What you carry at this position in your DNA and what research says about it.
Impulsivity and ADHD Risk: 5/10 evidence, 34 publications.
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Sample genotype (not yours): T/T
Lowest Dopamine Enzyme Activity and Higher Impulsivity Risk
A dramatic reduction in dopamine beta-hydroxylase activity characterizes this profile, resulting in higher dopamine and lower norepinephrine levels. Impulsive behaviors, adult ADHD, and adverse reactions to certain medications like disulfiram are more common.
What this genotype means: Up to 90% reduction in dopamine beta-hydroxylase enzyme activity; Higher risk of impulsivity, aggressive hostility, and adult ADHD; Increased risk of severe side effects from disulfiram.
Sample genotype (not yours): C/C
Normal Dopamine Enzyme Activity and Typical Impulsivity Risk
Normal, high-activity levels of the dopamine-converting enzyme characterize this profile. It provides a typical baseline for behavioral traits and a standard response to related medications.
What this genotype means: Normal, high-activity levels of dopamine beta-hydroxylase; Typical baseline risk for impulsivity and adult ADHD; Lower risk of adverse events from disulfiram.
Sample genotype (not yours): T/C
Intermediate Dopamine Enzyme Activity and Typical Impulsivity Risk
Moderately reduced dopamine beta-hydroxylase activity defines this intermediate profile, which generally maintains a typical behavioral outlook. However, the presence of one T allele still influences how the body processes certain medications.
What this genotype means: Approximately 50% reduction in dopamine beta-hydroxylase enzyme activity; Typical baseline risk for impulsivity and adult ADHD; Increased risk of side effects from disulfiram compared to CC.
Gene function and biological role
Gene Function: The DBH gene encodes dopamine beta-hydroxylase, an essential enzyme that converts dopamine into norepinephrine in the brain and sympathetic nervous system [1]. This chemical conversion is a key regulator of the balance between these two major neurotransmitters, directly shaping attention, mood, and stress responses [1] [2]. Variations in DBH activity can significantly alter the rate of dopamine clearance, leading to localized changes in neurotransmitter levels [2]. Because DBH is highly active in both central and peripheral nerves, its function influences not only cognitive traits but also cardiovascular responses [3].
Variant Impact: The rs1611115 variant, also known as C-1021T, is a functional single nucleotide polymorphism located in the promoter region of the DBH gene [1]. This genetic change directly controls how much of the dopamine beta-hydroxylase enzyme is produced, accounting for up to 52% of the variation in plasma DBH levels [4]. The T allele is a low-activity variant that dramatically reduces enzyme expression, whereas the C allele is associated with normal, high-activity levels [1] [4]. Specifically, individuals carrying two copies of the T allele have only about 10% of the enzyme activity seen in those with two copies of the C allele [5].
Key Insight: A single genetic letter change in the DBH promoter can reduce your body's dopamine-converting enzyme activity by up to 90%, shifting the delicate balance of brain chemicals.
Location: DBH. Chromosome 9 · 9q34.2 · 133.6 Mb
Estimated prevalence by population
Global 4.3%; European 4.4%; African 2.9%; East Asian 3.2%; South Asian 4.9%; Americas 7.9%; Ashkenazi 5.5%; Finnish 2.4%; Middle Eastern 7.9%; Amish 10.4%.
Estimated TT genotype frequency.
Global 32.2%; European 33.2%; African 28.4%; East Asian 29.2%; South Asian 34.4%; Americas 40.3%; Ashkenazi 36.0%; Finnish 26.2%; Middle Eastern 40.4%; Amish 43.7%.
Estimated TC genotype frequency.
Global 63.5%; European 62.3%; African 68.7%; East Asian 67.6%; South Asian 60.7%; Americas 51.8%; Ashkenazi 58.5%; Finnish 71.4%; Middle Eastern 51.7%; Amish 46.0%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Neurology & Mental Health
Neurodevelopmental Traits
Impulsivity and ADHD. Evidence: 3/10. Source: PMID 18982239. Increased Risk.
Addiction & Reward
Cocaine Therapy Response. Evidence: 5/10. Source: PMID 22906516. Poorer Response.
Headache & Migraine
Headache Drug Response. Evidence: 5/10. Source: PMID 25096645. Stronger Response.
Pharmacogenomics
Drug Metabolism Enzyme Activity
DBH Enzyme Activity. Evidence: 3/10. Source: PMID 24986918. ~90% Lower Activity.
Adverse Drug Reactions
Disulfiram Side Effects. Evidence: 5/10. Source: PMID 22760354. Increased Risk.
Showing effects for C/C genotype
Impulsivity and ADHD. Evidence: 3/10. Source: PMID 18982239. Typical Risk.
Cocaine Therapy Response. Evidence: 5/10. Source: PMID 22906516. Stronger Response.
Headache Drug Response. Evidence: 5/10. Source: PMID 25096645. Typical Response.
DBH Enzyme Activity. Evidence: 3/10. Source: PMID 24986918. Normal Activity.
Disulfiram Side Effects. Evidence: 5/10. Source: PMID 22760354. Typical Risk.
Showing effects for T/C genotype
DBH Enzyme Activity. Evidence: 3/10. Source: PMID 24986918. ~50% Lower Activity.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Homozygosity for the T allele results in a profound reduction of dopamine beta-hydroxylase (DBH) activity, leaving only about 10% of the normal enzyme levels [1]. This enzymatic bottleneck prevents the efficient conversion of dopamine to norepinephrine, leading to elevated dopamine levels in certain brain pathways [1] [2]. Research has linked this biochemical profile to specific personality traits, including higher impulsivity, aggressive hostility, and increased risk for adult ADHD [2]. Additionally, because the DBH enzyme is already highly depleted, taking the medication disulfiram (which further inhibits DBH) can trigger severe adverse effects such as extreme sedation or psychosis [1]. Affected individuals also tend to show a poorer response to disulfiram when used as a treatment for cocaine dependence [3]. However, studies suggest they may experience a better response to other treatments, such as naltrexone or levodopa [4].
Up to 90% reduction in dopamine beta-hydroxylase enzyme activity; Higher risk of impulsivity, aggressive hostility, and adult ADHD; Increased risk of severe side effects from disulfiram; Poorer response to disulfiram for cocaine dependence.
Sample genotype: CC (Homozygous)
Homozygosity for the C allele represents the most common genetic profile, producing normal, high-activity levels of the dopamine beta-hydroxylase (DBH) enzyme [1]. This ensures a standard rate of conversion from dopamine to norepinephrine, maintaining a typical balance of these neurotransmitters in the brain [1] [2]. There is no elevated genetic risk for impulsivity, aggressive hostility, or adult ADHD [2]. In medical contexts, having normal DBH levels means a significantly lower risk of adverse reactions to disulfiram [1]. Furthermore, clinical trials have shown that these individuals have a much better treatment response to disulfiram when used for cocaine dependence, showing a significant reduction in drug use compared to T allele carriers [3]. However, they may have a more typical, rather than reduced, likelihood of experiencing headaches during medication withdrawal therapies [4].
Normal, high-activity levels of dopamine beta-hydroxylase; Typical baseline risk for impulsivity and adult ADHD; Lower risk of adverse events from disulfiram; Better treatment response to disulfiram for cocaine dependence.
Sample genotype: TC (Heterozygous)
Heterozygosity for the T allele leads to an intermediate level of dopamine beta-hydroxylase (DBH) activity, typically around 50% of the level seen in CC homozygotes [1]. This moderate reduction is generally sufficient for normal brain chemistry, and there is no elevated risk for impulsivity or adult ADHD [2]. However, the partial reduction in DBH activity still has clinical relevance for medication responses [1]. Specifically, there remains an increased risk for adverse effects when taking disulfiram, as further chemical inhibition of already-reduced DBH levels can cause complications [1]. There is also a lower rate of success when using disulfiram to treat cocaine dependence [3]. On the positive side, studies indicate a decreased likelihood of headache and withdrawal symptoms during medication overuse headache therapies [4].
Approximately 50% reduction in dopamine beta-hydroxylase enzyme activity; Typical baseline risk for impulsivity and adult ADHD; Increased risk of side effects from disulfiram compared to CC; Decreased likelihood of headache during drug withdrawal therapy.
Variants with shared genetic architecture
rs6271 · DBH Gene · Chr 9 · Blood Pressure Regulation
rs1079596 · DRD2 Gene · Chr 11 · Impulsivity and Dopamine
rs2070762 · TH Gene · Chr 11 · Blood Pressure Risk
Dopamine-beta-hydroxylase in postural tachycardia syndrome.
Pharmacogenetic randomized trial for cocaine abuse: disulfiram and dopamine β-hydroxylase.
Pharmacogenetics of naltrexone and disulfiram in alcohol dependent, dually diagnosed veterans.
Content updated August 2026.
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