GLP-1 Drugs Work? The Question Should be Whether We’re Prescribing Them Correctly...

Andrew Kowalski, MD, FASN

I know that this is a very misleading title based on my positive stance on GLP-1s, but this is the problem that I have with periodicals and the misleading titles that they use as “clickbait.”

Unfortunately, you will only find out what the author is really writing about once you stomach your way though half the article and realize that this could have been stated at the beginning.

Titles like these also stimulate rumors that patients should stop these grounding breaking medications when they shouldn’t.

“Why every patient on semaglutide or tirzepatide needs a nutrition-and-muscle protocol from day one.”

A recent commentary in BBC Science Focus (May 2026) raised a concern that has been quietly circulating in obesity medicine, nephrology, and geriatric clinics for the past two years: GLP-1 and dual GLP-1/GIP receptor agonists are extraordinarily effective for weight loss, but the very mechanism that makes them work reduces appetite, slows gastric emptying, eating smaller meals and that CAN quietly tip patients into protein insufficiency, micronutrient depletion, and accelerated lean-mass loss if no one is watching.

The warning is valid. The conclusion, however, is not that we should pull back on these drugs. It is that we should stop prescribing them as monotherapy and start prescribing them inside a structured nutrition-and-muscle-preservation framework.

The reality is that the majority of providers, bothe primary care and specialists, have these conversations with patients…or else they should be. Decreased in intake will lead to decreased intake in protein and ultimately a loss inn muscle mass. This loss in muscle mass INCREASES your risk in many chronic diseases (cardiac, kidney, diabetes, brain health) that these shots are trying to protect you from. Having proper education in nutrition and focusing on a protein first approach is one way to curb these negative effects.

My concern is about the individuals who do not get these from a qualified provider, but are now able to purchase these online without restrictions or any key knowledge on what can happen if they do not think about their health long term.

What the data actually shows

In the SURMOUNT-1 body-composition substudy, tirzepatide produced striking weight loss, but the composition of that loss is the part clinicians need to internalize: roughly three-quarters of the weight lost was fat mass, and roughly one-quarter was lean mass. Semaglutide trials echo a similar pattern, dramatic fat-mass reduction with a non-trivial lean-mass signal in a subset of patients.

A 25% lean-mass component is not unique to GLP-1 therapy. It is, broadly, what the physiology of rapid weight loss looks like across modalities, including bariatric surgery and aggressive caloric restriction. The clinically meaningful question is not whether DXA shows a lower lean-mass number; it is whether the patient loses functional muscle, strength, bone density, and metabolic resilience; the variables that determine whether a patient ages well or accelerates into frailty.

That distinction matters. Lean-mass loss in a 38-year-old with sarcopenic obesity and a high baseline of muscle reserve is a different clinical event than the same percentage loss in a 72-year-old with CKD stage 3b, low grip strength, and a history of falls.

Where the “BBC Science Focus” piece is right, and where it stops short

The article is correct that micronutrient and protein monitoring protocols specific to GLP-1 therapy are not yet standardized. Current best practice is extrapolated from bariatric nutrition, obesity medicine, and the physiology of negative energy balance. That is a real gap, and it deserves the spotlight.

What the piece does not fully develop is that GLP-1 risk is NOT UNIVERSAL, and the patients at highest risk for nutritional injury are precisely the patients I see most often in my own practice:

- Older adults and the frailty-prone

- Patients with CKD, especially stages 3b–5 and post-transplant

- Patients with established or subclinical sarcopenic obesity

- Post-bariatric patients adding pharmacotherapy

- Patients on plant-predominant or vegetarian diets without a deliberate protein strategy

- Patients with persistent nausea, vomiting, or early satiety on dose escalation

- Patients with prior eating-disorder history

For these populations, GLP-1 therapy without a nutritional scaffold is not a neutral act. It is a setup for an entirely preventable medical induced problem.

The CRIMS lens: why this is a cardio-renal-metabolic question, not just a weight question

Within the framework I use clinically, Cardio-Renal-Inflammatory-Metabolic-Sarcopenia (CRIMS), muscle is not a cosmetic concern. Skeletal muscle is the body’s largest glucose-disposal organ, a major contributor to resting metabolic rate, a reservoir of amino acids during illness, and a powerful determinant of cardiovascular and renal outcomes. In CKD specifically, low muscle mass and low muscle quality are independently associated with mortality, hospitalization, and worse trajectories of kidney function.

In other words: the goal of GLP-1 therapy in a cardio-renal-metabolic patient is not weight loss. It is fat-mass loss with muscle preservation and metabolic restoration. The drug is one input. The protocol around it determines whether we deliver that outcome or quietly produce a thinner, weaker, more fragile patient.

A practical GLP-1 safety bundle

The following framework is what I use, and what I would advocate for as a standard of care in any clinic prescribing these agents at scale.

1. Baseline nutrition and function screen: Weight trajectory, 24-hour diet recall, protein intake estimate, GI symptom inventory, alcohol use, constipation history, and a brief frailty/sarcopenia assessment (grip strength, chair-stand test, gait speed where feasible).

2. Laboratory baseline, repeated at 3–6 months in higher-risk patients: CBC, comprehensive metabolic panel, magnesium, phosphorus where clinically relevant, iron studies and ferritin, vitamin B12, folate, 25-hydroxyvitamin D, and calcium/PTH when indicated. In CKD patients, this overlaps substantially with routine monitoring and adds little burden.

3. Protein target: For most patients without advanced CKD, a target of 1.2–1.6 g/kg/day using adjusted or goal body weight is reasonable, distributed across meals to support muscle protein synthesis. In advanced CKD, the target is individualized based on dialysis status, residual kidney function, and overall goals of care, but in nearly every case, “small appetite plus low protein” is the combination that produces sarcopenia, not protein itself.

4. Resistance training: Two to three progressive sessions per week, emphasizing compound movements; squats, hinges, presses, pulls, carries. This is not optional. Pharmacologic appetite reduction without a resistance-training stimulus is the single clearest recipe for lean-mass loss on GLP-1 therapy.

5. Fiber and hydration, titrated carefully: Beans and lentils, vegetables, berries, oats, chia and flax, and psyllium when needed. Fiber addresses both the constipation that frequently accompanies these drugs and the gut-microbiome health that is now understood to be central to cardio-renal-metabolic outcomes.

6. The “every bite counts” rule: When appetite is pharmacologically reduced, dietary quality matters more, not less. Protein first, plants second, ultra-processed foods last. Patients should understand this as a guiding principle, not a restrictive diet.

7. Function and body-composition tracking: Waist circumference, weight, grip strength, chair-stand performance, walking speed, and when available and indicated utilizing DXA or bioimpedance. The goal is to track what we actually care about, not just the scale.

8. Side-effect management: Slow titration, smaller and lower-fat meals during nausea, an aggressive constipation protocol, and a clear plan for what to do if oral intake collapses. A patient who is eating 600 kcal a day because of unmanaged nausea is NOT “responding well” to therapy. They are accumulating a problem.

The bottom line

The professional consensus emerging across obesity medicine, lifestyle medicine, and nephrology converges on a single point: GLP-1 and GLP-1/GIP receptor agonists are among the most consequential pharmacologic advances of the past two decades, and they deliver their best outcomes when embedded in a structured program of nutritional support, resistance training, micronutrient surveillance, behavioral care, and long-term follow-up.

The BBC Science Focus warning is not an argument against these drugs. It is a misleading argument against prescribing them casually. Obesity is a chronic disease. The tools we now have are powerful enough that the question is no longer whether we can produce weight loss, but whether we can produce the “right” weight loss, making it durable, muscle-preserving, metabolically restorative, and aligned with the cardio-renal-metabolic outcomes that actually shape a patient’s life.

That is a higher bar. It is also the bar we should be holding ourselves to.

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Andrew Kowalski, MD, FASN, is a practicing nephrologist specializing in cardio-renal-metabolic medicine and the developer of the CRIMS (Cardio-Renal-Inflammatory-Metabolic-Sarcopenia) clinical framework.