The topic has become unavoidable these days: no matter which way you turn, you run into references to incretin-mimetic drugs — yes, it does sound like it’s calling you a cretin, but I promise it isn’t — or GIP/GLP-1 receptor agonists — whether it’s on social media, at work, or because the hairdresser’s son found “the little jab” on some Korean website for fifty euros and swears it’s working wonders.
But what are these drugs really, what benefits can they offer, and what risks do they carry if used incorrectly? Let’s take a look together.
A few weeks ago, a patient proudly showed me her phone. On the screen was a photo of an injector pen, with a message from a friend underneath: “Look, I lost seven kilos in two months!”
I’ll admit I smiled for a moment.
Not because the news surprised me, but because scenes like this have been repeating constantly over the past few months. Obesity medications have entered everyday conversation. People talk about them on social media, on TV, in waiting rooms, even over dinner with friends. And yet, despite all this media attention, I can’t help wondering how many people have actually understood what these drugs are and how they work.
The first thing to clarify is that we’re not talking about a passing fad, nor about yet another miracle promise from the world of weight loss.
We’re talking about real medications, studied in large international clinical trials, that are substantially reshaping the therapeutic approach to obesity.
To understand why they matter, though, I need to take you a step back — from the drug to the disease it was developed to treat: obesity.
For many years, body weight was interpreted in an often overly simplistic way: eat less, move more, have more willpower, and the problem will sort itself out. If you can’t manage it, clearly you’re not trying hard enough.
Too bad reality is far more complicated than that.
Anyone who works every day with people trying to lose weight knows that motivation is rarely the missing ingredient. I’ve met patients capable of following extremely strict eating plans, weighing every gram of food, going to the gym four times a week, giving up dinners out, drinks with friends, even holidays, just to watch the number on the scale go down. And who then give up halfway through, or regain the weight — not always without interest — the moment the diet ends.
Today we know that obesity is a complex, chronic, multifactorial disease, shaped by genetic, hormonal, metabolic, psychological, environmental, and social factors.
We also know that when we lose weight, our body doesn’t necessarily register the event as a good thing. From its point of view, it might be a famine. So it puts a whole set of defense strategies into action.
Hunger increases. Fullness doesn’t last as long. Thoughts of food become more frequent. And as if that weren’t enough, energy expenditure tends to drop, especially after a restrictive diet that isn’t paired with proper training.
In other words, it’s as if the body keeps trying to drag us back to where we started.
It’s a remarkable evolutionary mechanism that helped our species survive for thousands of years. The problem is that today we live in an environment where food is available around the clock and opportunities for spontaneous movement have dropped dramatically.
That’s why obesity can’t and shouldn’t be treated as simply the result of bad choices.
Many people living with obesity fight this biological battle every single day. And they often fight it alone, carrying the weight of social stigma on top of everything else (that alone deserves an article of its own).
This is where GLP-1 receptor agonists come in — and, more recently, combined GIP/GLP-1 agonists.
When we eat, our gut naturally produces hormones called incretins. One of the most important is GLP-1 (Glucagon-Like Peptide 1), which helps regulate blood sugar, slows gastric emptying, and increases the feeling of fullness.
In other words, under normal conditions GLP-1 is produced naturally after a meal and tells the brain that food has arrived and that we can start feeling satisfied.
The new generation of drugs mimics or amplifies exactly these physiological signals. In other words, they help the brain register fullness more quickly and reduce the intensity of hunger.
Even though, put that way, it sounds almost like magic, it’s actually just physiology.
Let me put it bluntly: these drugs don’t “dissolve fat,” and they don’t magically speed up your metabolism.
They don’t turn a pizza into a salad.
Weight loss happens mainly because the person is able to eat less without constantly feeling the sense of deprivation that so often comes with traditional diets.
That’s a huge result, both from the patient’s personal point of view and from a clinical one.
One of my patients, living with obesity and prediabetes, whose doctor prescribed one of these drugs, described the experience to me in a very simple way: “For the first time, I can open a packet of biscuits without feeling like I have to finish it.”
Folks, that’s no small thing. It means being able to eat less without going through the same suffering you might have experienced in the past. For someone who has struggled with hunger for years, that’s a revolution.
The results seen in clinical trials are striking.
Depending on the drug used and the patient’s characteristics, weight loss can exceed 15% of initial body weight, and with some of the newest molecules, come close to 20%.
Numbers that, until just a few years ago, were nearly impossible to reach without bariatric surgery.
Let me open a (significant) parenthesis and say it again: be careful. These are still drugs. They must be taken exclusively under medical supervision, and like all drugs, they come with contraindications and side effects — most commonly affecting the digestive system: nausea, early fullness (you don’t say?), reflux, constipation and/or diarrhea, sometimes vomiting. In most cases these are temporary and manageable symptoms, but they can still significantly affect quality of life — which is why some people simply aren’t suitable candidates for this treatment. In short: they’re not for everyone, so please stop looking for them online. Parenthesis closed.
I said earlier that we’re looking at a revolution. But like all revolutions, this one risks being misunderstood.
The most dangerous — and unfortunately very common — misunderstanding is that these therapies are a shortcut. Or that they’re the definitive solution that makes everything else unnecessary.
None of that is true.
What is true, and proven, is that these drugs are extremely effective tools. But that doesn’t mean they’re stand-alone tools. Taking them isn’t enough to fix everything on its own.
Let’s start with what kind of weight is actually being lost. The word “slimming down” should really refer to losing body fat, not just losing weight in general. If, instead of losing mostly fat tissue, a person loses a significant share of lean and muscle mass, that’s a real problem.
Clinical studies have in fact shown that when the therapy isn’t paired with proper nutrition and the right kind of physical exercise (exercise, not just “activity”), lean mass can account for up to 40% of the weight lost. Which basically means taking a sledgehammer to your metabolism. And piling the weight back on at full speed the moment you stop the therapy.
So even though it might sound paradoxical (“why would I need a nutritionist when I’m already on the drug?”), it’s precisely when the drug works well and hunger drops that diet quality and lifestyle become absolutely central.
Why? Because the human body remains remarkably consistent, even in the age of these little jabs.
It still loves movement. It still needs sleep. It still responds to the quality of what we eat. And it still rewards those who manage to build habits that last.
The nutritionist’s role therefore becomes central — not just to help someone get adequate protein and encourage movement (strength training in particular), but to provide the kind of food education that turns habits into something lasting, effortlessly, even after reaching the desired weight and starting to taper the medication.
Because the drug can help you eat less, but it doesn’t teach you how to grocery shop, how to plan meals, how to handle a dinner out, or how to tell hunger apart from tiredness, boredom, or stress.
Without managing everyday life, once the desired weight is reached, the problem, unfortunately, isn’t solved for good.
In the end, the real revolution of these drugs isn’t that they let you lose weight without any effort.
It’s that they can finally give some people the chance to do what they’ve tried for years without succeeding: change.
A shot of confidence, and warm regards from your nutrition consultant,
Tatiana Gaudimonte
info@loveyourbody.ch
(image generated with AI)