What you carry at this position in your DNA and what research says about it.
Drug and Toxin Metabolism: 6/10 evidence, 9 publications.
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Sample genotype (not yours): T/T
Typical Drug and Toxin Clearance
Slower metabolism of valproic acid may increase the risk of side effects. Typical levels of bilirubin and normal clearance of environmental toxins are expected.
What this genotype means: Slower valproic acid metabolism; Typical bilirubin levels; Standard environmental toxin clearance.
Sample genotype (not yours): G/G
Altered Drug Clearance and Higher Bilirubin
Faster metabolism of valproic acid weakens its effect, while slower clearance of other compounds increases toxicity risks.
What this genotype means: Faster valproic acid clearance; Elevated plasma bilirubin levels; Increased risk of deferiprone toxicity.
Sample genotype (not yours): T/G
Intermediate Drug and Toxin Metabolism
Slightly altered clearance rates for certain medications and environmental compounds. Typical or slightly altered drug response.
What this genotype means: Intermediate valproic acid clearance; Typical to slightly variable bilirubin levels.
Gene function and biological role
Gene Function: The UGT1A10 gene belongs to the UDP-glucuronosyltransferase 1A family, which plays a critical role in the phase II detoxification pathway [1]. This gene family is responsible for glucuronidation, a process that attaches glucuronic acid to toxins, hormones, and drugs to make them water-soluble for excretion [1]. Although mapped to UGT1A10, this locus also dictates the function of UGT1A6, a major enzyme in the metabolism of common medications like aspirin and acetaminophen [2]. Proper functioning of these enzymes is essential for protecting tissues from chemical damage and clearing metabolic waste [1] [2].
Variant Impact: The rs6759892 variant is a missense mutation in the first exon of the UGT1A gene cluster, resulting in a Ser7Ala amino acid substitution [3]. This specific change defines the UGT1A6*2 haplotype, which is widely studied for its impact on enzyme activity [3]. The G allele encodes alanine, which is associated with altered glucuronidation rates for various drugs and environmental compounds [3] [4]. Depending on the substrate, this variant can either accelerate or slow down the clearance of therapeutic agents [4].
Key Insight: This single genetic change can cause you to clear some medications faster than normal while slowing down your ability to process other drugs and environmental toxins.
Location: UGT1A6. Chromosome 2 · 2q37.1 · 233.7 Mb
Estimated prevalence by population
Global 37.1%; European 35.9%; African 39.0%; East Asian 59.3%; South Asian 29.7%; Americas 43.8%; Ashkenazi 28.6%; Finnish 23.3%; Middle Eastern 36.8%; Amish 24.8%.
Estimated TT genotype frequency.
Global 47.2%; European 48.0%; African 46.9%; East Asian 35.4%; South Asian 49.6%; Americas 44.7%; Ashkenazi 49.8%; Finnish 49.9%; Middle Eastern 47.7%; Amish 50.0%.
Estimated TG genotype frequency.
Global 15.8%; European 16.1%; African 14.1%; East Asian 5.3%; South Asian 20.7%; Americas 11.4%; Ashkenazi 21.6%; Finnish 26.8%; Middle Eastern 15.5%; Amish 25.2%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Pharmacogenomics
Antiepileptic & Mood-Stabilizer Response
Valproic Acid Metabolism. Evidence: 6/10. Source: PMID 21806385. Slower metabolism.
Drug Metabolism Enzyme Activity
Deferiprone Response. Evidence: 5/10. Source: PMID 24036429. Typical response.
Chemical Sensitivity. Evidence: 3/10. Source: PMID 17424838. Typical resistance.
Organ Systems
Liver Function & Disease
Bilirubin Levels. Evidence: 6/10. Source: PMID 34343768. Typical levels.
Neurology & Mental Health
Sleep & Circadian Rhythm
Insomnia. Evidence: 6/10. Source: PMID 34343768. Direction unresolved.
Showing effects for G/G genotype
Valproic Acid Metabolism. Evidence: 6/10. Source: PMID 21806385. Faster metabolism.
Deferiprone Response. Evidence: 5/10. Source: PMID 24036429. Higher toxicity risk.
Chemical Sensitivity. Evidence: 3/10. Source: PMID 17424838. Higher sensitivity.
Bilirubin Levels. Evidence: 6/10. Source: PMID 34343768. Elevated levels.
Showing effects for T/G genotype
Valproic Acid Metabolism. Evidence: 6/10. Source: PMID 21806385. Typical metabolism.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele represents the typical genetic baseline for most metabolic pathways governed by the UGT1A family. For individuals taking the anti-seizure medication valproic acid, this genotype is associated with slower drug metabolism [1]. Slower clearance can lead to higher drug concentrations in the bloodstream, potentially increasing the risk of drug-induced liver injury or other side effects [1]. However, this genotype maintains typical glucuronidation activity for other compounds, resulting in normal bilirubin levels [2]. It also confers standard protection against environmental toxins like benzene and vinyl chloride [3]. No elevated risk for drug toxicity from deferiprone has been observed with this baseline genotype [4].
Slower valproic acid metabolism; Typical bilirubin levels; Standard environmental toxin clearance.
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele significantly alters the activity of the UGT1A6 enzyme. For valproic acid therapy, this genotype leads to faster drug metabolism, meaning the drug is often less effective [1]. However, for other substances, this variant is associated with decreased glucuronidation capacity [2]. This reduction can lead to elevated levels of plasma bilirubin [3]. It also increases the risk of drug toxicity when taking deferiprone, despite potentially showing a better initial therapeutic response [4]. Furthermore, reduced enzyme activity may increase susceptibility to DNA damage from environmental toxins like benzene [5].
Faster valproic acid clearance; Elevated plasma bilirubin levels; Increased risk of deferiprone toxicity; Higher sensitivity to environmental toxins.
Sample genotype: TG (Heterozygous)
Carrying one copy of the G allele results in intermediate enzyme activity for the UGT1A6 pathway. For individuals prescribed valproic acid, the drug reaches lower levels than in those with the T/T genotype [1]. This intermediate status may also lead to slight variations in the clearance of other common drugs and environmental chemicals [2]. Bilirubin levels are generally within the typical range, though minor fluctuations can occur [3]. The risk of adverse reactions to medications like deferiprone remains low and comparable to the general population [4].
Intermediate valproic acid clearance; Typical to slightly variable bilirubin levels.
Variants with shared genetic architecture
rs2070959 · UGT1A6 Gene · Chr 2 · Gallstone Risk
rs17863783 · UGT1A6 Gene · Chr 2 · Bladder Cancer Risk
rs1105879 · UGT1A6 Gene · Chr 2 · Colorectal Cancer Risk
Pharmacogenomics in aspirin intolerance.
Association of genetic variants in six candidate genes with valproic acid therapy optimization.
Content updated August 2026.
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