The Problem With Ozempic Isn’t Science. It’s Capitalism.

I dismissed GLP-1 drugs as a fad. Then I looked at the science. Here's what changed my mind. And what still worries me.

Oct 05, 2025

Welcome to Truth Be Told, the weekly food and fitness newsletter published by The Whole Truth Foods.

Editor’s note: This is Samarth Bansal, your Editor, and my turn to write the article today. (It’s been a while since I’ve written for my own publication—one of those occupational hazards of becoming an editor.)

This piece on GLP-1 drugs took me somewhere I didn’t expect. I started skeptical and ended up genuinely surprised by what the research showed. Read this to understand how these drugs actually work, what the clinical evidence shows, and why I think the real problem isn’t the science—it’s what happens when a medical breakthrough meets market incentives.

Also, a reminder: here is a short feedback form to help us understand how we’re doing. My team would really appreciate your time. And for any other thoughts, I am at samarth@thewholetruthfoods.com.

My first reaction to GLP-1 weight-loss drugs in 2023 was deep skepticism. Just another shiny new thing using “science” to sell me a shortcut—tapping into our endless chase for “perfection” through “easy” means.

I knew better. Because I know what weight loss feels like. Seven months, 20kg down: countless nights resisting that cookie at 10 PM; obsessing over the extra teaspoon of oil in the omelette because I was so precise about calories and macros; skipping meetups because I was so tired of the diet jokes. And gosh, those brutal moments when my body screamed for chocolate and I had to choose: give in or white-knuckle through it.

I’d run out of curse words for my own biology: “I’m doing this for us, my dear body, and you—your stupid hormones—won’t just cooperate?”

That’s what it took: enduring anxious micro-decisions, an uncomfortable obsession with my own body, so much learning. But it was worth it. It transformed my body (literally) and myself (metaphorically). I can’t imagine how I would have rebuilt my broken relationship with food without going through all of it.

So that gut feeling about weight-loss drugs stuck with me for a couple years because I didn’t dig into the actual science. When I finally did—over the last few months—I had a genuine change of mind.

Let me walk you through what I learned, why I changed my mind about these drugs, and yet, why I still wouldn’t recommend my uncle take them.

Before we get into Ozempic—or GLP-1 agonist drugs, which is what this family of medications is called—let’s get on the same page about how fat loss actually works.

Fat loss operates on one fundamental principle: energy balance. If you consume more calories than you burn, you gain weight. If you burn more than you consume, you lose weight.

Biologically, here’s what happens: when you burn more energy than you’re feeding your body, your body looks for alternative fuel sources—specifically, your stored fat. It breaks down that fat to get the energy it needs. And in the process, you lose weight.

Now this energy balance equation has two sides: calorie intake and calorie expenditure.

That’s where the distinction between food and exercise becomes sharp. You spend an hour sweating in the gym to burn 300-400 calories, but a chai and samosa puts all of that back. (Not fair.)

This is why controlling food intake is the single most important lever in fat loss. You have to eat in a deficit to hit your goals.

The problem—as I’ve written about before—is that our biology makes this harder than it sounds. It takes constant conscious effort to not eat more.

And this is exactly where GLP-1 drugs help: they suppress your appetite, you eat less, and you lose weight. (That’s all it does: no magic mechanism, no fancy fat burning—just the basics, assisted.)

How they do that is... interesting. Let me explain.

When we eat, our gut releases hormones that tell the body how to handle food: when to stop eating, how fast to digest, how much insulin to make. One of the most important hormones is GLP-1 (Glucagon-Like Peptide-1).

I find it kind of nuts that I’d never heard of GLP-1 in all my reading on fat loss. Because this hormone is actually on our side.

See what this little ally does: it reduces appetite by sending satiety signals to the brain, slows gastric emptying (so food leaves the stomach more slowly), and tells the pancreas to release insulin only when blood glucose rises. Put it all together, and GLP-1 helps you eat in control.

The villain in this story is an enzyme called DPP-4. It breaks down GLP-1 in about two minutes. So GLP-1 gets released and... it’s gone. The fullness effects it promises barely have time to show up.

Now think about it: wouldn’t it be amazing if GLP-1 could stick around longer, doing its thing without getting demolished by DPP-4?

This is exactly what drug scientists figured out how to do. Semaglutide—the medication inside Ozempic—is 94% structurally similar to the natural GLP-1 our body produces (meaning their molecular structures are nearly identical).

But here’s the key difference: it resists breakdown by DPP-4. The villain can’t kill this version of the hero.

And that changes things dramatically: while the naturally produced GLP-1 has a half-life of about 2 minutes, the injected semaglutide has a half-life of around 7 days—meaning those fullness signals stick around for days instead of minutes.

If there’s any “magic” with these weight-loss drugs, this is it.

That’s the theory. But theory isn’t enough. Because in biology, everything is connected. Change one thing and you change another. So we need to know what actually happens when people take these drugs.

Two critical questions: Do we have credible data showing these drugs help people lose weight? And even if they do, are we sure they’re not screwing up other bodily functions and creating new problems that didn’t exist before?

What we knew from before is that these drugs already helped diabetic patients. GLP-1 agonists were approved by the FDA for diabetes treatment back in 2005—so the class of drugs itself isn’t new. What’s new—and what recent clinical trials have tested—is whether they work for weight loss in non-diabetic people, and whether they’re any better than other weight-loss drugs.

The results have been convincing. Here are three key studies that paved the way to market approval.

1. STEP trials show GLP-1 works for weight loss

The STEP program (Semaglutide Treatment Effect in People with Obesity) was a series of large, global clinical trials that first showed semaglutide could cause major weight loss (even in people without diabetes).

In the flagship STEP 1 study, published in The New England Journal of Medicine in 2021, researchers took about 2,000 obese or overweight adults and randomly assigned them to one of two groups: one got a weekly injection of semaglutide (2.4 mg) plus basic lifestyle guidance, the other got a placebo injection plus the same guidance.

After 68 weeks, the results were striking: the semaglutide group lost an average of ~15% of their body weight, the placebo group lost only ~2.4%. In fact, nearly one in three people on semaglutide lost 20% or more of their weight—results that were previously seen only after bariatric surgery.

Meaning…. this is not just theory. It actually works.

2. SELECT trial shows GLP-1 goes beyond weight. It can help with heart health, too.

So far I’ve only talked about weight loss. But one of the most striking discoveries is that these drugs seem to help with far more than that.

This is why magazine covers like the one below. (Link to article.)

Take the SELECT trial, published in The New England Journal of Medicine in 2023. This one tested whether semaglutide could help heart disease patients. They studied over 17,000 adults who had overweight or obesity (but no diabetes) and a history of heart disease—heart attack, stroke, etc. Participants received either semaglutide 2.4 mg weekly or a placebo and were followed for about 3 years.

The results: those on semaglutide had a 20% lower risk of major cardiovascular events (heart attack, stroke, or cardiovascular death). And importantly, no new safety issues emerged.

Think about it: a drug originally for diabetes, now used for weight loss, was also proving to reduce the risk of dying from heart disease. Nuts.

That’s why in 2024, the FDA expanded Wegovy’s label to include cardiovascular risk reduction in people with obesity and heart disease.

3. Veteran Affairs study revealed more real-world evidence

The third study I want to share is one I first discovered through Derek Thompson’s journalism (former staff writer at The Atlantic). This is the massive Veterans Affairs study, published in Nature Medicine in 2024.

This one is different because it’s not a controlled trial. It analysed real-world data—electronic health records of more than 1 million U.S. veterans who were treated for diabetes.

Here’s Thompson describing what they found:

A team of scientists looked at more than 1 million patients with type 2 diabetes in the Veteran Affairs Medical System. They compared patients on GLP-1 drugs with those who been prescribed other meds.
GLP-1 drug usage was associated with a reduced risk of … just about everything bad: “substance use and psychotic disorders, seizures, neuro-cognitive disorders (including Alzheimer’s disease and dementia), coagulation disorders [e.g., means clotting], cardio-metabolic disorders, infectious illnesses and several respiratory conditions.”
When I initially read this study in January, it seemed too good to be true. Miracle drugs don’t exist. Perhaps, I thought, there were nuances that I’d missed. So I called up a co-author of the study, the Washington University physician-scientist Ziyad Al-Aly. On my podcast Plain English, Al-Aly told me that GLP-1 drug use really was associated with improvements across every biological system they studied. “They’re really remarkably beneficial, across multiple organ systems,” he said.

So here we are. There is real-world data to show that these drugs work. Remarkably well.

And yet, I have some concerns, and I didn’t recommend them to my uncle. Why?

Three reasons: biology, behavior, and capitalism. Let me explain.

Let’s start with biology.

If these drugs work so well, why do more than half of people stop taking them within a year?

For many, it’s just the cost: over a thousand dollars a month without insurance. No joke.

But even for those who can afford it, side effects are a major barrier: nausea, bloating, constipation, acid reflux—the same slowed digestion that keeps you full can also make you miserable. Some people adapt. Many don’t.

Then there’s something subtler: some users report that life on these drugs feels... muted. A bit… boring. Food becomes less interesting. Social drinking loses its appeal. The same mechanism that quiets hunger can sometimes quiet joy. (Not for everyone, of course.)

This shouldn’t surprise us. As Thomas Hager wrote in his book:

“No drug is good. No drug is bad. Every drug is both.”

The point is, every medication involves tradeoffs. The question is always: does the benefit outweigh the risk for you, specifically?

And here’s the thing about GLP-1s: we’re in the very early stages. What happens in 20 years? 30? We don’t know yet. There could be slow-developing issues we haven’t detected.

It’s possible. And no, those who flag aren’t fear-mongering. It’s just honest uncertainty.

But this is how medical science works. We don’t wait for 100% certainty before approving treatments, because waiting decades means denying known benefits to people who need help now. We make decisions based on the best available evidence, then keep watching.

So the science itself is sound. The drugs do what they’re designed to do. The side effects are documented. The unknowns are acknowledged.

If science isn’t the problem, what is?

Now second, human behaviour.

Think about what happens if someone takes these drugs without changing their underlying habits. The drug suppresses appetite, so they eat less and lose weight. But when they stop taking it, their appetite returns to what it was before.

And so if they haven’t built new eating patterns while on the drug, and they haven’t changed their relationship with food, the weight will almost certainly come back.

Moreover, if you lose weight rapidly without adequate protein and strength training, you lose muscle along with fat. And muscle loss is a real problem: it slows your metabolism, makes it easier to regain weight, and leaves you weaker than before. The drug doesn’t distinguish between fat and muscle—it just suppresses appetite. What you eat and how you move determines what you lose.

This isn’t unique to GLP-1s—it’s just how weight loss works. And it’s why medical guidance emphasises using these drugs alongside lifestyle changes: proper nutrition, strength training, and building sustainable eating patterns. The drug opens a window: it makes it easier to eat less, to resist cravings, to actually stick to changes that felt impossible before. But you still have to walk through that window. You still have to do the work.

And if you don’t—if you just rely on the drug alone—you’re setting yourself up for a painful cycle: lose weight, stop the drug (because of cost or side effects), gain it back, feel worse than before.

This is why I didn’t recommend it to my uncle. He wanted the results but wasn’t willing to change anything else about his life. No nutrition plan, no exercise, no rethinking his relationship with food. Just: “give me the shot.” And I knew how that story would end.

Now, I’m not interested in the moralistic hand-wringing about people “taking the easy way out.” Let people make their own choices about their bodies. Period.

The real risk is practical. Without the right support and commitment, these drugs can leave people more disappointed and more stuck than before they started.

The third problem—and the one that troubles me most—is capitalism.

Look, GLP-1 drugs make the most sense for people facing genuine medical risk. If you’re dealing with obesity-related diseases—diabetes, heart disease, metabolic syndrome—and lifestyle changes haven’t worked, these drugs can be life-changing. Possibly life-saving.

But that’s not how this will play out. We know it. Because the single biggest way to make money in healthcare is to feed on human anxiety. And our obsession with bodies, with thinness, with “optimization”? That’s fertile ground.

Big money creates powerful incentives—not just to help people who need it, but to expand the market as widely as possible. And we’re already seeing it. These drugs are being sought out for purely aesthetic weight loss. Celebrities are using them. Influencers are promoting them. In India, a black market has already emerged.

The companies will say the right things in their marketing: “Use alongside diet and exercise!” and “Consult your doctor!”

But many people are getting these drugs without proper medical supervision, without nutritional guidance, without understanding the commitment required.

Now do I trust pharmaceutical companies—whose entire business model depends on creating lifelong customers—to be cautious about who they sell to? No.

Do I trust them to be fully transparent about long-term risks as they emerge? History says I shouldn’t. This is the pattern we’ve seen before and the consequences show up years later.

And that’s where I have landed after immersing myself in the research: the problem with Ozempic isn’t the drug. It’s that we’ve turned a medical tool into a consumer product, marketed to insecurities rather than health needs.

The science is sound. The system is broken.

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