The belly that appeared and wouldn’t shift. The energy that got harder to hold onto. The feeling that the body had quietly changed the rules without telling you. If you’ve put all of that down to the menopause, you might be right. But there’s something else running underneath it — something I had too, without a single hormonal explanation for any of it.
I’m 53. Male. Nothing hormonal was happening to me. And yet what my blood tests documented across eight years maps almost exactly onto what you’ve been describing. The drift. The slow deterioration despite doing what I was told. The moment it all started moving in the wrong direction at once.
The mechanism has a name. And understanding it doesn’t require waiting for hormones to stabilise first.
What Was Actually Happening in My Blood Tests
October 2022. HbA1c 47 mmol/mol. One point from the diabetic threshold. Eight years on statins, gout pills, asthma inhalers, antihistamines. Every single blood test, the number crept up. Not dramatically. Just consistently. A slow drift in the wrong direction while I was doing everything I was supposed to be doing.
I thought I had several separate problems. My GP, to be fair, thought so too. A pill for each one. And the numbers kept moving.
What I didn’t understand then — and what took me years to properly figure out — is that those numbers weren’t separate problems. It was one mechanism expressing itself across multiple markers at the same time. And that mechanism had a name: insulin resistance. That was the thing I’d missed entirely.
The reason this matters for what you’re navigating is straightforward. My body had no hormonal transition to point to. No oestrogen fluctuating. No progesterone declining. And yet the same pattern appeared: belly fat accumulating in my 40s, energy getting harder to maintain, biomarkers drifting in the wrong direction year after year. Which means there’s something upstream of the hormonal picture. Something that was already running.
How Insulin Resistance Actually Works
Insulin’s job, in principle, is simple. You eat, glucose arrives in the bloodstream, insulin fires, your cells open up and let it in. Clean cycle. Works well when it operates occasionally.
The problem is what happens when that signal fires constantly.
Michael Mosley put this better than I’ve managed: it’s as though you’re constantly paying money into your bank account and finding it increasingly difficult to get it back out again. High insulin does exactly this with stored fat. The energy is present in substantial quantities. But the hormonal signal that would allow the body to release and burn it is suppressed. You’re not short of fuel. You’re locked out of it.
What builds that block? Constant glucose arriving. Constant insulin firing. Cells that hear the signal so many times they start to stop listening. That’s insulin resistance — not a disease that arrives suddenly, but a sensitivity that erodes quietly, over years, before anything shows up on a test.
Understanding it at 38 or 42 gives you more options than understanding it at 52. The mechanism doesn’t wait for a GP to label it.
What Hormones Actually Do to This Picture
I want to be careful here, because I’m a 53-year-old man and the audience I’m largely talking to is women navigating something I’ll never personally experience. What my data shows: insulin resistance can drive all of this without any hormonal change whatsoever. The belly that appeared after 40. The energy that got harder to maintain. All of it, in a male body, with nothing hormonal to point to.
What it doesn’t show — and what the research is clear about — is that hormones are irrelevant. They’re not.
Dr. Mindy Pelz, a functional medicine practitioner who has spent 25 years working with patients on exactly this, describes a hormonal hierarchy that stopped me when I first came across it. Cortisol and insulin, she says, have to be balanced before sex hormones can stabilise. If you’re addressing oestrogen directly without fixing what’s happening upstream with insulin, you’re working on the downstream effect while the upstream cause keeps running.
Now bring the traffic controller into it.
Oestrogen, when it’s present, acts as a redirector. It directs fat toward the hips and thighs — the pear shape that most women carry through their reproductive years. When oestrogen levels start to fluctuate in perimenopause, the controller goes off duty. Fat that would have followed the traditional route takes the default path instead: around the abdomen, visceral, metabolically active.
Nothing about the person’s behaviour changed. The controller stopped redirecting the traffic.
But here’s the bit I took a while to fully understand. The controller was already dealing with an overloaded system. If insulin resistance had been building for years, if there was already excess glucose arriving and cells already struggling to respond — when the controller went off duty, the situation got significantly worse, significantly faster. Two mechanisms compounding each other. My data shows what happens with just one of them. Yours may show what happens with both.
Christiane Northrup, a gynaecologist who has written extensively on perimenopausal health, put it plainly: insulin and stress hormones exacerbate oestrogen imbalance. A gynaecologist working with perimenopausal women. And insulin keeps turning up in the middle of the picture.
The Stress Piece — Worth Knowing
There’s a third element that connects to all of this. The adrenal glands use a common raw material — pregnenolone — to produce cortisol, oestrogen, DHEA, and progesterone. Under chronic stress, the adrenals receive an emergency instruction: all hands to the stress department. Every available unit goes to cortisol. Oestrogen and progesterone production drops. Not because the ovaries have stopped working. Because the building materials have been conscripted.
I had the cortisol piece too. Running a business under pressure, poor sleep, the kind of low-grade sustained stress that nobody flags because it’s just normal life. Fixing insulin sensitivity meant addressing all of it: not just food, but timing, sleep, and what chronic stress was doing upstream. Not one lever. The whole set of inputs.
The Most Common Misconception About Perimenopause Belly Fat
The most widespread assumption is that this is primarily a hormonal problem requiring a hormonal solution. The correlation is real. The timing is real. You’re doing what you always did and it’s not working anymore.
But the research — and my own data — suggests a more useful frame: hormonal change amplifies a metabolic dysfunction that was already building. The metabolic piece is addressable through lifestyle inputs regardless of where you are in the hormonal transition. It doesn’t require waiting for hormonal resolution.
Jessie Inchauspé, a biochemist who has followed the research on glucose and menopause closely, points to a 2020 Columbia University study showing that flattening glucose curves is associated with fewer menopause symptoms. Not just fewer metabolic problems. Fewer symptoms. Hot flushes, night sweats, insomnia — reduced in women managing their glucose response. Not “eat less.” Not “try harder.” A specific mechanism with a specific input.
I didn’t have hot flushes to track. But the direction of travel in my HbA1c data runs the same way. Reduce the glucose volatility, reduce the insulin load, and the downstream effects — whatever form they take in your body — may well improve.
The information most of us were given about midlife body change was simply incomplete. It pointed at the visible factor — hormones — without explaining what was already running underneath it.
What My Blood Tests Actually Showed
October 2022: HbA1c 47 mmol/mol. One point from the diabetic threshold. On statins, gout pills, asthma inhalers, antihistamines. Doing what I was told.
December 2023: Still pre-diabetic. Boxing Day, 18 stone. The last data point before anything changed.
February 2024: I went to my GP with what I’d been doing and said I wanted to try a supervised period without the medication. He wasn’t thrilled. But he said if I was going to do it, at least I was doing it properly. Monthly bloods for three months, then quarterly. He had my data. I had the measurements.
January 2025: HbA1c 40. Eleven months in. Normal range. Out of pre-diabetic territory for the first time in years.
April 2025: HbA1c 37 mmol/mol. Optimal. The lowest reading in NHS records going back to 2012.
And it wasn’t just the HbA1c. Same blood test, April 2025: CRP down 84%, from 6.2 to 1.0. ALT, the liver enzyme, down 67%. HDL up 15%. LDL down 32%. Cholesterol-to-HDL ratio within target range for the first time in eleven years on statins.
Eight biomarkers, all moving in the same direction, in the same window. Not because I targeted eight separate problems. Because the upstream mechanism changed.
My GP looked at the results and said — and I’m quoting — “Bloody hell, what’ve you been doing?”
I showed him the data. He said: whatever it is, keep doing it.
What the Timeline Actually Looked Like
Month one: not much. Energy inconsistent. Sleep a bit rough. Body adapting.
Month three: eating windows starting to feel manageable rather than difficult.
Month six: first meaningful comparison. HbA1c still elevated, but trending.
Month eleven: out of pre-diabetic range.
Month fourteen: optimal.
Not three weeks. Fourteen months. And it wasn’t a straight line. Ferritin dropped significantly partway through. Turned out there was an iron deficiency that needed investigating separately. Progress on one front doesn’t mean everything goes smoothly everywhere.
The mechanism I was addressing had been building over eight years of slow deterioration. The reversal needed to be consistent too. Not dramatic. Consistent.
That pattern — the mechanism running in the background before it shows up as anything labelled — is the same one operating across a lot of bodies. Mine had no hormonal complexity to it. But the underlying signal, the way insulin sensitivity erodes and then can be restored, runs the same way regardless.
I’ll leave that with you.
🎯 Key Takeaways
- The mechanism runs before the diagnosis: Insulin resistance builds over years without showing up on a test. Understanding it at 38 or 42 gives you more options than understanding it at 52.
- Hormones amplify what was already there: Oestrogen decline in perimenopause removes a redirector. But if insulin resistance was already building, two mechanisms now compound each other.
- Cortisol connects to the picture: Chronic stress conscripts the same raw materials the body uses to produce sex hormones. Reducing the stress load may return building materials to the hormone production line.
- The evidence points upstream: A 2020 Columbia University study found that flattening glucose curves is associated with fewer menopause symptoms — not just fewer metabolic problems. Fewer symptoms.
- The reversal took 14 months, not 14 days: Eight biomarkers moved in the right direction when the upstream mechanism changed. Not a straight line. Consistent.
Want to Start Tracking the Trend?
The fasting tracker I described — eating windows, fasting glucose, ketones if you’re measuring them, weekly check-ins — is in the description. It’s free. Worth building the habit before your next GP appointment so you’ve got something to show them.
👉 Get the 14-Day Rhythm Reset Guide (free)
💪 Want ongoing support? Join Rhythm Club for £30/month (includes FREE app access, community, and weekly accountability calls)
⚠️ Important: This is educational content based on evidence and personal experience. It is not medical advice. Speak to your GP before making changes to your fasting pattern, diet, or medication.
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