Liver

Why it does all of that, and not some other organ

One piece of plumbing explains the job list.

Blood leaving your gut does not rejoin the general circulation. It is collected into the hepatic portal vein and delivered straight to the liver first. Everything you absorb, whether that is food, alcohol, medicines or anything else you swallow, arrives there before it reaches your heart, your brain or anything else.

Two things follow, and they shape a great deal of what this page describes. The liver meets everything you take in at a far higher concentration than any other organ ever will. And it gets first refusal, so it can modify, store or destroy a substantial proportion of what arrives before the rest of you sees any of it. This is called first pass metabolism.

That is why some medicines have to be injected, because taken as a tablet they would be broken down before they ever reached the rest of you. It is why the liver does most of the body's drug and hormone processing. And it is why an organ whose job description reads like a list of unrelated tasks is in fact doing one thing. It stands between your gut and everything else.

What the profile looks at

The distinction most people miss is that a liver profile is really two tests wearing one name.

The enzymes, which are ALT, AST, GGT and ALP, live inside liver cells or line the bile ducts. They appear in the blood when those structures are damaged or stressed and leak. They are markers of injury, not of function, and a raised enzyme says something is going on rather than something is failing.

The proteins are the other half. Albumin is what the liver is manufacturing and bilirubin is what it is clearing. Total protein and globulin come with them, though a large part of globulin is antibodies, which are made by immune cells and not by the liver. Albumin and bilirubin move when the liver's capacity to do its work is genuinely reduced, which is a later and more serious issue than a leak.

A liver can be quietly damaged with normal proteins for a long time. It can also show raised enzymes for reasons that have nothing to do with disease, like a heavy lifting session. The two halves have to be read together.

The pattern matters more than any single number

The useful question is rarely whether one enzyme is raised. It is which of them is raised most, because the four come from different places and the pattern points somewhere.

ALT-dominant points at the liver cells themselves. ALT is the most liver-specific of the four, so when it leads, the liver is usually the story.

ALP-dominant points at the bile ducts, or at bone, because ALP comes from both. GGT is what separates them. A raised ALP with a raised GGT points at the biliary side. A raised ALP with a normal GGT points away from the liver entirely and towards bone, which is why the Minerals and bone section picks this up.

GGT-dominant, with everything else normal, is frequently not liver disease at all. See below.

And the ratio between AST and ALT provides information of its own. In fat-related liver disease, which many people have these days, ALT usually sits above AST. When AST ends up roughly double the ALT or more, alcohol moves up the list considerably. The ratio also tends to climb as scarring advances, which is why it appears inside the scores used to estimate fibrosis.

One pattern belongs to another section entirely. Raised ALT and AST with a normal GGT and a raised creatine kinase is muscle, not liver. The Muscle section explains why, and it is the most common false alarm in people who train.

GGT, and what it is actually for

GGT has a reputation as the alcohol enzyme, which is true but is not its job.

Its actual role is in recycling glutathione, the main antioxidant inside your cells. GGT sits on cell surfaces and breaks glutathione down outside the cell so the building blocks, cysteine in particular, can be taken back in and used to build more. It is part of the machinery that keeps a cell's antioxidant supply topped up, and it is not confined to the liver: it is also in the kidney, pancreas, lung and the lining of blood vessels.

It often rises because the liver makes more of it, not because anything has broken. Alcohol and a long list of ordinary medicines make liver cells produce more GGT, and the likeliest reason is that handling them runs glutathione down, which is the very thing GGT exists to help replace. That is an adaptation rather than an injury, and it is why an isolated raised GGT with a normal ALT, ALP and bilirubin often means nothing more than what somebody's liver has been asked to process lately.

A GGT inside the normal range still carries information. Higher GGT, still within the reference range, tracks with a higher risk of cardiovascular disease, of type 2 diabetes, of fat in the liver, and of death from any cause, and it does so after allowing for alcohol, smoking and the obvious confounders. ALT does not behave that way. A raised ALT predicts liver-related problems but is a much weaker signal for anything else. The leading explanation is that GGT is standing in for oxidative stress rather than for liver damage.

So based on that association, within the reference range a lower GGT is generally better than a higher one. That is not an argument for zero to become the target, and it is not a number to chase. It is a reason to read a high-but-normal GGT as information rather than as nothing.

What a normal ALT does and does not rule out

Read this before you read your own liver profile, because it is not what the reference range implies.

The conventional upper limit for ALT is not one agreed figure. UK labs set it anywhere from about 35 to 60 units per litre, and some use a lower one for women than for men. It was derived from reference populations that included a great many people with undiagnosed fatty liver. The most common cause of a raised ALT was sitting inside the group used to define normal, which pushed the limit up.

Thresholds worked out from metabolically healthy groups come out considerably lower. American gastroenterology guidance puts true healthy normal at 29 to 33 units per litre for men and 19 to 25 for women, and American liver guidance works to 35 for men and 25 for women. UK guidance has not followed. It accepts that the usual limits are probably too high, but it still leaves each lab reporting against its own range, so what counts as normal depends on who did the test.

And more importantly, a normal ALT is common in people who do have fat in the liver. Estimates run from about 25% all the way up to 80%, with the higher figures coming from scanning people who had no reason to suspect anything. A normal ALT is poor evidence of a healthy liver. It is reasonable evidence that the liver is not actively inflamed today, which is a much smaller claim.

So how do you actually find out

NICE says outright that routine liver blood tests should not be used to rule out fatty liver or the scarring that follows it. Which leaves the obvious question of what does.

The first step costs nothing, and you may already have the numbers. FIB-4 is a score worked out from 4 things: your age, your AST, your ALT and your platelet count. Any test that includes both a liver profile and a full blood count gives you 3 of the 4 and you supply the fourth. Free calculators for it are everywhere online. Below 1.3 makes advanced scarring unlikely. Above 2.67 is high risk and a reason to be seen. In between is the grey zone, which is where a lot of people land, and where a second test is needed.

Beyond that there are 2 better tests, and neither of them is something we sell. The ELF test is a blood test that measures 3 markers of scarring directly, and NICE treats a score of 10.51 or above as indicating advanced fibrosis. A FibroScan is an ultrasound probe pressed against the skin over the liver that measures how stiff it has become, and the same machine reports how much fat is in there at the same time. Both are available privately in the UK, and a FibroScan takes about 10 minutes.

The reason any of this is worth doing is that fat in the liver is reversible, early scarring can still improve, and advanced scarring largely does not. The point of finding out early is that early is the part you can still do something about.

The proteins, and the clock inside them

Albumin is made by the liver and is the main thing keeping fluid inside your blood vessels. It also has a half-life of about 3 weeks, which changes what a normal result means. Albumin is telling you the liver was manufacturing properly several weeks ago. It cannot fall quickly, so it is a poor marker of anything acute, and a good one for something that has been going on for a while.

Albumin also falls during inflammation, because the liver redirects its protein-making capacity. The Inflammation section explains that switch. And it is the same albumin that carries calcium and testosterone, which is why the Minerals and bone section pulls its three jobs together.

Bilirubin is not made by the liver but cleared by it, and the route explains the most common abnormal result on this profile. When red blood cells are recycled their haemoglobin is broken down, and bilirubin is what is left. It does not dissolve in water, so it travels to the liver stuck to albumin. The liver then attaches a sugar group to it, which makes it water-soluble and allows it to leave in bile.

Gilbert's syndrome is a common inherited reduction in the activity of the enzyme that attaches that sugar. Less conjugating capacity means bilirubin backs up mildly, and it backs up further during fasting, illness, stress and hard exercise, which is usually when people have blood taken. It causes no liver damage and needs no treatment. An isolated raised bilirubin in a well person, with normal enzymes and normal albumin, is most often this.

AST is only available with a venous sample because our lab's accreditation covers it for venous blood and not for capillary. AST is also one of the analytes most distorted by finger-prick collection. An abnormal number that means nothing is worse than 7 markers you can rely on.

What changes when the liver is under strain

The liver is another organ with a big reserve. Fat accumulating in the liver is now the most common liver problem we see today. It affects roughly a quarter to a third of adults, and it usually causes no overt issues at all for years. It was called non-alcoholic fatty liver disease (NAFLD) for decades and was renamed in 2023 to metabolic dysfunction-associated steatotic liver disease, which is a mouthful but is a better description, since it names what actually drives it rather than what does not.

When symptoms do arrive they include fatigue, discomfort under the right ribs, itching, yellowing of the skin or eyes, swelling of the abdomen or legs, and bruising more easily than usual. Most of those have many other explanations. The yellowing is the exception and is not vague at all. It means bilirubin is building up, which points either at the liver and bile ducts or at red cells being broken down faster than they can be cleared. And by the time any of these appear, a great deal has usually already happened.