What We Tell Our Patients About GLP-1 Medications

Ryan Bentley, MD, PhD, DC & Carley Dykstra, PA

GLP-1 medications are coming up more and more in our conversations with patients. People come in wanting a verdict: miracle drug or dangerous shortcut. And we understand why. The noise around this class of medications has made it genuinely hard to find a straight answer. Here is ours: they are neither. They are a tool. And like every tool in medicine, how you use them determines whether they help you or hurt you.

We were not early adopters on this class of medications. We watched the data develop. We evaluated the physiology. We looked at what was happening with our own patients who were doing everything right and still losing the fight against a metabolism that had stopped cooperating. And we came to a clear conclusion: for the right person, used the right way, within a structured clinical approach, GLP-1 medications are a legitimate and powerful tool. For the wrong person, used without a plan, they are an expensive way to lose muscle and miss the point entirely.

What These Medications Actually Do in Your Body

Your body already makes GLP-1. Every time you eat, cells in your small intestine release this hormone into your bloodstream, and it does several things simultaneously. It tells your pancreas to release the right amount of insulin. It signals your liver to ease off on glucose production. It slows how quickly food leaves your stomach, so you feel full longer. And it sends a message to the appetite centers in your brain that says “enough.”

These medications amplify that signal. They are not introducing something foreign into your system. They are turning up the volume on a conversation your body is already having with itself, a conversation that insulin resistance, chronic stress, and years of metabolic drift have gradually turned down to a whisper.

The medication we reach for right now is tirzepatide. You may have heard it called Mounjaro or Zepbound. Same medication, same company, same molecule. Mounjaro is approved for type 2 diabetes. Zepbound is approved for weight loss and sleep apnea. Your insurance company cares about that distinction. Your body does not.

What makes tirzepatide different from earlier GLP-1 medications like semaglutide (Ozempic, Wegovy) is that it works on two receptor systems simultaneously: GLP-1 and GIP (glucose-dependent insulinotropic polypeptide). GLP-1 handles appetite suppression, insulin timing, and gastric emptying. GIP amplifies insulin secretion and has direct effects on how your fat tissue functions. That dual mechanism is why the clinical results with tirzepatide have been more significant than what we saw with semaglutide alone. The SURMOUNT-5 trial, published in the New England Journal of Medicine, put both medications head-to-head in 751 patients over 72 weeks. The results were clear: tirzepatide produced an average of 20.2 percent body weight loss versus 13.7 percent with semaglutide. Nearly a third of tirzepatide patients lost 25 percent or more of their body weight. That is not a marginal difference. It shows up in the data, and it shows up in our clinic.

That said, semaglutide (Ozempic for diabetes, Wegovy for weight loss) remains a solid option for patients who respond well to GLP-1 receptor activation alone. Some patients tolerate one molecule better than the other. Some insurance plans cover one but not the other. We work with what your body responds to and what your situation allows. But when we have the choice, tirzepatide is where we start, because the dual mechanism addresses more of the metabolic picture at once.

The Food Noise Phenomenon

One of the most important things that happens when patients start these medications is something they struggle to describe at first. The best phrase we have heard came from a patient who told us, “The food chatter stopped. I don’t think about food all day anymore.”

That is not a side effect. That is a window into what was driving the weight problem in the first place.

Food noise is the constant mental commentary around eating. The intrusive loop of thinking about what you will eat next, the late-night pull toward the pantry when your body does not need fuel but your brain has a deeply wired connection between stress and the refrigerator door. Most of our patients who struggle with weight have lived with this noise for their entire adult lives. They assumed it was a willpower problem. A discipline problem. A personal failure.

In most, it was none of those things. It was a physiologic signal running too loud.

We had a patient in her early forties who exercised consistently, ate what most physicians would call a very healthy diet, and could not lose the thirty pounds she had been carrying for a decade. Her fasting insulin was elevated. Her HOMA-IR told the story of insulin resistance that had been building quietly for years. She was not failing at discipline. She was fighting a hormonal system that had drifted out of calibration.

When we addressed the insulin resistance with tirzepatide alongside maintaining a structured nutrition plan, the food noise dropped within the first month. For the first time, she could see her eating patterns clearly. The ten o’clock pull toward the kitchen was not hunger. It had never been hunger. And now, without that noise drowning out the signal, she could finally tell the difference.

That clarity is the window we want every patient to climb through. The medication quiets the noise long enough for you to see what is actually happening. What you build with that clarity determines whether the results last.

The Risks That Do Not Get Enough Attention

We want to be direct here, because the conversations in popular media almost never go deep enough on this. If this is not your first encounter with us, you know we love to take a deep dive.

The most significant risk with GLP-1 medications is muscle loss. When you eat substantially less, your body does not automatically pull all of its energy from fat. Without intentional effort, it will break down muscle to meet its needs. Your body treats muscle the way a company treats expensive employees during a budget cut. If revenue drops and nobody makes the case for keeping those employees, they get let go first. Resistance training is how you make that case. It tells your body that this muscle is being used, it matters, keep it. In our experience, the patients who were not doing structured resistance training were losing nearly as much lean mass as fat mass in the first three months. That is not a win. That is trading one metabolic problem for another, because muscle is the primary driver of your resting metabolic rate. Lose the muscle, and you have set yourself up for rebound the moment the medication stops, just like the yo-yo diets.

The second risk is nutrient deficiency. Think about the math. If your old diet was barely covering your magnesium, B12, and vitamin D needs at 2,200 calories a day, cutting to 1,400 calories without restructuring what you eat guarantees deficiency. You will feel it as fatigue, brain fog, poor sleep, and muscle cramps. And you will blame the medication when the real problem is that nobody restructured your nutrition to match your new intake.

These are not reasons to avoid the medication. They are reasons to use it within a clinical framework that accounts for them from day one.

How We Use These Medications at Vitalis-Health

This is where our approach differs from what most patients experience elsewhere. A prescription and a follow-up in three months is not a protocol. It is a hope and a prayer. Here is what we actually do.

Before we start, we test. Fasting insulin. HOMA-IR. Full metabolic panel. Vitamin D. B12. Magnesium. Omega-3 index. Inflammatory markers. We run genetic testing where appropriate to understand how your body processes nutrients and responds to metabolic interventions. We often get a body composition scan to establish your baseline body composition, so we know exactly where you are starting and can track whether you are losing fat or losing muscle. That distinction changes everything about how we manage your protocol.

Protein is the non-negotiable anchor. Every single day, your target is roughly one gram per pound of body weight, distributed across your meals. When you are eating less overall, protein becomes the thing you protect above everything else. It is the primary signal your body uses to preserve and build muscle tissue. Skimp on protein while taking a GLP-1 medication, and you are accelerating the very muscle loss that will undermine your results.

Healthy fats are structural, not optional. Every cell membrane in your body is built from fatty acids. Your hormones require fat to function. Prioritize omega-3 sources: fatty fish, walnuts, quality flaxseed. Add olive oil, avocado, and eggs. Do not use appetite suppression as an excuse to eat a low-fat diet. That is not a strategy. It is a mistake that will show up in your labs within ninety days.

Vegetables in volume. They provide the fiber, micronutrients, and phytonutrients your body needs when eating less, and they support the gut microbiome that plays a far larger role in metabolic health than most patients realize.

Targeted supplementation based on your labs, not a generic list. The gaps we monitor most closely include magnesium, B12, vitamin D, zinc, and omega-3 fatty acids. For patients concerned about muscle preservation (and that should be every patient on these medications), creatine monohydrate is supported by solid evidence and worth a direct conversation. We do not hand you a supplement list and send you to the store. We assess your baseline status, monitor as we go, and adjust based on what your labs actually show.

Resistance training is prescribed, not suggested. If you are on a GLP-1 medication and you are not doing structured resistance training at least three times per week, you are losing muscle. Period. This is not optional. This is part of the treatment protocol. We will help you build the program or connect you with someone who can.

We monitor throughout. This is not a prescription-and-refill arrangement. We are tracking your body composition, your labs, your energy, your strength, and your metabolic markers. If something is moving in the wrong direction, we catch it early and adjust. That is the standard of care at Vitalis-Health.

Who This Is For

We will be direct with you about something. These medications work best when they are part of a bigger plan. If you are already making an effort, eating thoughtfully, moving your body, and still hitting a wall that will not move, this is built for you. The medication gives biology a push when biology has stopped cooperating on its own.

If the plan is to take a weekly shot and change nothing else, we would rather have that honest conversation now and save you the frustration. We are not going to prescribe a tool and set you up to fail with it.

The goal is always to use these medications for a defined season. To use that window of reduced appetite and metabolic recalibration to build the habits, the muscle, and the metabolic momentum needed to sustain your results without being dependent on a weekly injection indefinitely.

What Is Coming Next: The Triple Agonist

The science in this space is moving fast, and we want you to understand where it is heading, because it matters for how we think about metabolic health.

The next development we are watching closely is retatrutide, a triple receptor agonist currently in Phase 3 clinical trials through Eli Lilly (great stock to buy now if you invest in the market). Where tirzepatide acts on two receptor systems (GLP-1 and GIP), retatrutide adds a third: the glucagon receptor.

That third receptor is what makes this genuinely different, not just incrementally better. Let us explain why.

Glucagon is the counter-regulatory hormone to insulin. When your blood sugar drops, glucagon tells your liver to release stored glucose. When you are stressed, cortisol rises, and glucagon plays a role in how your liver responds to that stress signaling. This is the mechanism behind the metabolic pattern we see in a large number of our patients: chronic stress drives cortisol up, cortisol signals the liver to dump glucose, insulin spikes to clear it, blood sugar crashes, cravings hit, you eat, and the cycle repeats. Those peaks and valleys. That rollercoaster of energy and hunger that has nothing to do with actual caloric need and everything to do with a stress response that has hijacked your metabolism.

Retatrutide’s glucagon receptor agonism does something elegant. It increases hepatic fat oxidation (your liver burns stored fat for fuel) and stimulates thermogenesis (your body burns more calories at rest). The GLP-1 component simultaneously reduces inappropriate glucagon secretion from the pancreas, smoothing out those stress-driven glucose dumps. And the GIP component improves insulin sensitivity so that when glucose does enter the bloodstream, your cells handle it efficiently instead of slamming the door shut.

The net effect is that the stress-metabolic cycle gets interrupted at multiple points simultaneously. Your liver burns fat instead of making more. Your resting energy expenditure increases. Your glucose control stabilizes. And the appetite suppression from GLP-1 means the crash-driven cravings lose their grip.

The clinical data reflects this. The Phase 2 trial, published in the New England Journal of Medicine, showed up to 24.2 percent body weight reduction at 48 weeks at the highest dose. The first Phase 3 result, TRIUMPH-4, was reported in December 2025: participants taking the 12 mg dose lost an average of 28.7 percent of their body weight, roughly 71 pounds, over 68 weeks. That is the largest weight reduction ever recorded for any medication in a Phase 3 trial. The 9 mg dose produced 26.4 percent. Placebo produced 2.1 percent. In a separate liver fat substudy, the highest doses reduced liver fat by over 80 percent within 24 weeks, and up to 93 percent of participants with fatty liver disease saw their levels return to normal. That liver fat number matters, because fatty liver is one of the clearest markers of the metabolic dysfunction driving the weight problem in the first place.

In terms of safety, retatrutide shares the gastrointestinal side effect profile common to the GLP-1 class: nausea, diarrhea, and constipation, mostly during dose escalation. The TRIUMPH-4 trial did identify a new signal worth watching: approximately 21 percent of participants on the 12 mg dose reported dysesthesia, an abnormal tingling or numbness sensation. Most cases were mild and did not lead to stopping the medication, but it is a finding that will need further evaluation as additional Phase 3 data comes in. Seven more Phase 3 trials are expected to report results in 2026.

We used to think that adding more receptor targets was just pharmaceutical marketing. More pathways, more complexity, more side effects, diminishing returns. What changed our thinking was looking at the specific patients in our practice who have done everything right with tirzepatide and still plateau. These are often the patients whose weight struggles are deeply connected to chronic stress, cortisol dysregulation, and the metabolic fallout that follows. The dual agonist does not fully address that layer. The triple agonist, mechanistically, should.

Tirzepatide remains our choice right now because the safety profile is well-established and the evidence base is strong. But retatrutide, as it moves through the approval process, will likely prove to be the right tool for the specific patient population whose metabolic dysfunction is being driven primarily by stress physiology. And for patients with concurrent fatty liver disease, the data is pointing toward a level of efficacy we have not seen before from any medication.

This is why we tell our patients: the medication or supplement we recommend today may not be the medication or supplement we recommend in two years, because the science keeps getting sharper. We stay current so your personalized protocol reflects the best available option, not last year’s thinking.

The Bridge

The body was designed with a remarkable capacity for self-regulation. We believe that design is intentional. These medications, used wisely, help restore the regulation that was always supposed to be there, before years of environmental exposure, metabolic stress, and modern food systems pulled it off course.

A GLP-1 medication is a bridge. It gets you across the gap between where your metabolism is stuck and where it can sustain itself. But what you build on the other side of that bridge is what determines your long-term health.

That is a tool that helps you find the path. Not a substitute for walking it.

If you want to understand whether this approach makes sense for you, reach out to our team at Vitalis-Health. We will look at your complete metabolic picture: your labs, your history, your genetics, and your goals. And we will build a plan that fits your actual biology, not a generic protocol.