The Surprising Benefits of GLP-1 Drugs Beyond Weight Loss
An opinion piece — not medical advice. This is where I currently stand on the evidence. As always, anything you’re considering should be discussed with your GP first.
With the news of Serena Williams returning to the tennis tour after four years away, the internet has been doing what the internet does — speculating wildly. A 43-year-old woman, four years out from elite competition, returning to one of the most physically demanding sports in the world. And among the theories floating around about how, one keeps coming up: GLP-1 drugs.
I’ll be honest. I don’t usually get excited about pharmaceutical treatments. A significant part of my clinical philosophy over the last 16 years has been built around finding root causes rather than managing symptoms — the whole reason I pursued functional medicine training, why nutrition and metabolic health sit at the centre of what I do, and why I’m generally sceptical of the idea that a drug is the answer to most things.
GLP-1 drugs have made me genuinely reconsider that scepticism. Not because of the weight loss — although it’s real and significant — but because of something else entirely. These medications appear to be doing things to the human body that nobody quite expected. Things that are deeply relevant to what I see in clinic every single day.
This article is my attempt to lay out where I currently stand, what the emerging research is showing, and why I think the conversation happening in scientific circles needs to filter through to everyday people a lot faster than it currently is.
So What Even Is a GLP-1 Drug?
GLP-1 stands for glucagon-like peptide-1. In plain language, it’s a small protein — technically a hormone — that your gut naturally produces when you eat. Its main job is to signal to your pancreas to release insulin, tell your liver to ease up on dumping glucose into your bloodstream, and communicate to your brain that you’re full. It’s essentially one of the body’s key messengers for managing energy and blood sugar.
The drugs — semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro) being the most well known — are GLP-1 receptor agonists. They mimic and amplify this signal. What makes them unusual is that GLP-1 receptors aren’t just in your digestive system. They’re distributed throughout the body — in the brain, the heart, the kidneys, the joints, the immune system. Which is why, when you flood those receptors with a drug that activates them, you start to see effects that go well beyond appetite and blood sugar.
It’s a bit like discovering that a light switch you thought only controlled one lamp is actually wired to half the house.
A quick word on the different drugs
You’ll hear semaglutide (Ozempic, Wegovy) and tirzepatide (Mounjaro) mentioned most, and people often ask me what the difference is. Broadly, the benefits overlap a lot. But anecdotally — and this lines up with what a lot of my patients report — tirzepatide tends to come with fewer of the nausea and digestive side effects that put people off semaglutide. It’s also more expensive, so for some people that’s the trade-off: pay more, tolerate it better, versus pay less and potentially deal with more side effects in the early stages. If you’re someone who tends to react strongly to medications generally, that’s worth raising with your GP.
Then there’s retatrutide, which is still working its way through trials but is generating a lot of attention. Where semaglutide and tirzepatide target one and two receptor pathways respectively, retatrutide targets three. Early trial data has shown weight loss results beyond anything seen with the current drugs, and the broader effects — on liver fat in particular — look even more pronounced. It’s not available yet, but given the trajectory of this whole drug class, I’d expect retatrutide and whatever follows it to become a much bigger part of this conversation over the next few years.
How I Got Interested
A few years ago, the only time I heard “Ozempic” was in the context of celebrity gossip. There was the usual pattern — a miracle solution sweeping through Hollywood, dramatic before-and-after photos, and the collective waiting for the inevitable wave of serious complications that would eventually follow. We’d seen it before with weight loss drugs. The jury always seemed to come back negative eventually.
This time felt different, though. The side effect profile was manageable. The scientific community wasn’t walking back its enthusiasm. And then my patients started talking.
The first few who went on GLP-1 drugs came back reporting something I hadn’t expected. Within weeks of starting — often before any significant weight change — they were noting improvements in joint pain. Knee osteoarthritis that had been grinding along for years, backs that had been periodically flaring, hip pain that had been resistant to everything we’d thrown at it. Better.
Now, I’m a sceptic by training. My first instinct wasn’t actually metabolic — it was psychological. A drug that produces visible change in your body relatively quickly could reasonably make someone feel more confident, more motivated, better about themselves. And we know that psychological wellbeing and pain perception are deeply intertwined. Someone who feels better about themselves tends to move more, sleep better, engage more with life. That alone could account for improvements in chronic pain without any direct pharmacological effect on the joints at all.
But I also knew from years of clinical experience that any meaningful improvement to metabolic health tends to produce improvements across multiple facets of health simultaneously. Better blood sugar regulation, better inflammatory control, better energy. If the drug improved metabolic function, the subsequent benefits would be significant regardless of whether the initial effect was psychological or metabolic.
So I had two reasonable explanations sitting in front of me. What I didn’t expect was what happened when I went further through the literature. I kept finding the same word popping up. Inflammation. Not just indirect effects on inflammation through weight loss. Direct, specific, GLP-1-receptor-mediated modulation of inflammatory pathways. In joint tissue. In cardiac tissue. In the kidneys. In the liver. Essentially everywhere these receptors live.
What the Research Is Actually Showing
This is where it gets genuinely interesting. I want to be clear that the science is still moving — some of this is well established, some is emerging — but the overall direction is consistent enough to take seriously.
Joints — and this is the part I find most relevant
A large study published in the BMJ looked at tens of thousands of people with diagnosed knee osteoarthritis over a fourteen-year period. It compared those who used GLP-1 drugs against a matched group who didn’t, controlling for age, weight, other health conditions, and healthcare access. The finding that stood out: people on GLP-1 drugs were significantly less likely to end up needing a total knee replacement — and that effect got stronger the longer they were on the medication and the newer the drug generation.
Now, the obvious explanation is weight loss. Less load on the joint, less wear, less eventual surgery. And that’s almost certainly part of it. But the benefits appear to happen independent of weight loss. Separate pilot trial data has shown signs of actual cartilage restoration in knee joints. Cartilage doesn’t regenerate — or so we’ve always been told. That it might do so with GLP-1 exposure points to something happening at the tissue level that weight reduction alone can’t account for. The researchers describe it as potential “disease- modifying activity” — meaning the drug may be changing the biology of what’s happening inside the joint, not just reducing mechanical stress on it.
For anyone who has been told their knee osteoarthritis is just going to keep progressing, that’s a meaningful shift in the conversation.
And joints aren’t isolated — there’s early data showing similar anti-inflammatory benefits in other forms of arthritis, including psoriatic arthritis, where disease activity improved before any weight loss had occurred.
Beyond joints
The same weight-loss-independent pattern keeps appearing across other organ systems. Heart disease risk drops significantly — and arterial inflammation, one of the main drivers, reduces almost immediately after starting the drug. Kidney protection appears to be almost entirely independent of weight loss. Fatty liver disease improves before the scales move. Even addiction research is finding benefits — alcohol, nicotine, gambling — through GLP-1 receptors in the brain’s reward pathways.
The list is growing. The theme is consistent: these drugs are doing something to inflammation and organ function that goes beyond the calorie equation.
What This Means From Where I Sit
I want to be careful here, because the science is still developing and I’ll always reserve the right to change my position if the evidence shifts. I’ve done it before and I’ll do it again — that’s what intellectual honesty requires.
But right now, looking at the cumulative picture, I think these drugs are being significantly under-utilised for the wrong reasons. The public conversation is almost entirely about weight. The scientific conversation is about something much larger — a class of medications with broad, direct anti-inflammatory and organ-protective effects that happen to also cause weight loss.
For my patients with longstanding osteoarthritis, chronic inflammatory pain, or joint problems that have been resistant to conventional treatment, I think this is absolutely worth a conversation with your GP. Not as a magic bullet. Not as a replacement for the fundamentals — because improving your diet, moving well, managing stress, and sleeping properly will always be the foundation. But there’s no contradiction in both things being true. Good lifestyle practices and a targeted short course of a medication that modulates inflammation — these aren’t mutually exclusive.
The analogy I keep coming back to is anti-inflammatory medication. Most of us are comfortable with the idea of someone doing a short course of a NSAID to get on top of acute inflammation while they do the rehab work. I think the evidence is building that GLP-1 drugs deserve to be thought about in a similar way — not as a permanent crutch, but as a tool that might help break a chronic inflammatory cycle while you work on the underlying drivers.
I also think the reclassification conversation happening in medical circles is justified. These are not simply “weight loss drugs” any more than statins are “cholesterol drugs.” The mechanism is broader and the clinical applications are widening.
A Note on How Healthcare Filters Evidence
There is a broader point here worth pausing on, because it says something about how healthcare systems process new information.
GLP-1 drugs entered public consciousness through a single, highly marketable lens — weight loss. That framing stuck, because it was the most commercially visible effect and the one that generated the most media coverage. But the science was always pointing somewhere more interesting. The weight loss was, in a sense, a side effect of something far more systemic being switched on.
This is not unusual. It reflects a pattern in how evidence travels through healthcare: the most legible finding — the one easiest to communicate, regulate and bill for — tends to define the drug in the public mind, sometimes for decades. The deeper mechanisms get discussed in journals and at conferences while patients, and even many clinicians, remain oriented around the headline.
It also raises a question worth asking about how we evaluate healthcare interventions more broadly. If a drug classified as one thing is producing significant benefits across multiple organ systems through mechanisms that were poorly understood at approval, what does that suggest about the adequacy of the frameworks we use to assess, fund and deploy new treatments? These are not abstract questions. They bear directly on which patients get access to which tools, and when.
I find that kind of systems-level question increasingly interesting — not just in the context of GLP-1 drugs, but across the healthcare system more broadly.
Some Important Cautions
No drug this widely discussed gets to exist without legitimate concerns, and I want to address a few directly.
Eating disorders and body image
This is the one I feel most strongly about. GLP-1 drugs are appetite suppressants, and they are being prescribed in a cultural moment already saturated with pressure around weight and body image. For people with a history of disordered eating — restricting, purging, or deeply distorted relationships with food and their bodies — these medications carry real risks that go beyond the physical. Appetite suppression can reinforce harmful patterns. The weight loss framing in media coverage makes it worse. If you or someone close to you has a history of an eating disorder, this conversation with your GP needs to include that history explicitly. It may not be a contraindication, but it needs to be part of the clinical picture. I would also encourage anyone in this category to have a conversation with a psychologist alongside any medical discussion.
Muscle loss and bone density
This was one of my earliest concerns, and it remains worth monitoring. When people lose weight rapidly, they typically lose some muscle mass alongside fat — and that has downstream effects on bone density, functional strength, and long-term metabolic health. Researchers like Ben Bikman, who were vocal early critics on this point, have more recently acknowledged that the lean mass concerns appear to have been somewhat overstated. Newer data suggests that much of what was being measured as “lean mass loss” was actually a reduction in liver mass and liver fat — which is, in fact, a health benefit, not a harm. Muscle strength, importantly, does not appear to drop in proportion to any modest reduction in muscle mass.
That said, we continue to believe strength training is essential for anyone on these medications. It is not optional. If you are commencing a GLP-1 medication and want guidance on how to structure resistance training alongside it, that is something we work with patients on directly at the clinic.
Cost and access
Ozempic is coming off patent, which should eventually bring its price down. Mounjaro still has a number of years of patent protection remaining, and at roughly $400 a month it remains simply out of reach for many people — particularly in a cost of living crisis. The equity question here is real. A drug class with this breadth of benefits becoming accessible only to those who can afford it is a health systems problem, not just a market one. It deserves more policy attention than it is currently getting.
A final Note on Serena
Whether Serena’s return works out or not is almost beside the point. What I find genuinely interesting is that a 43-year-old woman, who has spoken openly about how hard physical recovery has been since retirement and childbirth, might now have access to a tool that targets the chronic inflammatory burden her body has been carrying for decades of elite sport. If GLP-1 drugs are helping her manage that — great.
There’s a broader conversation to be had about body image, about the weight loss framing of these medications, and about who has access to them. Those are important conversations. But they shouldn’t crowd out the science. And right now, the science is pointing somewhere genuinely exciting.
I’ll keep reading. And I’ll keep updating my view as the evidence does what evidence does — shifts.
Further Reading
My suggestion is engaging with smart conversations so you can be better informed. Here are the ones I found most helpful.
1. GLP-1 Side Effects, Risks, and Who Should Actually Be Using Them — Dr Christine Guevara, interviewed by Dr Gabrielle Lyon
2. Nutrition for Satiety and Weight Loss — Dr Federica Amati, interview with Simon Hill
3. The Ozempic Expert: Ozempic Transforms Your Gut Microbiome — Dr Tyna Moore, interview with Steven Bartlett