A row of worn cast iron kettlebells on a gym floor

What Happens If You Stop Taking a GLP-1?

Somebody asks me this almost every week, usually some version of the same sentence. “How long do I have to stay on this?”

It is a fair question and it deserves a straight answer rather than a lecture. So here is what the data says happens, what I do about it, and the handful of situations where I think stopping is the right call.

Why you want to stop matters more than the fact that you want to stop

The first thing I ask is why.

The answers cluster into three groups, and they lead to three completely different conversations. Some people have hit their goal and believe they can hold it from here on their own. Some are looking at the monthly cost and doing math. And some are uneasy about taking any medication for years on end, the same way people feel about a blood pressure pill or a statin.

None of those are unreasonable. But the plan for a patient who cannot afford the drug looks nothing like the plan for a patient who is worried about what it is doing to them over a decade, and lumping them together as “wants to stop” wastes the visit.

What the evidence actually shows

The honest version is that most of the weight comes back, and it comes back faster than people expect.

The best synthesis we have is a 2026 systematic review and meta-regression in eClinicalMedicine that pooled 48 studies (1). About 60 percent of the weight lost during treatment is regained within 52 weeks of stopping. The curve is steep early, slows, and flattens out around 60 weeks, with regain plateauing near 75 percent of what was lost. Read the other direction, roughly a quarter of the loss is still there.

The individual trials tell the same story. In the STEP 1 extension, participants had lost 17.3 percent of body weight on semaglutide. A year after the drug and the lifestyle support both stopped, they had regained 11.6 percentage points, leaving a net loss of 5.6 percent, and 48 percent were still at least 5 percent below where they started (2). In SURMOUNT-4, people who came off tirzepatide regained about 14 percent over the following year while those who stayed on lost another 6.7 percent, and 82 percent of the group that stopped gave back more than a quarter of their loss (3).

Here is the part that gets left out of the headlines, and the part I care about more than the scale. The metabolic improvements unwind first. Around 70 to 80 percent of the blood pressure improvement is gone within 12 weeks of stopping. About half of the HbA1c improvement is back by 8 to 12 weeks (1). The weight takes a year to come back. The blood pressure takes three months.

That ordering is the reason I do not treat stopping as a neutral event in someone with hypertension or diabetes.

It is physiology, not a character flaw

I want to be clear about what that regain represents, because patients are brutal with themselves about it.

These drugs work on appetite signaling. Take the drug away and the signaling returns to where it was, which means hunger returns to where it was. The body defends the higher weight. Regaining is the expected biological result of removing the treatment, not evidence that somebody got lazy in month four.

I say this out loud in visits because the shame around regain is what stops people from coming back and restarting when they need to.

Most people stop anyway

Worth knowing: stopping is the norm, not the exception.

In a cohort of 125,474 adults starting these medications, 46.5 percent of those with type 2 diabetes and 64.8 percent of those without had stopped within a year (4). An analysis of 60,000 insured patients presented at ENDO 2026 found about four in ten stopped in the first year, and nearly six in ten by two years (5).

But look at what happens next in that same data. Of the people who stopped, 41.5 percent restarted within a year and 58 percent within two (5). This is not a drug people take once and abandon. It is a drug people fall off and climb back onto, usually after the weight starts coming back.

One more number, and it is the one that changed how I think about this. An integrated health system that added structured pharmacist onboarding and real follow-up got its one-year discontinuation rate down to 3.9 percent (6). Compare that to the 46 to 65 percent above. Most of the stopping in this country is not a drug problem. It is an access, cost and support problem.

What I actually do: lower the dose rather than stop

When somebody has reached a healthy weight, my preference is not to stop the medication. It is to lower the dose to the amount that holds the weight steady instead of the amount that keeps driving it down.

I will say plainly that the evidence here is thin. There are no randomized trials of tapering or maintenance dosing after weight loss, only small observational reports (7). So this is clinical judgment rather than a protocol, and I tell patients that.

What I like about it is that it answers the three concerns at once. It costs less. It involves less drug for people who are uneasy about long-term exposure. And it keeps the appetite brake partly engaged, which is the thing that actually prevents the rebound.

When the reason is cost

This is the most common real reason, and it has the most workable solutions.

First, the cash-pay programs. Eli Lilly and Novo Nordisk both sell direct now, and the prices are meaningfully better than they used to be. For a lot of patients that alone closes the gap.

Second, insurance, which is more winnable than people assume. If a patient carries a weight-related condition, and most do, there is often a path to coverage. Diabetes, prediabetes, hypertension, high cholesterol, GERD, obstructive sleep apnea. Those are not footnotes. They are the clinical justification that gets a prior authorization approved. It is worth the paperwork.

Third, switch the drug rather than abandon the class. Semaglutide instead of tirzepatide. Liraglutide instead of either. Not identical, but real.

Fourth, Medicare, and this is the part most patients have not heard. Part D still cannot pay for a drug prescribed for weight loss alone, because that exclusion sits in the statute and the 2025 attempt to reinterpret it was never finalized. What changed is the Medicare GLP-1 Bridge, which went live July 1, 2026 and runs through the end of 2027. It puts Foundayo, Wegovy and the Zepbound KwikPen at $50 a month for eligible beneficiaries (8). The Zepbound vials and single-dose pens are not in it, which is catching people out. If a patient was told no before last summer, that answer is worth getting again.

And if none of that works, we move to what is affordable. Bupropion and naltrexone as generics. Metformin. These are not equivalent to a GLP-1 and I do not pretend otherwise. They are considerably better than nothing, which is the actual alternative on the table.

Protecting muscle

If weight is going to move in either direction, I want as much of it as possible to be fat.

I target protein intake around 1.5 grams per kilogram. I want resistance training at least twice a week, and 30 minutes of aerobic activity five days a week. That applies while losing, while maintaining, and especially after stopping.

The concern worth naming is that we do not know whether regained weight comes back in the same proportions it left. If fat returns faster than muscle, somebody can land at their old weight with worse body composition than they had before treatment. The data on that is genuinely unsettled, so I am not going to overstate it. The defense is the same either way: protein and resistance training.

When I bring up the long-term question, and why not sooner

This is where I part company with a lot of advice.

I do not open with “this is a lifelong medication.” Early on, we do not yet know whether the drug will even work for this person, and plenty of patients arrive with reservations already sitting in the back of their minds. Leading with a life sentence can talk somebody out of a treatment that might have changed their health, before anyone knows if it helps.

So I raise it as we approach maintenance, when there is something real to discuss: this is working, here is what holding onto it looks like.

When I support stopping

Not every stop is a mistake. I will back the decision in a patient who becomes pregnant, who cannot tolerate the side effects, who genuinely cannot afford it after we have worked the options, or who is not able to use it safely. That last one covers skipping the lab work, taking it in ways it was not prescribed, or developing disordered eating patterns such as bingeing and purging or restricting toward anorexia. It also covers losing more weight than is healthy and not sticking to the maintenance plan.

In those situations stopping is the correct medical decision, not a failure of resolve.

Restarting

People restart. It is common, and I treat it as a normal part of the course rather than a setback.

If somebody has been off for more than about a month, we go back to introductory dosing and step up again. Restarting at the dose you left off at is how people end up with a week of nausea they did not need to have.

For clinicians

Three things worth carrying into your own visits.

Ask the why before you negotiate the how, because cost, goal attainment and long-term safety worry need different responses.

Counsel on the cardiometabolic rebound, not only the weight. Your patient with hypertension will give back most of their blood pressure improvement inside three months, which is a faster and more clinically meaningful change than the scale (1).

And treat the discontinuation statistics as a system signal rather than a patient-adherence story. A 3.9 percent one-year discontinuation rate in a supported program, against 46 to 65 percent in the broader population, tells you where the problem actually lives (4,6).

The Bottom Line

Stopping a GLP-1 means most of the weight comes back, typically around 60 percent of it within a year, with the blood pressure and blood sugar improvements unwinding much faster than that.

That is physiology rather than failure. If you have reached a healthy weight, lowering the dose is usually a better move than stopping outright. If cost is the problem, there is more room to work than most people realize, between cash-pay pricing, prior authorization based on the conditions you already have, switching agents, and the Medicare GLP-1 Bridge if you are on Medicare. And if you do stop, protect your muscle, and come back without embarrassment if the weight starts climbing. Restarting is common and it works.

Related Reading

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Wegovy and Zepbound Cash Pay Prices Without Insurance (2026 Update)
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Does Mounjaro Lower Your Risk of Heart Attack and Stroke?
Foundayo vs. the Wegovy Pill: Comparing the Two New Weight Loss Pills
More on Weight Loss & Metabolic Health

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. Budini B, Luo S, et al. Trajectory of weight regain after cessation of GLP-1 receptor agonists: a systematic review and nonlinear meta-regression. eClinicalMedicine. 2026. https://pmc.ncbi.nlm.nih.gov/articles/PMC13043475/
  2. Wilding JPH, Batterham RL, Davies M, et al. Weight regain and cardiometabolic effects after withdrawal of semaglutide: The STEP 1 trial extension. Diabetes Obes Metab. 2022;24(8):1553-1564. https://pmc.ncbi.nlm.nih.gov/articles/PMC9542252/
  3. Cardiometabolic Parameter Change by Weight Regain on Tirzepatide Withdrawal in Adults With Obesity: A Post Hoc Analysis of the SURMOUNT-4 Trial. JAMA Internal Medicine. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2841273
  4. Discontinuation and Reinitiation of Dual-Labeled GLP-1 Receptor Agonists Among US Adults With Overweight or Obesity. JAMA Network Open. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2829779
  5. Endocrine Society. More than half of those who stop GLP-1s restart within a year. ENDO 2026, presented June 14, 2026. https://www.endocrine.org/news-and-advocacy/news-room/2026/sontha-press-release-endo-2026
  6. Health System Pharmacies Keep Patients on GLP-1 Therapy. American Journal of Managed Care. https://www.ajmc.com/view/health-system-pharmacies-keep-patients-on-glp-1-therapy
  7. Scripps. Patients Maintained Weight Loss After Reducing GLP-1 Treatment Frequency. https://www.scripps.org/news_items/8102-scripps-patients-maintained-weight-loss-after-reducing-glp-1-treatment-frequency
  8. Medicare GLP-1 Bridge: Information for Providers. Centers for Medicare & Medicaid Services. https://www.cms.gov/medicare/coverage/prescription-drug-coverage/medicare-glp-1-bridge/information-providers
A pharmacist standing in front of shelves of medicines

Compounded Semaglutide and Tirzepatide: What to Know Now

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.

Related Reading

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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.

Is Obesity a Brain Problem? How the Body Controls Weight

Patients ask me some version of this constantly: “Why can’t I just eat less and lose the weight?” On the surface it sounds like a fair question. Obesity is a chronic disease with a great deal of biology behind it, and the brain sits at the center of that biology. Treatment that ignores this tends to fail, and the patient usually gets blamed for the failure.

Research from Dr. Sabrina Diano at Columbia University lays out how the brain regulates weight and why it matters clinically.

The central nervous system runs energy balance through two systems. The hypothalamus handles hunger and fullness, the homeostatic side. The hedonic pathway, running on dopamine, responds to reward. That second system is why cravings and emotional eating feel as forceful as they do (Lenoir et al., 2007; Samaha et al., 2020).

Within the hypothalamus, the arcuate nucleus holds two opposing groups of neurons. NPY/AgRP neurons drive eating when energy runs low. POMC/α-MSH neurons suppress appetite when energy is adequate. Both communicate with the PVN, VMH, and LH, and the result is a negotiated balance between intake and expenditure (Diano, 2024; Gropp et al., 2005).

The body feeds signals into that system constantly. Fat tissue releases leptin, which should reduce appetite, except that many patients with obesity develop leptin resistance and the signal lands blunted (Zhang et al., 1994). Adiponectin helps regulate insulin and fat metabolism, and levels fall in obesity (Mahmoud, 2022). After meals, insulin, GLP-1, PYY, and amylin generate satiety. Ghrelin, made in the stomach, climbs before meals and drives hunger. In Prader-Willi syndrome it runs abnormally high (Drucker & Holst, 2023).

Diet interferes with the signaling directly. High-fat, high-sugar foods provoke inflammation in the hypothalamus that disrupts how these neurons talk to each other, through oxidative stress and breakdown of melanocortin pathways (Kim et al., 2019; Diano, 2023). Obesity also generates low-grade inflammation throughout the body, visceral fat especially, which worsens insulin resistance (Mukherjee et al., 2023).

Genetics complicates it further. A few single-gene mutations cause obesity outright, but most cases involve many genes each nudging risk slightly. Epigenetics matters too: maternal obesity during pregnancy can alter gene expression in the child and raise their risk decades later (Farooqi et al., 2003; Mahmoud, 2022; Catalano & Shankar, 2017).

The gut microbiome is another piece, with lower microbial diversity and more gut inflammation both tracking with obesity (Vezza et al., 2020). Environmental chemicals including BPA and phthalates can disrupt hormone signaling and tilt the body toward storing fat (Heindel et al., 2015).

All of this explains the part patients find most demoralizing, which is why weight loss is so hard to hold onto. The body defends a set point. Weight comes down, metabolism slows, hunger hormones rise, and regain becomes the likely outcome (Diano, 2024).

Consider what that looks like in practice. Someone loses 20 pounds through real effort, and then finds themselves hungrier than they have ever been while burning fewer calories at rest. Nothing about their discipline changed. Their body is defending the weight it had before.

Recognizing obesity as a biologically regulated condition changes the approach. Treatment has to work on several fronts at once: nutrition, behavioral strategy, medication, and sometimes surgery. GLP-1 receptor agonists like liraglutide and semaglutide, and dual agonists like tirzepatide, act on these pathways directly, which is a large part of why they work as well as they do.

Obesity is physiology, environment, and genetics interacting. Personal choice is in there somewhere, well downstream of the rest. Understanding that gives us better tools and considerably more patience.

Related Reading

Why Is Losing Weight and Keeping It Off So Hard? How Do You Actually Lose Weight? A Doctor Explains What Brain Scans Show About Appetite and Overeating Food Addiction and Obesity: How the Brain Is Involved Why Your Body Fights to Regain the Weight You Lost

Scott Rennie, D.O.

References

Diano, S. Physiology and Pathophysiology of Obesity, Columbia University, 2024.

Zhang Y, et al. Nature, 1994;372(6505):425-32.

Gropp E, et al. Nature Neuroscience, 2005;8(10):1289-91.

Farooqi IS, et al. NEJM, 2003;349(6):570-8.

Drucker DJ, Holst JJ. Diabetologia, 2023;66(4):651-64.

Kim DW, et al. Cell Metabolism, 2019;30(1):110-122.

Mukherjee R, et al. Front Endocrinol, 2023;14:1154067.

Heindel JJ, et al. Nat Rev Endocrinol, 2015;11(11):653-61.

Mahmoud AM. Int J Mol Sci, 2022;23(3):1225.

Catalano PM, Shankar K. BMJ, 2017;356:j1.

Vezza T, et al. Antioxidants, 2020;9(7):578.

Lenoir M, et al. PLoS One, 2007;2(8):e698.

Samaha AN, et al. Neurosci Biobehav Rev, 2020;113:198-213.

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.

Doctor Supervised Weight Loss: What Works Long Term

Telling patients to eat less and move more doesn’t cut it. Obesity is a chronic disease, and progress requires structured, ongoing, individualized care. The hardest part clinically is making sure the weight that comes off is fat rather than muscle.

Losing muscle costs more than strength. It costs independence, recovery capacity, and eventually survival. Older adults and patients with low baseline activity are the most exposed. Poorly managed weight loss produces sarcopenia, the loss of muscle mass and function. Layer excess fat on top and you get sarcopenic obesity, where a patient looks heavy and is functionally weak and metabolically compromised at the same time.

The European Working Group on Sarcopenia in Older People sets out how to catch it early. It starts with loss of strength, measured by grip strength or a chair-stand test. DXA or BIA can confirm low muscle mass. Poor strength plus low mass plus reduced physical performance defines severe sarcopenia. These definitions give us a framework to act before decline becomes permanent (Cruz-Jentoft et al., Age Ageing, 2019).

Muscle mass predicts survival on its own. Appendicular Lean Mass Index, lean tissue in the arms and legs divided by height squared, is a reliable measure, and people in the top quartile carry substantially lower all-cause mortality than those in the lowest, even after adjusting for BMI and comorbidities (Srikanthan & Karlamangla, Am J Med, 2014). Put plainly, a patient with stronger arms and legs has better odds of living longer regardless of what the scale says.

Strength testing matters as much as mass. Low grip strength tracks with higher mortality from cardiovascular disease, cancer, and respiratory illness. Poor lower-body strength, showing up as slower gait speed or difficulty rising from a chair, tracks with frailty, hospitalization, and long-term disability.

Both measures are cheap and fast, and both are underused. Grip strength needs a dynamometer and a hand to put it in, which rules it out of any remote encounter. The 30-second sit-to-stand doesn’t. A hard chair, arms crossed over the chest, as many stands as the patient can complete in thirty seconds, counted by whoever is watching. It works over video as well as it works in a room, and it yields a number worth tracking across visits. One usable functional measure beats a chart full of weights.

Nutrition is the cornerstone of preserving muscle during weight loss. The baseline protein RDA of 0.8 g/kg/day is inadequate for many adults, particularly older patients and anyone in a calorie deficit. The evidence supports closer to 1.2 to 1.6 g/kg/day, and up to 2.0 g/kg/day in some medically supervised cases (Paddon-Jones et al., Am J Clin Nutr, 2015; Bauer et al., J Am Med Dir Assoc, 2013). Spacing intake across meals rather than loading it at dinner sustains muscle protein synthesis better. Whey and casein, soy, eggs, and blended plant sources all work.

Calculating a target in patients with obesity is genuinely awkward. Actual body weight overshoots. Ideal body weight undershoots. Adjusted body weight is the usual compromise, and reasonable clinicians disagree about which to use. For a 5’6″ patient, a target weight around 73 kg at 1.5 g/kg puts the daily goal near 110 grams, which is a number a patient can actually work with.

Exercise has to include both resistance and aerobic work. Resistance training protects and builds lean mass. Aerobic activity improves cardiovascular and metabolic health. A 2022 systematic review and meta-analysis found the combination conferred the greatest mortality risk reduction, and notably found that weight training alone wasn’t associated with lower mortality among people doing no aerobic exercise (Shailendra et al., Am J Prev Med, 2022). For a patient that translates to brisk walking or cycling most days plus two or three weekly strength sessions using bands, weights, or bodyweight.

Think of muscle like a retirement account. Build it and hold it early, so it is there when it is needed. A patient in their seventies who lands in the hospital with pneumonia can lose a large fraction of their reserve to a few days of immobility and poor intake. If the reserve was thin going in, the decline may be permanent, and it shows up later as falls, fractures, and lost independence. Investing ahead of time changes that trajectory.

Medication is a real adjunct, and it has to be paired with strategies that protect lean tissue. GLP-1 receptor agonists produce substantial weight loss, and a meaningful fraction of that loss is lean mass. Adequate protein and resistance training are the mitigation strategies with actual evidence behind them, and body composition deserves monitoring wherever it is available rather than weight alone.

As clinicians, we need to screen past BMI. Ask about physical activity. Get a functional measure. Consider dietary adequacy. Refer to dietitians, physical therapists, or trainers where it helps, and even a single session with a trainer improves safety and confidence with resistance work. Set goals patients can hold: one to two pounds a week of fat loss while protecting muscle.

Obesity treatment is chronic care. The point is helping patients hold strength, mobility, and independence while metabolic health improves, and preserving muscle sits at the center of that.

Related Reading

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Scott Rennie, D.O.

References:

1. Cruz-Jentoft AJ, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019;48(1):16-31. https://pubmed.ncbi.nlm.nih.gov/30312372/

2. Srikanthan P, Karlamangla AS. Muscle mass index as a predictor of longevity in older adults. Am J Med. 2014;127(6):547-553. https://pubmed.ncbi.nlm.nih.gov/24561114/

3. Paddon-Jones D, et al. Protein and healthy aging. Am J Clin Nutr. 2015;101(6):1339S-1345S. https://pubmed.ncbi.nlm.nih.gov/25926511/

4. Bauer J, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013;14(8):542-559. https://pubmed.ncbi.nlm.nih.gov/23867520/

5. Shailendra P, et al. Resistance Training and Mortality Risk: A Systematic Review and Meta-Analysis. Am J Prev Med. 2022;63(2):277-285. https://pubmed.ncbi.nlm.nih.gov/35599175/

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.