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Gilbert's Syndrome Symptoms: What They Feel Like, and the Blood Tests That Confirm It

Gilbert's syndrome is a common, usually harmless inherited condition that makes bilirubin run a little high. Here are its symptoms and triggers, what the blood tests show, and how a clinician tells it apart from liver disease and hemolysis.

Published

November 2, 2026

Read time

10 min read

Medically reviewed by

Rhonda Collins, FNP-C

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Gilbert’s syndrome is a common inherited condition in which the liver processes bilirubin more slowly than usual, so bilirubin in the blood runs a little high. Many people have no symptoms at all. When symptoms do appear, the main one is mild, short-lived yellowing of the whites of the eyes or the skin, usually brought on by fasting, illness, dehydration, stress or hard exercise ^[1][2]. It does not damage the liver and needs no treatment ^[2][3].

The useful question for most people is not “do I have symptoms?” but “is my high bilirubin really Gilbert’s?” That answer comes from the pattern across a few blood tests: a raised indirect bilirubin with a normal direct bilirubin, normal liver enzymes and no sign of red blood cells breaking down ^[3][4]. This article explains each part of that pattern and what it means when a result does not fit.

What Gilbert’s syndrome is

Bilirubin is the yellow pigment made when old red blood cells are broken down. Before the body can get rid of it, the liver attaches a sugar-like molecule to it, a step called conjugation, which turns it into a water-soluble form that leaves in bile ^[1]. The enzyme that does this is bilirubin-UGT, made from instructions in the UGT1A1 gene ^[1].

In Gilbert’s syndrome, changes in UGT1A1 leave people with roughly 30 percent of normal enzyme activity ^[1]. Unconjugated bilirubin, the form measured as indirect bilirubin, then builds up a little in the blood ^[1].

• The cause. In many populations the most common change is a variant called UGT1A1*28, in the promoter region that controls how much enzyme is made. It usually causes Gilbert’s syndrome when a person inherits two copies, one from each parent ^[1]. In Asian populations a different type of UGT1A1 change is more common ^[1].
• How common it is. MedlinePlus Genetics estimates that it affects 3 to 7 percent of Americans ^[1]. Across populations, published estimates range from about 2 percent to 20 percent depending on ancestry ^[2][3].
• Who notices it. It is usually recognized in adolescence, often around puberty, and it is diagnosed more often in men than in women ^[1][3].
• Why it is usually harmless. The liver itself is healthy. People with Gilbert’s syndrome have normal liver enzymes and liver structure, no increased risk of cirrhosis, and an excellent outlook ^[3]. Observational studies have even linked it with lower rates of cardiovascular disease, although these are associations rather than proof of a protective effect ^[3].

Not everyone who carries the gene changes has raised bilirubin. Other factors, such as slightly faster red cell turnover or slower movement of bilirubin into the liver, seem to decide whether it shows up on a blood test ^[1].

Gilbert’s syndrome symptoms

About 30 percent of people with Gilbert’s syndrome have no signs or symptoms and find out only when a routine blood test shows a raised bilirubin ^[1]. For the rest, symptoms are mild and come and go.

Episodes of mild jaundice

The characteristic symptom is a short episode of jaundice: a yellow tinge to the whites of the eyes, and sometimes the skin ^[1][4]. MedlinePlus Genetics notes that bilirubin very rarely rises high enough to cause visible jaundice ^[1]. When it does, the yellowing fades as the trigger passes, and it can recur on and off throughout life ^[4].

Common triggers

Episodes usually follow a stress on the body. The triggers named most often are ^[1][2][4]:

• going without food for a long time, including fasting or skipping meals
• dehydration
• illness, such as a cold or other infection
• vigorous exercise or physical exertion
• emotional or physical stress
• menstruation

Fatigue and abdominal discomfort

Some people with Gilbert’s syndrome report tiredness or abdominal discomfort ^[1]. These symptoms are real for the people who have them, but they are not a clear feature of the condition. Clinical reviews describe the typical person with Gilbert’s syndrome as having no abdominal pain, itching, pale stools or dark urine, and a normal examination ^[3]. Ongoing digestive symptoms or fatigue are therefore worth investigating in their own right, rather than being put down to Gilbert’s.

What Gilbert’s syndrome does not cause

Gilbert’s syndrome does not cause dark urine, pale stools, itching or abdominal pain ^[3]. The extra bilirubin is the indirect form, which travels in the blood bound to albumin ^[5]. Dark urine, pale or clay-colored stools, itching, fever or ongoing abdominal pain point to a liver or bile duct problem instead ^[5][6]. Our guide to bilirubin in urine explains that distinction.

What the blood tests show

Gilbert’s syndrome has a recognizable blood test pattern ^[3][4]:

• Total bilirubin is mildly raised. MedlinePlus reports it is most often below 2 mg/dL ^[4]. Reviews describe levels that fluctuate between about 1 and 5 mg/dL, rising with triggers such as fasting ^[3].
• Most of it is indirect (unconjugated) bilirubin. The direct (conjugated) fraction stays normal ^[4].
• The level moves from test to test. A result can be normal one week and raised the next, depending on what you ate, how well hydrated you were and whether you were unwell ^[1][3].

A total bilirubin result alone cannot show this pattern. The American College of Gastroenterology recommends that a raised total bilirubin be split into its direct and indirect fractions, because a raised direct bilirubin usually means liver disease or a blocked bile duct ^[7]. Our guides to high total bilirubin and high indirect bilirubin cover the other causes of each result.

At Mito, the fractionated bilirubin test reports total, direct and indirect bilirubin from one blood draw.

How Gilbert’s syndrome is told apart from liver disease and hemolysis

A high indirect bilirubin has two main explanations. Either the liver is conjugating it too slowly, as in Gilbert’s syndrome, or the body is making too much because red blood cells are breaking down faster than normal, which is called hemolysis ^[2][5]. Liver disease is the other possibility a clinician wants to exclude ^[2][7]. Gilbert’s syndrome is diagnosed by ruling out both, not by a single test ^[2][3].

Normal liver enzymes: ALT, AST, ALP and GGT

In Gilbert’s syndrome, the liver tests other than bilirubin are normal ^[3].

• ALT and AST rise when liver cells are injured ^[7].
• ALP rises when bile flow is impaired, and GGT helps show whether a raised ALP comes from the liver or from bone ^[7][8].

Normal results across all four make liver disease much less likely as the cause of a raised bilirubin ^[3]. Our article on liver enzymes explains what each one measures. The hepatic function panel covers ALT, AST, ALP, total and direct bilirubin, albumin and total protein in one test. GGT is a separate GGT test.

A normal blood count and reticulocyte count

To rule out hemolysis, clinicians look at the red blood cells themselves.

• A complete blood count (CBC) shows whether there is anemia ^[9].
• A reticulocyte count measures young red blood cells. A high count can mean the bone marrow is replacing cells that are being destroyed, as in hemolytic anemia ^[10].
• Haptoglobin and lactate dehydrogenase (LDH) are among the tests used to investigate suspected hemolysis ^[9].

In Gilbert’s syndrome these markers of hemolysis are absent ^[3]. A CBC and a reticulocyte count are both available at Mito, and our reticulocyte count reference page explains the marker.

Repeat or fasting bilirubin

Because bilirubin in Gilbert’s syndrome moves around, a raised indirect bilirubin on repeated testing supports the diagnosis ^[3]. Some clinicians use a fasting test, in which a period of calorie restriction is followed by a recheck, since fasting reliably pushes bilirubin up in Gilbert’s syndrome ^[3].

This has a practical side when you compare results. Some panels are drawn fasting. Mito’s comprehensive metabolic panel, for example, asks for a 12-hour fast. If you have Gilbert’s syndrome, a fasting draw may show a higher bilirubin than a test taken after a normal breakfast ^[3][4]. Comparing results taken under similar conditions avoids reading a trigger as a trend.

Genetic testing is rarely needed

Gilbert’s syndrome is caused by a gene change, but genetic testing is not needed to diagnose it ^[4]. The blood test pattern is usually enough ^[3].

Reading the pattern

When a high bilirubin is not Gilbert’s syndrome

The diagnosis does not fit, and the result needs further investigation, when any of these is present ^[2][3][7]:

• A raised direct bilirubin. Gilbert’s syndrome affects only the indirect fraction. Our guide to high direct bilirubin covers what it means.
• Abnormal liver enzymes, such as a raised ALT, AST, ALP or GGT.
• Anemia or a high reticulocyte count, which suggest hemolysis.
• Dark urine, pale stools or persistent itching ^[5].
• A bilirubin well above the mild range typical of Gilbert’s syndrome, or one that keeps rising. Much higher indirect bilirubin can come from hemolysis or from Crigler-Najjar syndrome, a rare and more severe condition caused by changes in both copies of UGT1A1 ^[1][2].
• Symptoms beyond mild jaundice, such as abdominal pain that does not go away, fever or weight loss ^[4][5].

A previous diagnosis of Gilbert’s syndrome does not protect against other problems later. A new pattern of results deserves a fresh look rather than being assumed to be the same condition.

Living with Gilbert’s syndrome

Management is reassurance and knowing the diagnosis. Gilbert’s syndrome does not need treatment, and no specific diet or lifestyle change is required ^[3][4]. Its main clinical importance is that a raised bilirubin can be mistaken for liver disease and investigated again and again ^[3].

Some people find that long fasts, skipped meals or dehydration bring on episodes of yellow eyes, and choose to avoid them. That is a matter of comfort rather than a medical need, because the episodes do no harm ^[3][4].

Medicines and Gilbert’s syndrome

The same UGT1A1 enzyme clears some medicines, so Gilbert’s syndrome is worth telling every prescriber about.

• Irinotecan, a chemotherapy drug used mainly for colorectal cancer, is inactivated by UGT1A1. People with two copies of UGT1A1*28 are more likely to develop low white cell counts on it, and its prescribing information addresses this ^[11].
• Atazanavir, an HIV medicine, blocks UGT1A1 and raises indirect bilirubin, sometimes enough to cause jaundice. The risk is highest in people with two reduced-function UGT1A1 variants such as UGT1A1*28 ^[12].

Reviews list other medicines whose handling may be altered, though this rarely leads to toxicity ^[3].

When to see a clinician

See a clinician if yellowing of the eyes or skin appears for the first time, so the cause can be confirmed, or if any of the signs in the “not Gilbert’s” list above appear. Seek care promptly for jaundice with dark urine, pale stools, fever or abdominal pain that does not go away.

Where to start

If a blood test showed high bilirubin, start with a fractionated bilirubin test, which shows whether the rise is indirect or direct, and a hepatic function panel, which checks the liver enzymes at the same time. A comprehensive metabolic panel is an alternative that adds kidney, electrolyte and glucose markers to the liver tests, though it reports total bilirubin only. If those point toward hemolysis, a reticulocyte count and a CBC are the next step.

References

1. MedlinePlus Genetics. Gilbert syndrome. National Library of Medicine.
2. Grant LM, Faust TW, Thoguluva Chandrasekar V, John S. Gilbert Syndrome. StatPearls. Treasure Island (FL): StatPearls Publishing; updated 2024.
3. De Silva AP, Nuwanshika N, Niriella MA, de Silva HJ. Gilbert’s syndrome: The good, the bad and the ugly. World J Hepatol. 2025;17(2):98503.
4. MedlinePlus Medical Encyclopedia. Gilbert syndrome. National Library of Medicine.
5. Fargo MV, Grogan SP, Saguil A. Evaluation of Jaundice in Adults. Am Fam Physician. 2017;95(3):164-168.
6. MedlinePlus. Bilirubin Blood Test. National Library of Medicine.
7. Kwo PY, Cohen SM, Lim JK. ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries. Am J Gastroenterol. 2017;112(1):18-35.
8. MedlinePlus. Gamma-glutamyl Transferase (GGT) Test. National Library of Medicine.
9. MedlinePlus Medical Encyclopedia. Hemolytic anemia. National Library of Medicine.
10. MedlinePlus. Reticulocyte Count. National Library of Medicine.
11. Dean L. Irinotecan Therapy and UGT1A1 Genotype. In: Medical Genetics Summaries. National Center for Biotechnology Information; updated 2018.
12. Gammal RS, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for UGT1A1 and Atazanavir Prescribing. Clin Pharmacol Ther. 2016;99(4):363-369.

Frequently asked questions

What are the triggers for Gilbert's syndrome?

The usual triggers are going without food for a long time, dehydration, illness such as a cold or other infection, vigorous exercise, stress and menstruation. Each can push bilirubin up for a while, sometimes enough to make the whites of the eyes look slightly yellow. Levels fall back once the trigger passes.

What should you avoid with Gilbert's syndrome?

No specific diet or lifestyle restriction is required, because the condition is benign. Many people notice that long fasts, skipped meals and dehydration bring on episodes of yellow eyes, so they choose to avoid them. It is also worth telling every prescriber that you have it, because the same enzyme handles some medicines, such as the cancer drug irinotecan.

Can Gilbert's syndrome cause digestive problems?

Some people with Gilbert's syndrome report abdominal discomfort or tiredness, but clinical reviews describe the typical person as having no abdominal pain, itching, pale stools or dark urine. Because Gilbert's syndrome does not damage the liver or gut, ongoing digestive symptoms should be checked for another cause rather than put down to it.

Can you take anything for Gilbert's syndrome?

Gilbert's syndrome does not need treatment, and no medicine is routinely prescribed for it. Management is reassurance and knowing the diagnosis, so a raised bilirubin is not mistaken for liver disease and repeatedly investigated.

Is Gilbert's syndrome serious?

No. It is a benign genetic variation in how the liver processes bilirubin. It does not cause liver damage or raise the risk of cirrhosis, and the outlook is excellent. Its main practical importance is that it can look like liver disease on a blood test, and that it changes how the body handles a few medicines.