Everyone’s talking about GLP-1s right now. You’ve probably had the conversation yourself — with a friend, in a group chat, maybe with your own GP. And I understand why. For a lot of women, these medications are the first thing that’s actually moved the number on the scale in years.
But here’s what I want to open for conversation with you for a moment, because it matters more than the drug itself: GLP-1s are popular right now because insulin resistance has become the default state for midlife women. This is a pattern I am seeing daily in clinic, and it’s one that’s deeply tied to what’s happening hormonally through perimenopause and menopause.
The medication is targeting something real. What it isn’t doing is addressing why that something developed in the first place. And that gap is exactly what I want to discuss today.
Why midlife exacerbates insulin resistance…
Let’s start with the biochemistry, because once you understand this, so much of what’s happened to your body over the last few years stops feeling mysterious.
Estrogen plays a role in your menstrual cycle; however, it also plays a direct role in how sensitive your cells are to insulin — it helps keep the signalling pathway open, so insulin can do its job efficiently and your pancreas doesn’t have to work overtime. As estrogen fluctuates and ultimately declines through perimenopause, that protective effect declines with it. Your cells become measurably less responsive to insulin, simply as a consequence of the hormonal shift you’re moving through.
At the same time, progesterone — which has its own calming, insulin-sensitising influence — is often the first hormone to drop in perimenopause, sometimes years before estrogen becomes erratic. And let’s layer this with cortisol, your primary stress hormone, which tends to run higher through this life stage, whether from disrupted sleep, an overloaded nervous system, or the sheer mental load most women carry into and beyond their late 40s. Cortisol directly opposes insulin’s action. It tells your liver to release more glucose, right when your cells are already struggling to clear it.
So you have three hormonal shifts converging at once — fluctuating and declining oestrogen, declining progesterone, and rising cortisol — and every one of them pushes in the same direction: toward insulin resistance.
This is what your body does at this stage of life. Insulin resistance in midlife isn’t the exception. Given what’s shifting hormonally, it’s close to what we’d expect.
There’s another piece I want to name, because I think it gets missed constantly: the sheer exhaustion so many women are carrying right now isn’t just tiredness. It’s not that they’re scheduling too much or something a good night’s sleep fixes. For a lot of women, it’s the mental load — the constant background task of remembering, planning, and anticipating everyone else’s needs — running all day quietly, every day, whether or not anything is actually happening. That kind of unresolved, always-on stress keeps cortisol elevated in a low, sustained way rather than the short, sharp bursts cortisol is actually built for. And sustained cortisol is one of the more direct things working against your insulin right now.
Where GLP-1s fit — and where they stop
This is where GLP-1 medications come in, and why they work so well for so many women.
GLP-1 is a hormone your own gut already produces after eating. It slows gastric emptying, increases satiety, and improves insulin secretion. The medications mimic that hormone at a much higher, sustained level than your body produces naturally. For someone whose insulin resistance has progressed to the point of significant weight gain, that mechanism can genuinely help — appetite settles, portions shrink without a fight, food noise reduces, and often for the first time in years, the scale starts moving.
I’m not here to tell you GLP-1s don’t work. They do exactly what they’re designed to do.
What I want you to understand is what they’re not designed to do. They don’t correct the oestrogen decline that’s reducing your insulin sensitivity. They don’t lower the cortisol that’s working against you overnight. They don’t rebuild the muscle mass that — biochemically — is your single largest reservoir for clearing glucose out of your bloodstream. And they don’t touch the inflammatory load, the gut function, or the nervous system dysregulation that so often sit underneath the whole picture.
This is exactly why the rebound weight gain conversation around GLP-1s has become so common. When the medication stops — whether by choice, by cost, or because the body’s response changes over time — and none of the underlying drivers have been addressed, the insulin resistance that was there at the start is often still there. Sometimes it’s worse, because muscle mass was lost alongside fat mass while on the medication, and muscle is precisely the tissue you need for long-term insulin sensitivity. The appetite suppression goes. The underlying physiology doesn’t.
What actually closes the gap
This is what I want to explain: whether or not you ever take a GLP-1, the actual work is the same. It’s about addressing the reasons your cells became insulin resistant in the first place.
That means looking at the whole picture — supporting the nervous system so cortisol isn’t running in overdrive around the clock, rebuilding and preserving muscle so your body has somewhere to send glucose, and calming the inflammatory processes that keep insulin signalling reduced. None of this is about not being able to control your eating or another restrictive eating diet. It’s about working with the specific mechanisms driving the resistance.
This is also precisely why root-cause support matters most alongside a GLP-1, or instead of it. If you’re using one of these medications, addressing the underlying insulin resistance is what protects the results once you stop — it’s the difference between the weight coming back and it staying off. And if you’re not using one of these medications, this work can shift the trajectory before you ever need to have that conversation with your GP.
Where you can start…
Berberine-containing herbs, if used properly. It gets talked about constantly, but most content stops at “it lowers blood sugar.” What’s rarely explained is that it works through the same AMPK pathway as metformin — part of why research directly compares the two.
Clinically, what’s more interesting is what happens downstream: the compound berberine also shifts gut microbiome composition, increasing bacteria that produce short-chain fatty acids, which independently support insulin sensitivity through the gut-liver axis. It’s also poorly absorbed with a short half-life, which is why dosing it once a day, without attention to timing around meals, tends to under-deliver compared to what the research protocols actually used.
Your nervous system isn’t just “stressed” — it’s stuck. Here’s what I mean by that. Your vagus nerve is the thing that actually switches you out of fight-or-flight mode and back into rest-and-digest mode, and most women in midlife are barely able to do this.
One of the simplest ways in is your breath — making your exhale longer than your inhale, even just a few rounds of it, sends a direct signal down that nerve to bring your cortisol down. I know that sounds almost too small to matter, but it works within minutes, not weeks. And there is a lot of research around this.
A cold water change at the end of your shower, even if it’s just on your face, does something similar. None of this is about being calmer for the sake of it. Every bit of cortisol you bring down is one less thing working against your insulin.
The post-meal walk. Muscle contraction itself opens a separate glucose doorway into your cells, called GLUT4, completely independent of insulin. A short walk after eating — even ten minutes — pulls glucose out of your bloodstream through a pathway that bypasses insulin resistance altogether. It’s not about burning calories. It’s a direct biochemical workaround, and one of the few interventions that works immediately, the same day, rather than needing weeks to show an effect.
Insulin resistance in midlife isn’t a verdict. It’s a signal, one that’s been building through a completely explicable hormonal process—and one that responds well once you address the drivers, not just the downstream symptom of appetite and weight.
If you’ve been wondering why the number on the scale won’t move no matter what you try, or you’re on a GLP-1 and want to protect your results long term, that’s exactly the conversation worth having. Let’s look at the whole picture together.
Teressa,
Naturopath | Clinical Nutritionist | Biochemist
Gold Coast Naturopath, Gold Coast Health, Naturopath Australia, Gold Coast Wellness, Holistic Health, Insulin resistance, Naturopathic Medicine, Functional Health, Midlife, Personalised Healthcare
