What you carry at this position in your DNA and what research says about it.
Gallstone Risk: 10/10 evidence, 19 publications.
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Sample genotype (not yours): G/G
Typical Gallstone Risk
Efficient bilirubin clearance maintains baseline levels and supports typical gallbladder health.
What this genotype means: Optimal bilirubin clearance; Typical gallstone risk; Slightly higher LDL cholesterol.
Sample genotype (not yours): G/T
Slightly Elevated Gallstone Risk
A minor reduction in enzyme efficiency leads to slightly higher bilirubin levels and a modest increase in gallstone risk.
What this genotype means: Modestly elevated bilirubin levels; Slightly increased gallstone risk; Altered statin pharmacokinetics.
Sample genotype (not yours): T/T
Elevated Gallstone Risk
Significantly higher bilirubin levels increase the likelihood of developing pigment-based gallstones.
What this genotype means: Significantly elevated bilirubin levels; Nearly twofold higher gallstone risk; Altered drug metabolism pathways.
Gene function and biological role
Gene Function: The UGT1A10 gene is part of the uridine diphosphate-glucuronosyltransferase 1A complex, a critical gene cluster on chromosome 2. This family of enzymes is responsible for glucuronidation, a major detoxification pathway in the body [1]. Through this process, the liver attaches glucuronic acid to fat-soluble toxins, drugs, and metabolic waste products to make them water-soluble for excretion [1]. A primary substrate of this enzyme family is bilirubin, a yellow byproduct of normal red blood cell breakdown [2]. Proper functioning of these enzymes prevents the toxic accumulation of unconjugated bilirubin in the bloodstream and tissues [2].
Variant Impact: The rs6742078 variant is an intronic genetic change located within the UGT1A gene cluster. Although it is classified as an intron variant, it serves as a highly accurate proxy for functional promoter variations in the neighboring UGT1A1 gene [1]. Specifically, it is in strong linkage disequilibrium with the UGT1A1*28 allele, which reduces gene expression and impairs bilirubin clearance [1]. Consequently, this single nucleotide polymorphism is one of the strongest genetic determinants of baseline serum bilirubin levels in the general population [3].
Key Insight: This genetic variant explains up to twenty percent of the total variation in human blood bilirubin levels, making it a primary driver of benign jaundice and gallstone susceptibility.
Location: UGT1A1. Chromosome 2 · 2q37.1 · 233.8 Mb
Estimated prevalence by population
Global 41.9%; European 46.2%; African 32.4%; East Asian 76.4%; South Asian 35.0%; Americas 45.8%; Ashkenazi 38.2%; Finnish 33.5%; Middle Eastern 44.9%; Amish 33.0%.
Estimated GG genotype frequency.
Global 45.0%; European 43.5%; African 49.0%; East Asian 22.0%; South Asian 48.3%; Americas 43.7%; Ashkenazi 47.2%; Finnish 48.8%; Middle Eastern 44.2%; Amish 48.9%.
Estimated GT genotype frequency.
Global 13.1%; European 10.3%; African 18.6%; East Asian 1.6%; South Asian 16.7%; Americas 10.4%; Ashkenazi 14.6%; Finnish 17.7%; Middle Eastern 10.9%; Amish 18.1%.
Estimated TT genotype frequency.
Showing effects for G/G genotype
Organ Systems
Digestive & Gut Disorders
Gallstones. Evidence: 3/10. Source: PMID 23753274. Typical Risk.
Liver Function & Disease
Bilirubin Levels. Evidence: 10/10. Source: PMID 19414484. Typical Levels.
Cardiovascular & Metabolic
Lipids & Cholesterol
LDL Cholesterol. Evidence: 6/10. Source: PMID 39024449. Slightly Higher.
Pharmacogenomics
Lipid-Lowering Drug Response
Atorvastatin Response. Evidence: 4/10. Source: PMID 38493369. Typical Response.
Neurology & Mental Health
Sleep & Circadian Rhythm
Insomnia. Evidence: 8/10. Source: PMID 34343768. Associated.
Showing effects for G/T genotype
Gallstones. Evidence: 3/10. Source: PMID 23753274. ~9% Increased Risk.
Bilirubin Levels. Evidence: 10/10. Source: PMID 19414484. ~16% Higher.
LDL Cholesterol. Evidence: 6/10. Source: PMID 39024449. Typical.
Atorvastatin Response. Evidence: 4/10. Source: PMID 38493369. Altered Response.
Showing effects for T/T genotype
Gallstones. Evidence: 3/10. Source: PMID 23753274. ~1.9x Higher Risk.
Bilirubin Levels. Evidence: 10/10. Source: PMID 19414484. ~90% Higher.
LDL Cholesterol. Evidence: 6/10. Source: PMID 39024449. Slightly Lower.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Efficient processing of cellular waste products is a hallmark of this genotype. The presence of two copies of the G allele ensures optimal expression of the glucuronidation enzymes [1]. Bilirubin is processed and excreted rapidly, keeping blood levels within the standard reference range [1]. Because bile composition remains balanced, the risk of developing pigment-based gallstones is not elevated [2]. Additionally, this genotype is associated with a typical response to common medications metabolized by the UGT pathway [3]. However, a slight genetic predisposition toward higher LDL cholesterol levels has been observed in large cohort studies [4].
Optimal bilirubin clearance; Typical gallstone risk; Slightly higher LDL cholesterol.
Sample genotype: GT (Heterozygous)
Slightly reduced glucuronidation capacity characterizes this heterozygous genotype. Carrying one copy of the T allele is associated with a modest sixteen percent increase in baseline serum bilirubin levels [1]. While this minor elevation is generally harmless and does not cause clinical jaundice, it slightly alters the chemical composition of bile [1]. Over time, this minor imbalance can lead to a small, nine percent increase in the risk of developing symptomatic gallstones [2]. The genotype also influences how the body processes certain medications, such as statins, potentially altering drug exposure levels [3]. On the positive side, a slight genetic trend toward lower LDL cholesterol levels is associated with this variant [4].
Modestly elevated bilirubin levels; Slightly increased gallstone risk; Altered statin pharmacokinetics.
Sample genotype: TT (Homozygous)
Substantially reduced enzyme activity leads to a notable accumulation of unconjugated bilirubin in the bloodstream. Carrying two copies of the T allele is associated with an average ninety percent increase in serum bilirubin levels [1]. This elevation is highly characteristic of Gilbert syndrome, a benign liver condition that can cause mild, intermittent jaundice during periods of stress or fasting [2]. Because the liver excretes excess bilirubin into the gallbladder, the risk of developing symptomatic pigment gallstones is nearly doubled [1]. This altered metabolic rate also impacts the processing of various therapeutic drugs, potentially increasing the risk of side effects from medications like atorvastatin [3]. Conversely, higher circulating bilirubin may act as a mild natural antioxidant, and this genotype is linked to slightly lower LDL cholesterol [4].
Significantly elevated bilirubin levels; Nearly twofold higher gallstone risk; Altered drug metabolism pathways.
Variants with shared genetic architecture
rs887829 · UGT1A1 Gene · Chr 2 · Bilirubin and Heart Health
rs10929302 · UGT1A1 Gene · Chr 2 · Drug and Bilirubin Clearance
rs4148323 · UGT1A1 Gene · Chr 2 · Bilirubin and Drug Metabolism
Extreme bilirubin levels as a causal risk factor for symptomatic gallstone disease.
Genome-wide association meta-analysis for total serum bilirubin levels.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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