What you carry at this position in your DNA and what research says about it.
Bilirubin and Heart Health: 10/10 evidence, 44 publications.
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Sample genotype (not yours): C/C
Typical Bilirubin Levels and Heart Risk
This genotype is associated with standard liver enzyme activity and typical levels of bilirubin in the blood. You have a baseline risk for coronary artery disease and gallstones.
What this genotype means: Typical bilirubin clearance; Standard risk for gallstones; Normal response to UGT1A1-metabolized drugs.
Sample genotype (not yours): C/T
Slightly Elevated Bilirubin Levels
Carrying one copy of the T allele slightly reduces your liver's ability to clear bilirubin, leading to mildly elevated levels. This generally does not cause health issues but can slightly alter drug metabolism.
What this genotype means: Mildly elevated bilirubin; Slightly increased risk of drug-induced hyperbilirubinemia; Typical cardiovascular risk profile.
Sample genotype (not yours): T/T
Higher Bilirubin and Lower Heart Risk
Two copies of the T allele significantly raise your bilirubin levels, which is characteristic of Gilbert syndrome. This provides a protective effect against heart disease but increases gallstone and drug toxicity risks.
What this genotype means: Significantly elevated bilirubin (Gilbert syndrome); Lower risk of coronary artery disease; Increased risk of gallstones and drug toxicities.
Gene function and biological role
Gene Function: The UGT1A1 gene belongs to a cluster of genes encoding UDP-glucuronosyltransferases, which are essential enzymes responsible for metabolizing and eliminating various compounds from the body [1]. UGT1A1 is the primary enzyme responsible for converting bilirubin into a water-soluble form so it can be safely excreted by the liver [2]. When these enzymes have reduced activity, bilirubin levels in the blood rise [2]. While very high levels of bilirubin can cause visible jaundice, mildly elevated levels are actually associated with a lower risk of cardiovascular issues [3]. Conversely, lower levels of bilirubin are linked to higher rates of cardiovascular disease and hypertension [3].
Variant Impact: The rs887829 variant is located near the UGT1A1 gene and is in complete linkage disequilibrium with the well-known UGT1A1*28 promoter variant [2]. The T allele of this variant acts as a marker for decreased expression of the UGT1A1 enzyme in the liver [2]. This reduction in enzyme activity slows down the clearance of bilirubin, leading to higher circulating levels of this natural antioxidant [4]. It also alters how the body processes several prescription medications, including certain chemotherapies and cholesterol-lowering drugs [5]. Because of its strong effect on bilirubin levels, this variant is a primary genetic driver of Gilbert syndrome [2].
Key Insight: Having two copies of the T allele can increase your baseline bilirubin levels up to four-fold, which is the hallmark of Gilbert syndrome. While this sounds alarming, mildly elevated bilirubin acts as a powerful natural antioxidant that is linked to a significantly lower risk of coronary artery disease.
Location: UGT1A1. Chromosome 2 · 2q37.1 · 233.8 Mb
Estimated prevalence by population
Global 41.3%; European 46.1%; African 30.4%; East Asian 76.4%; South Asian 34.9%; Americas 45.7%; Ashkenazi 38.1%; Finnish 33.4%; Middle Eastern 44.9%; Amish 33.2%.
Estimated CC genotype frequency.
Global 45.1%; European 43.6%; African 49.5%; East Asian 22.0%; South Asian 48.4%; Americas 43.8%; Ashkenazi 47.2%; Finnish 48.8%; Middle Eastern 44.2%; Amish 48.8%.
Estimated CT genotype frequency.
Global 13.6%; European 10.3%; African 20.1%; East Asian 1.6%; South Asian 16.8%; Americas 10.5%; Ashkenazi 14.6%; Finnish 17.8%; Middle Eastern 10.9%; Amish 18.0%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Organ Systems
Liver Function & Disease
Bilirubin Levels. Evidence: 10/10. Source: PMID 19414484. Typical Levels.
Digestive & Gut Disorders
Gallstones. Evidence: 4/10. Source: PMID 22558097. Typical Risk.
Cardiovascular & Metabolic
Heart Disease
Coronary Artery Disease. Evidence: 4/10. Source: PMID 23642732. Typical Risk.
Pharmacogenomics
Antimicrobial & Antiviral Response
Atazanavir Response. Evidence: 9/10. Source: PMID 26148204. Typical Response.
Showing effects for C/T genotype
Bilirubin Levels. Evidence: 10/10. Source: PMID 19414484. Slightly Elevated.
Gallstones. Evidence: 4/10. Source: PMID 22558097. Slightly Higher Risk.
Atazanavir Response. Evidence: 9/10. Source: PMID 26148204. Intermediate Risk.
Showing effects for T/T genotype
Bilirubin Levels. Evidence: 10/10. Source: PMID 19414484. Significantly Higher.
Gallstones. Evidence: 4/10. Source: PMID 22558097. Higher Risk.
Coronary Artery Disease. Evidence: 4/10. Source: PMID 23642732. Lower Risk.
Atazanavir Response. Evidence: 9/10. Source: PMID 26148204. Higher Toxicity Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Having two copies of the C allele means your liver produces typical amounts of the UGT1A1 enzyme [1]. This enzyme efficiently processes bilirubin, keeping your circulating levels within the standard reference range [1]. While normal bilirubin levels are healthy, you do not receive the extra cardiovascular protection associated with higher levels of this antioxidant [2]. Your risk for coronary artery disease remains at the population average [2]. Additionally, your liver processes medications like atazanavir and irinotecan normally, with a low risk of drug-induced jaundice [3].
Typical bilirubin clearance; Standard risk for gallstones; Normal response to UGT1A1-metabolized drugs.
Sample genotype: CT (Heterozygous)
This genotype results in a moderate reduction in the expression of the UGT1A1 enzyme in the liver [1]. With only one copy of the T allele, your body still produces enough enzyme to prevent significant bilirubin buildup under normal conditions [1]. However, you may experience slightly higher baseline bilirubin levels than those with the C/C genotype [2]. This mild elevation is generally harmless and does not provide the strong cardiovascular protection seen in T/T homozygotes [3]. You may have a slightly increased risk of mild side effects, such as elevated bilirubin, when taking certain medications like atazanavir or specific chemotherapies [4].
Mildly elevated bilirubin; Slightly increased risk of drug-induced hyperbilirubinemia; Typical cardiovascular risk profile.
Sample genotype: TT (Homozygous)
Having the T/T genotype significantly reduces the expression of the UGT1A1 enzyme, leading to much higher levels of serum bilirubin [1]. This genetic profile is the primary cause of Gilbert syndrome, a benign liver condition characterized by intermittent, mild jaundice [1]. Interestingly, because bilirubin is a powerful natural antioxidant, this elevation is linked to a substantial reduction in the risk of coronary artery disease [2]. However, the slower clearance of bilirubin also increases your susceptibility to gallstones [3]. Furthermore, you are at a higher risk for side effects and toxicity when taking drugs metabolized by this pathway, such as irinotecan or atazanavir [4].
Significantly elevated bilirubin (Gilbert syndrome); Lower risk of coronary artery disease; Increased risk of gallstones and drug toxicities.
Variants with shared genetic architecture
rs6742078 · UGT1A1 Gene · Chr 2 · Gallstone Risk
rs10929302 · UGT1A1 Gene · Chr 2 · Drug and Bilirubin Clearance
rs4148323 · UGT1A1 Gene · Chr 2 · Bilirubin and Drug Metabolism
A Genome-wide Association Study of Circulating Levels of Atorvastatin and Its Major Metabolites.
UGT1A1 is a major locus influencing bilirubin levels in African Americans.
Genome-wide association meta-analysis for total serum bilirubin levels.
A genome-wide association study of total bilirubin and cholelithiasis risk in sickle cell anemia.
Content updated August 2026.
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