When I stopped my cholesterol medication in February 2024, I expected the numbers to blow up. That’s what everyone said would happen. Stop statins suddenly, they said, and your LDL rebounds. Your body compensates. You’re taking a real risk.
What happened instead was this: fourteen months later, my LDL had dropped 32%. My cholesterol-to-HDL ratio, the number that actually matters for cardiovascular risk, had reached target for the first time since 2016. And I hadn’t taken a single statin.
I’ve got NHS blood tests going back to 2012 in a folder. The whole trajectory, on medication and off it, all documented. What those tests show about what actually drives cholesterol, and why statins addressed one part of the picture while something else was running quietly underneath, is what this post is about
The Idea I’d Believed for Eleven Years
The conventional reasoning goes roughly like this. High cholesterol is a risk factor for heart disease. Statins reduce cholesterol. If your numbers are high, you take the medication and manage from there. And if you start doing something unconventional, like fasting or cutting out food groups, your cholesterol could swing unpredictably. So keep taking the medication and change things carefully, if at all.
That’s not an unreasonable position. The guidelines exist because the evidence exists. Elevated LDL, over time, does appear in the same frame as cardiovascular risk. Statins do reduce LDL in clinical trials. None of that is contested.
I believed it for eleven years. I took the medication. I had the blood tests. I attended the reviews. And all the while, without either me or my GP fully registering it, the trend was going the wrong way.
The idea I’d accepted, the one embedded in every prescription renewal and every reassuring “the medication is working” conversation, was that statins were addressing the problem. My data going back to 2012 suggest something different. The medication was suppressing one number while the underlying driver kept running.
Eleven Years on Medication – What the Numbers Actually Showed
April 2012. First test where cholesterol is flagged. Total cholesterol 7.5 mmol/L. GP note: need to speak to doctor. Atorvastatin 40mg begins. Standard first-line treatment. Nothing controversial about that decision at the time.
Here’s what the data looked like across the years that followed.
By December 2016, ezetimibe was added. Dual therapy now. You’d expect the numbers to have dropped and stayed down. They didn’t. They moved around but kept climbing across subsequent tests. The cholesterol-to-HDL ratio, which is actually the more useful measure because it shows the balance of what’s circulating rather than just the raw total, had reached 6.2 by then. Up from 4.7 in 2012. That means my cardiovascular risk profile, by the ratio measure, had worsened 32% across nine years on dual medication.
By July and August 2020: total cholesterol 7.3 to 7.4. Still prescribed. Still being reviewed. December 2023: total cholesterol 8.0 mmol/L. LDL 5.6. That’s 27% worse than the 4.4 it was when the statin conversation started in 2012. HDL: 1.3 and declining. Ratio: 6.2.
December 2023 is also when my GP looked at those results and told me everything looked fine. Stay on the medication. That was his honest read of the situation, and from a managed-care perspective, it wasn’t wrong. I was on the medication. The medication was doing its job of suppressing one enzyme. But the trajectory, when you lay out all eleven years together, told a different story.
There was one more number in that December 2023 test I wasn’t paying much attention to at the time. ALT, the liver enzyme. 69, which is 73% above the upper reference limit. Statins are known to put pressure on the liver. I filed that one away.
Eleven years. Multiple blood tests. Cholesterol never below 6.0 on medication. Ratio: unchanged at 6.2. Trend across the full period: upward.
What Changed in February 2024
Boxing Day 2023. I stopped eating the way I’d eaten for most of my adult life. 18:6 fasting. Eating window from noon to six. Non-UPF food. Nothing more complicated than that at the start.
My prescriptions had lapsed in October 2023 when I moved surgery. By mid-February 2024, the remaining medication had run out. I made the decision not to renew. I want to be clear about that: there was no prior GP conversation about stopping. I had years of tests in a folder, I’d watched the trajectory, and I made that call unilaterally. I disclose that every time, because I’d never suggest anyone do the same. The monitoring that followed was transparent with my GP, and that monitoring is what made it possible to track what happened next.
What I remember from that period was waiting for the spike. The internet is quite clear on this. Stopping statins suddenly can cause a rebound. Cholesterol shoots up. I’d been on the medication for over eleven years. I genuinely expected something to blow up.
Nothing blew up.
One month later, March 2024. First blood test off all medication. Total cholesterol 7.0. Not dramatic yet. But the liver enzyme, the one I’d filed away: ALT down from 69 to 28. In one month. A 59% improvement. My GP’s words at that review: this is better than on statins.
What Fourteen Months Off Medication Actually Showed
Let me walk through the cholesterol data specifically, because this is where the story is.
March 2024, one month off medication: total 7.0. LDL 4.7, already down from the 5.6 peak. That’s a 16% improvement in the first month.
April 2025, fourteen months off medication: total 7.11. LDL 3.8, down 32% from the 5.6 peak. HDL: 1.5, up from 1.3. That’s a 15% improvement in HDL. Ratio: 4.7, within target. For the first time since 2016.
November 2025, twenty-one months off medication: total 6.77. Ratio: 4.8, holding within target. The LDL figure in this test uses the Sampson equation, which calculates rather than measures directly, so I don’t compare it to the April figure. The ratio is the honest number. And the ratio has held.
And then the liver. By November 2025: ALT 10. Down from 69 in December 2023. An 86% reduction. Lowest reading in records going back to 2012s. That one genuinely surprised me. I was watching the cholesterol numbers. The liver came with it, quietly.
To put the full picture plainly: on statins across eleven years, the cholesterol-to-HDL ratio worsened by 32% and never reached target. Off statins across fourteen months, the ratio improved to within target and has held there. That is one person’s data. N=1. NHS blood tests going back to 2012, all of it documented. I’m not a cardiologist. I can’t tell you exactly which variable drove each number. But I can tell you what the measurements show.
Why Statins Couldn’t Address the Driver
Here’s the mechanism, as best I understand it.
LDL cholesterol is essentially a delivery driver that keeps dropping parcels at the wrong address, specifically inside your arterial walls, where they accumulate and cause problems. HDL is the returns driver. It picks up the misdelivered parcels and takes them back to the liver to be processed properly. What you want is fewer wrong-address deliveries and a strong returns service. That’s the simplified version of why the ratio matters more than the raw total. A high total with an excellent returns service tells a completely different story to a high total with almost no returns.
What drives LDL out of balance, and this took me a while to understand, isn’t primarily fat in your diet. Your liver makes most of your cholesterol. And what tells the liver to produce more isn’t dietary fat. It’s refined carbohydrates and the insulin response they trigger. Sarah Berry, nutrition scientist at King’s College London and Chief Scientist at ZOE, has documented this clearly: diet alone can reduce LDL by up to 30%, equivalent to statin-level effect. She’s also described the mechanism precisely: excess refined carbs cause the liver to convert those carbs to saturated fat, which then suppresses the very receptor responsible for clearing LDL from your blood. That’s not a fringe position. That’s King’s College research.
Statins work by blocking an enzyme the liver uses to produce cholesterol. That does reduce LDL in many people. What statins don’t do is address the insulin signal that’s telling the liver to overproduce in the first place. The fasting shortened my eating window and removed most of the refined carbohydrates that were driving that signal. When the signal changed, the liver started behaving differently.
The delivery driver problem didn’t need the van blocking the road. It needed the dispatch centre to stop sending the wrong jobs.
What This Does and Doesn’t Mean
I want to be careful here, because this is where the N=1 framing matters most.
My data suggests that for me, the driver behind eleven years of rising cholesterol wasn’t something statins could fix. The numbers went up on the medication for eleven years. They came down off it, during a period when I’d changed what and when I was eating. That’s the honest read of what the records show. It’s one person’s data. It’s not a clinical trial.
There are people for whom statins are genuinely the right call. High-risk cardiac patients. Significant family history. People who’ve already had a cardiac event. That conversation is between you and your GP, and it’s a different conversation to mine. I’m not suggesting my journey maps onto yours.
What I’d invite you to consider is the mechanism underneath. The way the liver responds to insulin load, the way eating patterns affect what gets produced and what gets cleared, that process doesn’t start when someone hands you a prescription. It runs quietly for years before anyone puts a name on it. The numbers that show up in a cholesterol panel are the downstream signal of something happening upstream.
If your GP has mentioned your numbers are worth keeping an eye on, or if you’re already on medication and wondering what else might be going on, understanding the upstream driver before or alongside the medication conversation is, in my view, more useful than ignoring it. That’s what data going back to 2012 looks like from where I’m standing. Your read of your own data may come out differently. That’s how it should work.
🎯 Key Takeaways
- The ratio matters more than the total: The cholesterol-to-HDL ratio is a better risk indicator than raw total cholesterol. Mine worsened 32% on dual medication across nine years and reached target within fourteen months off it.
- The liver is the production site: Most cholesterol is made by your liver, not absorbed from food. What drives overproduction is insulin load from refined carbohydrates, not dietary fat.
- Statins address one enzyme: They reduce cholesterol production via one pathway. They don’t address the insulin signal that drives the liver to overproduce in the first place.
- The liver responded quickly: ALT dropped 59% in the first month off statins, and 86% over twenty-one months. The liver strain from long-term statin use isn’t always felt in real time.
- N=1 is still data: One person, one record, all documented. It’s not a clinical trial. But it’s a pattern worth examining alongside your own numbers and GP.
Ready to Start Your Own Rhythm Reset?
If the mechanism in this post has made you curious about what changing your eating window and food quality might do for your own biomarkers, the 14-Day Rhythm Reset Guide is the place to start. It covers how I structured the eating window during this period, what the reasoning was, and how to build from day one without making it complicated.
👉 Get the 14-Day Rhythm Reset Guide (free)
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🔽 Read the Video Transcript
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⚠️ 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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