ReadYourDNA

Bilirubin

Where your DNA places you among other people, and the studies behind it.

General information

Not tailored to your result, and not medical advice

Avoid Prolonged Fasting And Dehydration: Bilirubin is processed in the liver by the enzyme UGT1A1, the step that lets it be excreted. In Gilbert syndrome, a common inherited reduction in that enzyme's activity, UGT1A1 runs at only 30% to 50% of normal capacity, and dropping intake to around 400 kcal a day can raise bilirubin two to three fold within 48 hours. Fasting, dehydration, febrile illness, menstruation and physical exertion are all listed as common precipitants. Regular meals and adequate fluids keep that pathway from being stressed unnecessarily, and fluctuations triggered this way are described as benign and self-limiting. StatPearls (NCBI Bookshelf)

Get Visible Yellowing Looked At: Mild movement in bilirubin is common and usually harmless, but visible yellowing of the skin or the whites of the eyes is not something to interpret at home. The NHS lists alcohol-related liver disease, gallstones, hepatitis, pancreatitis and sickle cell disease among the causes, and says to ask for an urgent GP appointment or get help from NHS 111 when yellowing appears. Itchy skin, darker urine and paler stools alongside it are worth mentioning. Keeping alcohol intake low is the behavior most directly under your own control on the liver side of this pathway. NHS

Quit Or Avoid Smoking: Smoking is consistently associated with lower serum bilirubin. The authors describe bilirubin as an endogenous antioxidant and treat that rise as one of the changes that follow quitting, though the shift itself is small. Quitting is worth doing for reasons that have nothing to do with this marker, but smoking status is one of the few everyday behaviors with a measurable, repeatable effect on it. Nicotine & Tobacco Research (PubMed)

Account For Hard Endurance Exercise: Hard endurance exercise, running in particular, causes a mild intravascular hemolysis driven by repeated foot strike impact together with hyperthermia, dehydration, oxidative damage and shear stress. Hemoglobin released from ruptured red cells feeds the same heme breakdown pathway that produces bilirubin, and unconjugated bilirubin sits alongside haptoglobin and LDH among the markers used to support a hemolysis picture, though it is the less specific of them. Reviewers describe the effect as typically mild and almost self-limiting, completely resolving within 24 to 48 hours. If a blood test happens to follow a hard training block, that context is worth mentioning to the clinician reading it. Annals of Translational Medicine (PMC)

Treat Protective Claims With Caution: Observational studies repeatedly find that people with mildly higher bilirubin have less cardiovascular and metabolic disease, and bilirubin is often called protective on that basis. When researchers instead used a common UGT1A1 variant as a natural experiment, carriers had clearly higher bilirubin but showed no significant association with any of the 19 conditions tested. Measured bilirubin, in the same work, tracked with 15 of those 19 conditions and with several hundred clinical diagnoses overall, which led the authors to conclude that the apparent benefits are likely due to confounding. The honest reading is that a higher number is not in itself something to chase through lifestyle. Clinical Pharmacology & Therapeutics (PMC)

Genetics vs Environment

How much of this is genetic?

Genetics explains 50% of why people differ in this trait. The rest is environment, daily habits and chance.

Heritability estimate: Twin and family studies estimate the heritability of total serum bilirubin at roughly 48-58% (e.g. Framingham heritability ~49%); UGT1A1 is the dominant locus, with its top variant explaining about 18% of variance (Johnson AD et al., Hum Mol Genet 2009)

About Bilirubin

Background and further reading

Bilirubin is a yellow-orange pigment formed when hemoglobin from worn-out red blood cells is broken down. It travels to the liver, where the enzyme UGT1A1 attaches sugar molecules to it (conjugation), making it water-soluble so it can be excreted in bile and eliminated. Doctors measure total bilirubin in routine blood panels as a marker of liver function and red-blood-cell turnover. Mildly elevated bilirubin is common and usually harmless; markedly high levels can cause jaundice, a yellowing of the skin and the whites of the eyes.

Genetic Basis: Blood bilirubin level is one of the most strongly heritable common biomarkers, with a large share of person-to-person variation explained by a single gene. The dominant signal is UGT1A1, which encodes the enzyme that conjugates bilirubin. A common variation in its promoter (the TA-repeat, often reported as UGT1A1*28, tagged by variants such as rs887829) reduces enzyme production, so bilirubin clears more slowly and blood levels run higher. Inheriting two lower-activity copies is the basis of Gilbert's syndrome, a benign condition present in an estimated 3-10% of people that causes mild, fluctuating unconjugated hyperbilirubinemia. A second well-established locus, SLCO1B1, encodes a liver transporter (OATP1B1) that helps move bilirubin from the blood into liver cells. A genome-wide meta-analysis confirmed UGT1A1 and SLCO1B1 as the principal loci influencing total serum bilirubin.

Other Factors: Because it neither exclusively favors nor harms health, bilirubin is best read as a neutral biomarker. In people with a Gilbert's-type genetic background, levels tend to rise transiently during fasting, dehydration, physical stress, or intercurrent illness, and this is expected rather than a sign of liver disease. Higher bilirubin can also reflect increased red-blood-cell breakdown (as in some anemias) or reduced clearance, while non-genetic causes of low readings include certain medications. Bilirubin is a potent antioxidant, and observational studies have linked mildly higher levels to favorable cardiovascular and metabolic markers, though this remains an association rather than an established benefit. A genetic score describes an underlying tendency and is not a substitute for a measured blood test.

How this was calculated

The published research behind your score, and the variants it draws on.

Study Details

12 published scores from 5 studies

The bilirubin score combines 12 polygenic scores drawn from 5 published studies.

Truong B (2024). Integrative polygenic risk score improves the prediction accuracy of complex traits and diseases. Cell Genom: 3.0M

Ding Y (2022). Polygenic scoring accuracy varies across the genetic ancestry continuum in all human populations bioRxiv: 980k

Privé F (2022). Portability of 245 polygenic scores when derived from the UK Biobank and applied to 9 ancestry groups from the same cohort Am J Hum Genet: 120k

Raben TG (2023). Biobank-scale methods and projections for sparse polygenic prediction from machine learning. Sci Rep: 7k

Sinnott-Armstrong N (2021). Genetics of 35 blood and urine biomarkers in the UK Biobank. Nat Genet: 3k

Further reading

Johnson AD, Kavousi M, Smith AV, et al. Genome-wide association meta-analysis for total serum bilirubin levels. Human Molecular Genetics (2009)

Bosma PJ, Chowdhury JR, Bakker C, et al. The genetic basis of the reduced expression of bilirubin UDP-glucuronosyltransferase 1 in Gilbert's syndrome. New England Journal of Medicine (1995)

Related Traits

These traits are influenced by some of the same genes and variants as this one

HbA1c: Glycated hemoglobin, reflecting average blood sugar levels over the past 2-3 months.

LDL Cholesterol: Low-density lipoprotein cholesterol - the primary causal driver of atherosclerosis and cardiovascular disease.

ALT (Liver Enzyme): A liver enzyme measured in routine blood tests; higher levels often reflect liver stress.

Back to All Traits

Content updated August 2026.

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