-scale

Should We Be Concerned About Muscle Loss With GLP-1s?, Medscape: https://www.medscape.com/viewarticle/should-we-be-concerned-about-muscle-loss-glp-1s-2026a1000p67

Increasing GLP-1 Use Raises Muscle Loss Concerns, Medscape: https://www.medscape.com/viewarticle/increasing-glp-1-use-raises-muscle-loss-concerns-2026a1000p4h

Deep Dive: GLP-1, Muscle Loss and What It Means, Medscape: https://www.medscape.com/c99/p10/are-concerns-glp-1s-and-muscle-loss-real-or-overblown-2026a1000gdz

New GLP-1 Therapies Enhance Quality of Weight Loss by Improving Muscle Preservation, American Diabetes Association: https://diabetes.org/newsroom/press-releases/new-glp-1-therapies-enhance-quality-weight-loss-improving-muscle-0

Drug enhances muscle repair during GLP-1 weight-loss treatment in mice, Stanford Medicine: https://med.stanford.edu/news/all-news/2026/06/muscle-glp-1.html

Retatrutide FDA Approval Status 2026, freemedicaljournals.com: https://freemedicaljournals.com/blog/retatrutide-fda-approval-status-2026/

Results From Amgen’s Phase 2 Obesity Study of Monthly MariTide, Amgen: https://www.amgen.com/newsroom/press-releases/2025/06/results-from-amgens-phase-2-obesity-study-of-monthly-maritide-presented-at-the-american-diabetes-association-85th-scientific-sessions

Spiral staircase with glowing blue arrow indicating growth percentages of +15%, +35%, +58%, +60%, culminating at 100%.

Wegovy 7.2 mg: Who Should Consider the Higher Dose?

On By Dr. Scott RennieIn Weight Loss & Metabolic Health1 Comment

Wegovy just got a new top rung on the ladder. In March of this year, the FDA approved a higher, 7.2 mg dose of semaglutide, marketed as Wegovy HD, for adults with obesity or overweight. This is a new ceiling on a drug we already know well. Same drug. Higher rung. I think it’s worth walking through what the data actually shows before deciding who in your practice, or mine, is a good candidate for it.

The approval leaned on two trials, STEP UP and STEP UP T2D, both 72-week phase 3 studies. In STEP UP, which enrolled adults with obesity but without type 2 diabetes, patients on 7.2 mg lost an average of 20.7% of body weight, compared with 15.6% on the standard 2.4 mg dose and 3.9% on placebo, a meaningful jump and not a marginal one. Almost a third of patients on the higher dose, 31.2%, lost a quarter or more of their starting body weight. In the companion trial, STEP UP T2D, which looked at patients with obesity and type 2 diabetes, the numbers were lower but still substantial: 14.1% average weight loss, with about a fifth of patients losing 20% or more. That gap between the diabetes and non-diabetes cohorts isn’t surprising. We see it consistently with GLP-1 therapy, and it’s a good reminder to set expectations differently for patients with T2D up front.

Here’s the part that matters most for how I’ll actually use this in practice: Wegovy HD isn’t a starting dose. The label requires that a patient have already tolerated 2.4 mg for at least four weeks before stepping up, and the escalation is meant for patients where additional weight loss is clinically indicated, meaning the 2.4 mg dose hasn’t gotten them where they need to be. So the ideal candidate is someone who’s already on semaglutide, tolerating it reasonably well, but has plateaued short of their goal or still has a lot of excess weight to lose relative to their comorbidities. Think of a patient who’s been on 2.4 mg for six months, lost maybe 10-12% of body weight, tolerates the GI side effects fine, but still has a BMI well into obesity range with sleep apnea or hypertension that hasn’t fully responded. That’s the kind of case where I’d bring up 7.2 mg. It’s not for someone just starting therapy, and it’s not for someone who’s struggling with nausea or GI symptoms at the lower dose. If they can’t tolerate 2.4 mg, going higher solves nothing.

Which brings up the safety side, because the tradeoff here is real.

Overall tolerability at the higher dose was described as similar to what’s been seen with 2.4 mg, with GI effects like nausea, vomiting, constipation, and abdominal pain remaining the most common complaints. But two numbers stood out to me. Dysesthesia, essentially altered or abnormal skin sensation, occurred in 22% of patients on 7.2 mg versus 6% on 2.4 mg and 0.3% on placebo. That’s not a side effect I’d been counting on discussing much with patients on standard-dose semaglutide, and it’s one I’ll need to specifically ask about at follow-up visits once patients move up. I’ve seen the same pattern in my own patients, the ones who dose escalate quickly on standard Wegovy dosing, well before anyone gets near 7.2 mg. The trial data and my own visit notes agree on that one. Dose reductions due to adverse events were also more common at the higher dose, 18.5% versus 12.4% on 2.4 mg, and discontinuation due to side effects ran around 5.4%. The higher dose isn’t a free upgrade. You’re trading tolerability for more weight loss, and that’s a conversation to have explicitly with the patient rather than assume they’d automatically want the escalation.

One safety finding from STEP UP deserves more attention than it got. Dysesthesia, meaning abnormal skin sensation, was reported by 22.9 percent of patients on 7.2 mg against 6.0 percent on 2.4 mg and 0.5 percent on placebo. I go through what that means and how to counsel for it in my article on GLP-1 skin and nerve pain.

From a practical standpoint, Wegovy HD is expected to be available through pharmacies and telehealth channels starting in April, delivered in a single-dose pen. I don’t think this changes how I approach a new patient starting on semaglutide at all, the same titration principles from 2.4 mg still apply. What it does is give me another option for the subset of patients who’ve done well but not well enough, and who’ve shown they can handle the medication without major GI intolerance. That’s a narrower group than “everyone on Wegovy,” and I’d resist the urge, mine or a patient’s, to jump to the higher dose just because it’s now available. The data supports it for the right patient. It doesn’t support treating it as the new default starting point.

Scott Rennie, D.O.
Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Sources:

FDA approves high-dose Wegovy 7.2 mg for adults with obesity, Healio: https://www.healio.com/news/endocrinology/20260319/fda-approves-highdose-wegovy-72-mg-for-adults-with-obesity

FDA approves Novo Nordisk’s new Wegovy HD injection, delivering the highest weight loss to date for a Wegovy injection, PR Newswire: https://www.prnewswire.com/news-releases/fda-approves-novo-nordisks-new-wegovy-hd-injection-delivering-the-highest-weight-loss-to-date-for-a-wegovy-injection-adding-to-its-already-expansive-clinical-profile-302718982.html

STEP UP Trial Shows Higher Dose of Wegovy Produces Significant Weight Loss in Adults With Obesity Without Diabetes, Applied Clinical Trials Online: https://www.appliedclinicaltrialsonline.com/view/wegovy-weight-loss-obesity-diabetes

Compounded Semaglutide and Tirzepatide: What to Know Now

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

When patients ask me about compounded weight loss drugs like semaglutide and tirzepatide, I take a deep breath. The topic is complicated and keeps changing. I won’t just tell patients to avoid them. They’re already looking for these options, and my job is to help them navigate the risks safely.

Dr. Beverly Tchang’s “swim safely” analogy fits well. We can’t stop people from diving into the ocean of compounded products, but we can at least give them floaties: information, caution, and tools to make better decisions. (Tchang, Medscape)

Here’s how I explain it to patients and colleagues, updated with the most recent data.

Why compounded versions exist

When semaglutide and tirzepatide injections were in short supply a few years ago, patients turned to compounding pharmacies that offered custom formulations, often at a lower price. (GoodRx)

In late 2024, the FDA ended the declared shortage of tirzepatide. (Stat News) By early 2025, semaglutide (Ozempic and Wegovy) followed. Once the shortages ended, enforcement ramped up against compounded versions. (GoodRx)

Now, compounded versions are only legal in narrow circumstances, such as when a patient has a medical need that can’t be met by an approved product. (GoodRx)

In December 2024, the FDA sent warning letters to several companies selling unapproved GLP-1 drugs labeled “for research use only.” (Reuters) Some of these contained no active ingredient, incorrect salt forms, or inconsistent potency. (Verywell Health)

Key risks and what to look for

Not all compounding pharmacies operate at the same standard. A friendly local pharmacist doesn’t necessarily mean the product is safe. Dr. Tchang’s checklist gives a good framework for evaluating any compounded GLP-1 medication. A simplified version: look for a pharmacy where the medication is prescribed by a licensed provider, there are no disciplinary actions on file, the pharmacy has been in business for more than a year, only semaglutide base is used (not a salt form), and the facility is FDA-registered or FDA-inspected; it should also be able to ship sterile drugs safely to all 50 states.

If a compounding pharmacy cannot meet these criteria, that’s a red flag. Ask directly for documentation. If they can’t provide it, walk away.

Some compounders also mix in vitamins or preservatives to make their product “different” from the brand name; that may sound harmless, but combining untested additives with peptides can change how the drug behaves. (GoodRx)

A few are promoting oral or sublingual forms of semaglutide and tirzepatide. These seem attractive for patients who don’t like injections, but they haven’t been validated in clinical trials, and absorption is unpredictable. (Omada Health)

Even small changes in formulation or dosing can interrupt treatment and cause rebound weight gain or side effects.

How I approach this with patients

When a patient says, “I found a compounding pharmacy that sells it for half the price,” I acknowledge their concern. Access and cost are real issues. But I explain that the regulatory situation has changed. If an FDA-approved version is available, that’s the standard we should use first.

I encourage patients to ask the pharmacy for their certificate of analysis, sterility test results, and ingredient source; if the pharmacy hesitates or says it’s proprietary, that’s enough reason to stop.

One patient of mine was on a compounded semaglutide microdose that wasn’t commercially available, at least as she described it to me. I never could pin down what she was actually getting. The compounder wouldn’t release potency data either. We moved her to a low-dose commercial version instead. Weight loss slowed a little. Safety and consistency improved, and I knew what was in the pen.

We also reviewed manufacturer assistance programs and insurance coverage. Many patients don’t realize that drug makers often cap out-of-pocket costs for brand medications; cost confusion is one of the biggest drivers behind compounded use.

The FDA’s BeSafeRx campaign

The FDA has an ongoing public safety campaign called BeSafeRx, designed to help patients and providers verify the legitimacy of online pharmacies and compounded drug sources; it offers tools to check pharmacy licenses, identify red flags, and report suspicious products.

It’s a good resource for anyone considering buying compounded or online medications; I often share it directly with patients so they can see what trustworthy sourcing looks like.

You can find the BeSafeRx information at:

https://www.fda.gov/drugs/buying-using-medicine-safely/besaferx-your-source-online-pharmacy-information

What’s changed recently

The REDEFINE trial (NEJM, 2025) studied cagrilintide combined with semaglutide (CagriSema) and showed about 20.4 percent weight loss over 68 weeks, compared with 14.9 percent with semaglutide alone; that kind of data will shape treatment algorithms going forward. GoodRx reports that the FDA’s grace period for compounding GLP-1s has officially ended for both tirzepatide and semaglutide, though some pharmacies still market “custom” or “non-identical” formulations, and regulators are watching closely.

Approach this without judgment if you’re a clinician. Patients are trying to find affordable solutions. And they often trust what they see on social media more than official channels; we can help most by staying informed, asking questions, and documenting carefully. Patients should be cautious for a different reason. Ask your provider to review any compounded medication before you use it, make sure your pharmacy meets every item on that checklist, and use resources like the FDA’s BeSafeRx to verify safety.

Knowledge and transparency remain the best safeguards.

Scott Rennie, D.O.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Binge Eating Disorder Signs and Treatment in Adults and Kids

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Binge Eating Disorder, or BED, is one of the eating disorders I screen for most often in practice. Clinicians define it as repeated episodes of eating a large amount of food in a short period of time while feeling a loss of control during the episode. BED involves episodes that feel compulsive: the person cannot stop eating even when full or uncomfortable. This goes well beyond a second helping at dinner or an indulgent dessert.

The diagnostic criteria for BED require both that large amounts of food are consumed in a discrete time frame and that there is a sense of loss of control while eating. The episodes are also linked to behaviors such as eating more rapidly than normal, eating until uncomfortably full, eating when not hungry, eating alone because of embarrassment, and feeling disgusted or guilty afterward. At least three of those behaviors must be present. The episodes need to occur at least once a week for three months, cause distress, and they are not followed by purging behaviors like in bulimia.

Here’s a hypothetical that illustrates the pattern: someone sits down in the evening and works through an entire pizza and a half-gallon of ice cream in under two hours, not from hunger but because they can’t stop. They feel physically ill afterward. Ashamed, too. The cycle repeats weekly or more often. I’ve seen a real version of this on video visits. One of my patients was managing things with intermittent fasting, and it worked in the sense that the scale moved, but every time the eating window opened back up, they took in way more calories than they needed. The fast itself was setting up the binge.

Children complicate this picture. For kids under 12, researchers have proposed a related diagnosis called Loss of Control Eating Disorder, or LOC-ED (Tanofsky-Kraff et al., 2008). The issue is that children may not consume amounts of food that adults would consider objectively large, but they still experience the same loss of control. In this group, the definition focuses on the subjective sense of being unable to stop eating. The proposed criteria mirror those of BED but apply specifically to children younger than 12. The episodes still need to happen at least once a week for three months and cause distress.

Picture a hypothetical case in pediatrics: a 10-year-old who sneaks into the kitchen at night, eats snack foods quickly, and can’t stop once started. The amount might look modest by adult standards. For a child, it’s significant. What matters is the loss of control, not the portion size. Wrappers hidden in the trash. A refusal to eat breakfast the next morning. Those are often the only clues a parent gets.

Treatment is available for both BED and LOC-ED. For adults with BED, the most evidence supports cognitive behavioral therapy, which helps patients identify triggers, restructure eating patterns, and address guilt and shame. Interpersonal therapy has also been shown to help, especially when social stress is a driver. Some patients benefit from medications. SSRIs have modest benefit for binge frequency, and lisdexamfetamine is the only medication currently approved by the FDA for BED in adults. Nutritional counseling and structured meal planning are usually part of the approach.

I should be direct about where I actually fit into this picture. I don’t manage BED treatment myself. Real treatment leans heavily on behavioral health, and in my current telemedicine positions I don’t have the coordination with a therapist or eating-disorder specialist that this really requires. What I do is screen for it on video visits: ask the direct questions, name what I’m seeing, and refer out from there.

For children with LOC-ED, treatment recommendations are less formalized since the diagnosis itself is still considered research-based. The focus is often on family-based behavioral therapy, involving parents in setting up structured eating schedules and reducing situations where loss of control is most likely to occur. Addressing mood or anxiety symptoms is important, since these are often linked to eating episodes. Nutrition support is also key, both for the child and for parents trying to guide food choices. Medications are not first-line in children.

Recognizing BED or LOC-ED is important because both conditions are linked to higher rates of obesity, depression, and medical complications if untreated. Many people don’t come forward because of shame or because they don’t realize their pattern is a diagnosable disorder. Asking direct questions about eating behaviors, especially around loss of control, can uncover these conditions and open the door to treatment.

If this description fits you or someone you know, talk with a healthcare provider. Early recognition, especially in children, can change the trajectory and reduce the risk of chronic problems.

Scott Rennie, D.O.
Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

References:

Allison KC, Tarves EP. Treatment of night eating syndrome. Psychiatr Clin North Am. 2011;34(4):785-796. doi:10.1016/j.psc.2011.08.002

McCuen-Wurst C, Ruggieri M, Allison KC. Disordered eating and obesity: associations between binge-eating disorder, night-eating syndrome, and weight-related comorbidities. Ann N Y Acad Sci. 2018 Jan;1411(1):96-105. doi: 10.1111/nyas.13467. PMID: 29044551; PMCID: PMC5788730

Tanofsky-Kraff M, Marcus MD, Yanovski SZ, Yanovski JA. Loss of control eating disorder in children age 12 years and younger: proposed research criteria. Eat Behav. 2008;9(3):360-365. doi:10.1016/j.eatbeh.2008.03.001

What Is an Obesity Medicine Board Certified Doctor?

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

More family physicians, myself included, are choosing to become certified through the American Board of Obesity Medicine. The credential looks small on paper. What sits behind it is a real change in how we handle obesity and the conditions that travel with it.

ABOM certification is open to physicians who can show advanced knowledge in preventing, evaluating, and treating obesity. There are two routes. One is 60 hours of continuing medical education credits in obesity-related topics, half of which must specifically address obesity treatment. The other is an accredited obesity medicine fellowship. Either way, candidates then sit for a 4-hour exam covering the physiology and pathophysiology of obesity, nutrition and behavioral treatment, medications, surgery, and bias in care.

Why go through all that? We are the ones patients come to first. About 40% of U.S. adults have obesity, and it is tied to diabetes, heart disease, infertility, arthritis, and worse outcomes with infections. Yet most of us had very little structured training on obesity in medical school or residency. I certainly didn’t. ABOM fills that gap with something more useful than repeating “eat less, move more.”

Patients are also asking harder questions than they used to. GLP-1 medications like semaglutide and tirzepatide changed the conversation. People have worked out that weight regulation is physiology, not character. They want to know whether medication makes sense for them, what the risks are, and what else they should be doing. Certification puts you in a better position to answer that honestly and to build a plan that lasts longer than a few months.

For me, the certification built confidence. I know how to adjust anti-obesity medications, screen for related conditions like PCOS or fatty liver, and talk about weight without stigma. Patients notice. They feel taken seriously when obesity gets treated as the chronic medical condition it is.

One case stays with me. A patient in her fifties came to me with obesity and prediabetes, worn down after years of failed diets. Using what I’d learned, I recognized she was a candidate for pharmacotherapy. We started semaglutide, and we built a plan around meal structure, activity, and sleep. Within months her A1c had come back into the normal range and her energy had returned.

Colleagues are seeing benefits too. A physician I know in rural Missouri became ABOM-certified and quickly became a regional referral point. Practices in nearby towns began sending her patients rather than having them drive hours to an urban obesity clinic. In an underserved area, that is the difference between getting treated and not.

For doctors considering it, the field is growing quickly. More than 11,500 physicians in the United States and Canada now hold the certification, up from roughly 9,800 a year earlier. Insurers are beginning to recognize obesity medicine, which means more treatments get covered when a certified physician is guiding them. You also end up connected to a national group of people working on one of the largest drivers of chronic disease we have.

So the certification is a line on a CV. It is also the reason I practice differently than I did before I sat the exam, and that is the part that reaches patients.

Scott Rennie, D.O.

Sources:

American Board of Obesity Medicine: https://www.abom.org

Johnson-Rabbett B, et al. An Update on the American Board of Obesity Medicine (ABOM): 2017-2024. Obesity. 2025. doi:10.1002/oby.70013

CDC/NCHS. Obesity and Severe Obesity Prevalence in Adults: United States, August 2021-August 2023. NCHS Data Brief No. 508: https://www.cdc.gov/nchs/products/databriefs/db508.htm

Flegal KM, Kruszon-Moran D, Carroll MD, Fryar CD, Ogden CL. Trends in Obesity Among Adults in the United States, 2005 to 2014. JAMA. 2016;315(21):2284-2291.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Why the Scale Isn’t the Best Measure of Weight Loss

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

When patients bring up weight loss, the number on the scale is almost always the first thing out of their mouth. The scale is a poor narrator. What is being lost, fat or muscle or some mix of the two, matters as much as how much of it is gone. That distinction is body composition, and it drives health, function, and what happens years down the line.

Research from Dr. Dympna Gallagher and colleagues has mapped how body composition shifts during weight loss, and how activity, resistance training in particular, protects muscle through it.

Not all weight loss is the same. Weight comes off as a mix of fat and fat-free mass, the latter including muscle, water, and bone. Work from the 1980s estimated that 20 to 30 percent of the weight lost on a standard diet comes from lean mass (Webster et al., 1984). That fraction is not fixed. Age, diet quality, activity, and the speed of loss all move it. Steady loss of about half a kilogram a week protects muscle better than anything faster (Council on Scientific Affairs, JAMA 1988). This matters because Framingham data link muscle loss to higher mortality while fat loss lowers risk (Allison et al., 1999).

Exercise changes the arithmetic. Gallagher’s review and work from Beavers and colleagues found that structured exercise cuts muscle loss during weight reduction nearly in half. In one trial in older adults, resistance training brought lean mass loss down from 16 percent to 10 percent (Beavers et al., 2017). Resistance work beat aerobic exercise at preserving muscle even when both groups lost similar total weight, and combining them produced the best result: more fat lost, better strength, better mobility (Davidson et al., 2009).

Body composition also drifts with age even when the scale holds steady. The Health ABC study found people gradually losing skeletal muscle and subcutaneous fat while gaining visceral fat and fat within muscle tissue (Newman et al., 2005). Less muscle with more central fat raises metabolic risk and costs mobility, and it is a large part of why sarcopenic obesity shows up in older adults.

Bariatric surgery offers a natural experiment in what happens under very large weight loss. Gallagher’s group found that surgical patients lost substantial fat while holding onto muscle long term, provided nutrition stayed adequate and they resumed activity afterward (Davidson et al., 2018). Skeletal muscle remained relatively stable at five years despite major reductions in fat mass.

What I tell patients comes down to this. Do not manage your health by the scale alone. Protect the muscle. Resistance training two or three times a week, adequate protein while calories are restricted, and goals you can actually sustain. A 5 to 10 percent reduction over roughly 20 weeks improves metabolic risk and is realistic for most people (Wadden et al., 1996). I would rather track grip strength or how many chair stands someone can do than watch the scale week to week, because those numbers tell me whether the weight coming off is the weight we wanted to lose.

That is the whole point of paying attention to composition. Losing fat while holding muscle buys better health, more independence, and better metabolic outcomes. Resistance training is not an optional extra here. It belongs in the treatment plan alongside everything else.

Scott Rennie, D.O.

References

Gallagher D. Body Composition Changes with Weight Loss, Including Physical Activity Regimens. Columbia University, 2022.

Wadden TA et al. Am J Clin Nutr. 1996;63(3 Suppl):294S-298S.

Council on Scientific Affairs. JAMA. 1988;260(17):2547-2551.

Webster JD et al. Can J Appl Sport Sci. 1984;9(3):111-118.

Allison DB et al. Int J Obes Relat Metab Disord. 1999;23(1):1-7.

Beavers KM et al. Obesity. 2017;25(9):1476-1483.

Davidson LE et al. Arch Intern Med. 2009;169(2):122-131.

Davidson LE et al. Obesity. 2018;26(3):500-506.

Newman AB et al. Am J Clin Nutr. 2005;82(4):872-878.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Is Yo-Yo Dieting Bad for You? Weight Cycling Explained

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

A lot of my patients describe the same arc. They work hard, lose weight, feel good for a while, and then months or years later it comes back. That repeated loss and regain is weight cycling. It is common, and it is hard on people both physically and emotionally.

The question I hear most often is whether it is even worth trying if the weight is coming back anyway. The research answers that more clearly than it used to, and the answer is yes.

Weight cycling generally means repeated intentional loss followed by unintentional regain. Some researchers set the bar at a 10 percent change in body weight occurring three or more times. Depending on the study, it affects 20 to 35 percent of men and up to half of women (Montani et al., 2015).

Why does the weight return? Biology pushes back harder than most people anticipate. After weight loss, resting energy expenditure falls further than body size alone would predict, and this metabolic adaptation can persist for years, meaning the body burns less than expected (Fothergill et al., 2016). Hormones move too. Leptin drops, hunger hormones climb, and patients end up hungrier and less satisfied by meals than they were before (Sumithran et al., 2011). The body also tends to compensate for exercise by raising appetite. Together these explain why maintenance is the hard part, not the losing (Thomas et al., 2012).

The real question is whether the cycling itself does damage. Large reviews and cohort studies have not found strong evidence that weight cycling raises mortality or major chronic disease risk when the weight loss is intentional and supervised (Mehta et al., 2014). Some work suggests regain may favor fat over muscle, visceral fat especially, though the findings are inconsistent (Mackie et al., 2017).

The psychological picture is better than most people assume. Foster and colleagues found that patients who regained weight still reported improvements in mood, hunger, and eating behavior after the loss phase (Foster et al., 1996). Other work has found no consistent long-term harm from the pattern itself (Osborn et al., 2011).

So should patients keep trying? The National Task Force on the Prevention and Treatment of Obesity concluded in 1994 that weight cycling should not deter people from attempting weight loss, and that position has held up (National Task Force, JAMA 1994). The benefits of intentional loss, lower blood pressure, better lipids, better glucose control, better quality of life, generally outweigh the risk of regaining.

One of my patients lost about 8 percent of her body weight through diet and walking. A year later most of it had come back. During the stretch she kept it off, though, her blood pressure normalized and she came off one of her antihypertensives. The weight returned. The benefit she got during that window was real and measurable, and the research says her experience is the rule rather than the exception.

What I steer patients toward is sustainable habit rather than another aggressive diet. Regular activity, consistent eating patterns, decent sleep, and watching the trend line instead of the daily number. A setback does not undo the progress. Staying connected to support, whether that is a clinician, a dietitian, or counseling, matters more than most people expect.

Weight cycling is real and it is discouraging. It is not a reason to stop. Even temporary weight loss buys real health, and the useful reframe is to treat weight management as ongoing care rather than a project with an end date.

Scott Rennie, D.O.

References

Montani JP et al. Obesity Reviews. 2015.

Fothergill E et al. Obesity. 2016.

Sumithran P et al. NEJM. 2011.

Thomas DM et al. Obesity. 2012.

Mehta T et al. Obesity Reviews. 2014.

Mackie GM et al. Obes Res Clin Pract. 2017.

Foster GD et al. J Consult Clin Psychol. 1996.

Osborn CY et al. Ethn Dis. 2011.

National Task Force on the Prevention and Treatment of Obesity. Weight cycling. JAMA. 1994;272(15):1196-1202.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.

Do Weight Loss Supplements Work? What Research Shows

On By Dr. Scott RennieIn Weight Loss & Metabolic HealthLeave a comment

Patients ask me about supplements constantly. They have seen an ad promising fast results from something natural and want to know whether it is worth a try. The answer is duller than the advertising. The evidence behind most weight loss supplements is thin, and the safety problems are not.

Paul R. Thomas at Columbia University’s Institute of Human Nutrition has reviewed this literature. What he and others find is that these products mostly do not work. The studies that exist tend to be small, short, and funded by the companies selling the product. Where a benefit shows up, it is small. Garcinia cambogia came in at under a kilogram of difference against placebo. That is not what patients are hoping for when they buy it, and it is not remotely close to what lifestyle change or an FDA-approved medication will do (Thomas, 2022).

The marketing claims sort into a few categories. Appetite suppression is credited to hoodia, glucomannan, and saffron. Metabolic or energy boosting gets attributed to caffeine, green tea extract, and bitter orange. Fat absorption blocking is the pitch for chitosan, and reduced fat synthesis for CLA and garcinia cambogia. The proposed mechanisms sound reasonable. The measured effects are close to nothing.

Safety is the more serious issue. Supplements do not have to be proven safe or effective before they are sold, because they are regulated closer to food than to drugs. The FDA can generally act only after harm is documented, which leaves a wide window. Independent testing has repeatedly turned up quality failures, including heavy metal contamination and doses that do not match the label. Some products have been found to contain banned or genuinely dangerous drugs, among them sibutramine, pulled from the market over cardiovascular risk, and phenolphthalein, a carcinogen (Tucker et al., 2018).

The harm is documented rather than theoretical. Roughly 23,000 emergency department visits a year in the United States are attributed to supplements, and weight loss and energy products account for most of them. The usual presentations are palpitations, chest pain, and tachycardia, and the patients are disproportionately young adults in their twenties and early thirties (Geller et al., 2015).

When patients ask what to do, I tell them to be careful. If they are going to use something, single-ingredient products from established national brands are the safer end of the pool, ideally with third-party verification such as USP or NSF. Avoid proprietary blends that will not disclose what is in them. Be suspicious of anything promising to melt fat. If they have a reaction, stop the product, keep the bottle, and report it to Poison Control and the FDA’s MedWatch program.

Supplements are everywhere and the evidence does not support them. Nutrition, physical activity, behavioral support, and where appropriate FDA-approved medication remain both more effective and considerably safer than whatever is currently being advertised.

Scott Rennie, D.O.

References

Thomas PR. Weight Loss Supplements. Columbia University Institute of Human Nutrition, 2022.

Geller AI et al. Emergency Department Visits for Adverse Events Related to Dietary Supplements. NEJM. 2015;373:1531-1540.

Tucker J et al. Unapproved Pharmaceutical Ingredients Included in Dietary Supplements Associated With US Food and Drug Administration Warnings. JAMA Network Open. 2018;1(6):e183337.

Board Certified in Obesity Medicine and Family Medicine

This blog is for educational purposes only and does not constitute individual medical advice. Always consult your own physician before making changes to your health, medications, or treatment plan.