Your GP has flagged your liver enzymes. Maybe more than once. And you’ve been told, more or less, not to worry about it. “Abnormal, but expected.” That phrase has been said to more people than anyone has counted. What it actually means is: elevated, yes, but elevated in the way we’d expect given everything else going on. Not alarming enough to investigate. Not normal enough to ignore.
I had that conversation in 2012. My ALT — the main liver enzyme marker — was at 37. Just inside the normal range. By December 2023, it was at 69. That’s 73% above the upper limit. Twenty months later, it was 10. That’s an 86% drop, tracked against NHS blood test data going back to 2012.
The story of how that happened is more complicated than I expected. And the phrase “abnormal, but expected” is worth unpacking properly, because it tells you quite a lot about why this number gets ignored more often than it should.
Your GP has flagged your liver enzymes. Maybe more than once. And you’ve been told, more or less, not to worry about it. “Abnormal, but expected.” That phrase has been said to more people than anyone has counted. What it actually means is: elevated, yes, but elevated in the way we’d expect given everything else going on. Not alarming enough to investigate. Not normal enough to ignore.
I had that conversation in 2012. My ALT — the main liver enzyme marker — was at 37. Just inside the normal range. By December 2023, it was at 69. That’s 73% above the upper limit. Twenty months later, it was 10. That’s an 86% drop, tracked against NHS blood test data going back to 2012.
The story of how that happened is more complicated than I expected. And the phrase “abnormal, but expected” is worth unpacking properly, because it tells you quite a lot about why this number gets ignored more often than it should.
[Note to Neil: Add YouTube embed once video is published]
What ALT Is Actually Telling You (And Why “Normal Range” Is A Wide Range)
ALT stands for alanine aminotransferase. It’s a protein that lives inside liver cells. When those cells are under stress or damaged, they leak ALT into the bloodstream. So when your GP runs a liver function test, they’re not directly measuring the liver. They’re measuring how loudly the liver is complaining.
The NHS reference range sits at up to 40 iu/L. Most GPs treat a result inside that range as a green light. But the upper limit of normal was set to capture the majority of the population — and when the majority of the population is carrying some degree of metabolic stress, “normal” and “healthy” are not quite the same thing. My April 2012 reading was 37. Just under the ceiling. I was told it was fine. It wasn’t investigated further. And yet the number had been climbing.
This matters because the mechanism that drives ALT upward often runs for years before it shows up in symptoms. By the time it becomes something a GP investigates further, the underlying process has typically been running quietly in the background for a long time.
Benjamin Bikman has spent his career researching insulin resistance, and one of the clearest things he has identified is its relationship to the liver specifically. Insulin resistance is the strongest known predictor of non-alcoholic fatty liver disease — it increases the risk 15-fold. And NAFLD has gone from being virtually unheard of 30 years ago to affecting roughly one in three people in Western countries. Not a niche condition. The workplace around you.
So what is the mechanism? When your primary fat storage systems are overloaded — when fat cells are at capacity, glycogen stores are topped up, and energy keeps arriving — the body needs somewhere to put the overflow. Think of your house with every room full and someone still delivering boxes. Eventually you start using the airing cupboard. The one under the stairs, behind the boiler, the space that was never meant for long-term storage. You start stacking things in there that do not belong. It gets crowded, it gets warm, it gets problematic.
That is what happens to the liver when ectopic fat accumulates. The organ is built for processing fat, not storing it permanently. Fat stacks up inside the hepatocytes — the liver cells themselves. They get stressed. ALT leaks out. The number on your blood test goes up.
Insulin resistance accelerates this because elevated insulin keeps fat locked in storage — fat cells cannot release stored energy into circulation when insulin is high. So more incoming energy gets redirected into overflow sites. The airing cupboard fills up faster.
The Thing Nobody Mentioned About The Gut
Here is the part that genuinely stopped me when I came across it.
A 2022 study published in Nature Medicine by Abraham Meijnikman and Max Nieuwdorp at Amsterdam University Medical Centers measured portal vein ethanol concentrations in people with and without fatty liver disease. The portal vein is the main channel between the gut and the liver. What they found was that gut bacteria in people with NAFLD were fermenting carbohydrates and producing enough ethanol to reach concentrations in the portal vein above the legal drink-drive limit. The liver was clearing it before it reached the rest of the bloodstream. That is why people had no intoxication symptoms. But the liver was doing this processing work constantly, silently, every single day.
Think of the liver as a Royal Mail sorting office. Everything that arrives from the gut comes through here first — nutrients, hormones, and, it turns out, alcohol that your own microbiome produced. A sorting office handles the throughput fine on a normal day. But when the gut is disrupted by years of the wrong food, the sorting office starts receiving volumes it was not built to process. Parcels pile up. The cells doing the work get stressed. ALT rises.
The research group also found that these ethanol levels rose significantly after eating, not during fasting. What you eat and what your gut microbiome does with it directly affects what arrives at the liver. This is not a small finding. Most people, if they think about their liver at all, think about alcohol intake. But non-alcoholic fatty liver disease has nothing to do with drinking. The same mechanism runs from years of ultra-processed food and chronically elevated insulin, with no units of alcohol involved. One in three. That is not a drinking problem statistic.
My Numbers, 2012 to 2025
I want to lay out the full data trail here, because individual readings are not the story. The trend is.
April 2012: ALT 37 iu/L. Just inside normal range. GP noted, no action needed.
December 2023: ALT 69 iu/L. 73% above the upper limit of 40. GP note: “abnormal, but expected.” I was on statins, overweight, and carrying multiple metabolic issues simultaneously. An elevated liver enzyme was, from the system’s perspective, part of the package. It was not investigated further.
March 2024: ALT 28 iu/L. One month after stopping statins, changing to a predominantly non-UPF diet, and beginning extended fasting. Down from 69 to 28. A 59% drop in a single month.
November 2025: ALT 10 iu/L. Twenty months into the transformation. The lowest reading in NHS blood tests going back to 2012. A GP letter arrived in December 2025 confirming the result: optimal. Liver enzymes optimal. Off all risk lists.
That is the 86% drop the title refers to. December 2023 to November 2025. 69 to 10.
The Honest Version: I Don’t Know Which Lever Did the Most Work
Here is where I want to be precise, because this matters.
I cannot tell you which lever moved the ALT most. I have tried to isolate it from the data. The data does not isolate it.
Statins can raise ALT in some people. The mechanism is worth discussing with your GP — not a conclusion to draw from a YouTube video. But there is a known connection in certain patients, and my GP was aware of it. When I stopped the statins, part of the initial drop may reflect the removal of that contribution.
Weight loss is also strongly associated with ALT reduction, particularly with the reduction of ectopic hepatic fat. The weight was coming off simultaneously. That almost certainly contributed.
The food change — removing most ultra-processed food — would have altered what was arriving at the liver via the portal vein. Based on the Amsterdam research, that is not a trivial variable. And the extended fasting introduced gaps in which the gut was not processing incoming food at all. A motorway cannot be resurfaced while cars are still on it.
All of those things ran together. Anyone who tells you they know which one did the most work is simplifying a multi-variable picture into something cleaner than the data supports. I am not going to do that. What I can say is that the combination worked, and that the ALT was the marker that moved most.
There is a principle that made sense of the 20-month arc for me. For disease to progress, injury must outpace healing. For recovery to happen, healing must outpace injury. That is the whole of it. You do not need to reverse everything at once. You need to tip the balance and keep it tipped. Two steps forward and one step back is still progress. The first month after stopping statins and changing inputs gave a big signal. The following 19 months were the compound interest.
I was not targeting the liver. The HbA1c and the cholesterol were the headline markers I was watching. ALT was on the panel because it is always on the panel. When it moved, it moved further than anything else. I did not expect that.
What This Might Mean If Your GP Has Flagged Your Liver Enzymes
If you have had a liver enzyme result flagged — particularly ALT — here are the questions worth taking to your GP rather than leaving on a shelf.
Is this a one-off result, or has it been trending upward across multiple tests? A single elevated reading tells you relatively little. A pattern across two or three years tells you considerably more. Ask to see the trend, not just the latest number.
Is there a possibility that a current medication is contributing? Statins are one example. Several other medications have hepatic effects worth reviewing with your GP. This is not a reason to stop anything. It is a reason to have an informed conversation about monitoring.
What is the target, not just the upper limit? “Normal” and “optimal” are different things. Ask what the number would look like if everything was running well.
Can we retest in three months after I have made some food changes? That comparison point is valuable. ALT responds to input changes relatively quickly. Your GP can help you track whether what you are doing is working.
On the food side: the clearest lever I can point to — the one I ran during the 70-Day Rhythm Reset that I am most confident contributed — was removing ultra-processed food from the majority of meals. Not perfect, not zero UPF, but the majority. Two meals a day built from ingredients you can recognise. The gut microbiome responds to this. Based on the Amsterdam research, what you feed the microbiome directly affects what it produces in the portal vein.
The 12-hour overnight fast was the floor for the eating window. Not aggressive. Not extended fasting out of nowhere. Just not eating after 8pm and not eating before 8am. That gap matters. The gut needs time when it is not processing incoming food to repair, to reset, to do the maintenance work that cannot happen while the system is busy.
Timeline to expect: three months is the minimum for a meaningful retest if you are changing food inputs. My one-month result was unusual. If you are on statins or any medication your GP put you on for metabolic reasons, do not change anything without a conversation first. That is the version of this worth taking to a GP appointment. Not the YouTube video. The questions.
Key Takeaways
- ALT measures how loudly your liver is complaining: When liver cells are stressed, they leak this enzyme into the bloodstream. A rising number, even inside “normal” range, is a trend worth watching
- Insulin resistance sits upstream of fatty liver: It increases the risk 15-fold. One in three people in Western countries are now affected by NAFLD
- Your gut microbiome affects what arrives at the liver: Research from Amsterdam UMC found gut bacteria in NAFLD produce measurable alcohol the liver silently clears — changed by what you eat
- Multi-variable honesty matters: The 86% ALT drop happened alongside statin cessation, weight loss, food change, and fasting running simultaneously. The data does not isolate one cause
- The trend across years is more informative than a single reading: Ask your GP for the pattern, not just the latest number
Ready to Start Your Own Rhythm Reset?
If the data in this post has made you curious about what changing your food inputs and eating window could do for your own markers, the 14-Day Rhythm Reset Guide covers the fundamentals: eating windows, non-UPF food choices, and how to build a rhythm your body can work with. It is where most people start.
👉 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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