What you carry at this position in your DNA and what research says about it.
Antidepressant Response: 5/10 evidence, 25 publications.
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Sample genotype (not yours): A/A
Mixed Antidepressant Response and Higher Side Effect Risk
Presence of the double A allele is associated with a higher likelihood of responding to certain antidepressants like citalopram. However, this profile also carries an increased risk of experiencing drug toxicity and side effects from several common psychiatric medications.
What this genotype means: Enhanced response to citalopram; Increased risk of SSRI toxicity; Higher risk of olanzapine side effects.
Sample genotype (not yours): A/G
Typical Antidepressant Response and Side Effect Risk
A heterozygous genetic profile generally results in a typical response to most antidepressant medications. The risk of experiencing drug-induced side effects or toxicity remains at a baseline level.
What this genotype means: Typical response to citalopram; Baseline risk of SSRI side effects; Slightly improved response to venlafaxine.
Sample genotype (not yours): G/G
Typical Side Effect Risk and Mixed Response
A double G allele combination is associated with a typical risk of side effects but a mixed response profile depending on the specific antidepressant. Response to citalopram may be lower, while response to venlafaxine or fluoxetine may be enhanced.
What this genotype means: Lower response rate to citalopram; Enhanced response to venlafaxine; Typical risk of drug toxicity.
Gene function and biological role
Gene Function: The HTR2A gene encodes the serotonin 2A receptor, a key protein involved in transmitting chemical signals across brain cells [1]. Serotonin is a neurotransmitter that regulates mood, sleep, anxiety, and appetite [1]. This receptor is the primary target for many atypical antipsychotics and is modulated by selective serotonin reuptake inhibitors [2]. Variations in this gene can alter receptor density or signaling efficiency in the brain [3]. These changes are heavily studied for their influence on how people respond to psychiatric medications [2].
Variant Impact: Located within an intron of the HTR2A gene, rs7997012 is a common genetic marker. Although it does not directly change the amino acid sequence of the serotonin receptor, it may influence gene expression or splicing. This genetic marker is widely investigated in psychiatric pharmacogenomics, particularly regarding antidepressant efficacy [2]. Research indicates that the variant plays a role in predicting treatment remission and side effect susceptibility [4]. It is also studied in the context of anxiety disorders and treatment resistance [5].
Key Insight: The same genetic variant can increase the effectiveness of one antidepressant while simultaneously raising the risk of side effects for another.
Location: HTR2A. Chromosome 13 · 13q14.2 · 46.8 Mb
Estimated prevalence by population
Global 12.4%; European 17.8%; African 0.5%; East Asian 6.8%; South Asian 16.7%; Americas 9.8%; Ashkenazi 7.9%; Finnish 30.5%; Middle Eastern 9.8%; Amish 14.5%.
Estimated AA genotype frequency.
Global 37.9%; European 48.8%; African 13.6%; East Asian 38.5%; South Asian 48.3%; Americas 43.1%; Ashkenazi 40.4%; Finnish 49.4%; Middle Eastern 43.0%; Amish 47.1%.
Estimated AG genotype frequency.
Global 49.7%; European 33.5%; African 85.9%; East Asian 54.8%; South Asian 34.9%; Americas 47.1%; Ashkenazi 51.7%; Finnish 20.0%; Middle Eastern 47.2%; Amish 38.4%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Pharmacogenomics
Antidepressant & Psychiatric Drug Response
Citalopram Response. Evidence: 5/10. Source: PMID 18803430. Stronger Response.
SSRI Side Effects. Evidence: 5/10. Source: PMID 24192302. Higher Risk.
Venlafaxine Response. Evidence: 5/10. Source: PMID 22006095. Typical Response.
Olanzapine Side Effects. Evidence: 5/10. Source: PMID 19636338. Higher Risk.
Fluoxetine Response. Evidence: 5/10. Source: PMID 29975559. Typical Response.
Showing effects for A/G genotype
Citalopram Response. Evidence: 5/10. Source: PMID 18803430. Typical Response.
SSRI Side Effects. Evidence: 5/10. Source: PMID 24192302. Typical Risk.
Venlafaxine Response. Evidence: 5/10. Source: PMID 22006095. Stronger Response.
Olanzapine Side Effects. Evidence: 5/10. Source: PMID 19636338. Typical Risk.
Showing effects for G/G genotype
Citalopram Response. Evidence: 5/10. Source: PMID 18803430. Poorer Response.
Fluoxetine Response. Evidence: 5/10. Source: PMID 29975559. Stronger Response.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Clinical studies show that homozygous A allele carriers treated with citalopram have an improved therapeutic response, including an eighteen percent reduction in the absolute risk of treatment failure [1]. Despite this potential benefit, the same genetic profile is linked to a significantly higher risk of drug toxicity when taking several selective serotonin reuptake inhibitors, including fluoxetine, paroxetine, and sertraline [2]. There is also an increased likelihood of experiencing adverse side effects when prescribed the atypical antipsychotic olanzapine [3]. In contrast, response rates to other medications like venlafaxine may be typical rather than enhanced [4]. Understanding these patterns helps researchers map out how genetic variations influence the balance between drug efficacy and tolerability.
Enhanced response to citalopram; Increased risk of SSRI toxicity; Higher risk of olanzapine side effects.
Sample genotype: AG (Heterozygous)
Heterozygous individuals typically exhibit a standard response pattern to common selective serotonin reuptake inhibitors like citalopram [1]. The likelihood of achieving remission or experiencing treatment-limiting side effects is considered average compared to the general population [2]. However, some research suggests a slightly improved response to the serotonin-norepinephrine reuptake inhibitor venlafaxine [3]. Standard clinical guidelines do not currently recommend altering medication choices or dosages based solely on this genotype [4]. Most individuals with this genetic profile tolerate standard psychiatric therapies well without elevated risks of drug toxicity [2].
Typical response to citalopram; Baseline risk of SSRI side effects; Slightly improved response to venlafaxine.
Sample genotype: GG (Homozygous)
Homozygous G allele carriers often show a reduced likelihood of responding successfully to citalopram, with a higher rate of treatment non-response compared to A allele carriers [1]. Conversely, this genotype is associated with a significantly better response and higher remission rates when treated with venlafaxine [2]. There is also evidence of improved clinical outcomes and higher remission rates in children and adolescents treated with fluoxetine [3]. Fortunately, the risk of experiencing severe drug toxicity or adverse side effects from these medications remains low and typical [4]. These contrasting response rates highlight the complexity of serotonin receptor genetics in determining medication efficacy.
Lower response rate to citalopram; Enhanced response to venlafaxine; Typical risk of drug toxicity.
Variants with shared genetic architecture
rs6311 · HTR2A Gene · Chr 13 · Antidepressant Side Effects
rs6313 · HTR2A Gene · Chr 13 · Serotonin Receptor Function
rs6314 · HTR2A Gene · Chr 13 · Episodic Memory
Temperament profiles, 5-HT2A genotype, and response to treatment with SSRIs in major depression.
Pharmacogenetics in major depression: a comprehensive meta-analysis.
Content updated August 2026.
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