What you carry at this position in your DNA and what research says about it.
Mood and Stress Sensitivity: 5/10 evidence, 57 publications.
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Sample genotype (not yours): C/C
Higher Risk of Mood and Stress Sensitivity
Having two copies of the C allele is associated with an increased risk of depression and anxiety. It also significantly influences response rates to several antidepressant and antipsychotic drugs.
What this genotype means: Increased risk of depression and anxiety; Significantly reduced serotonin release; Poorer response to certain antidepressant and antipsychotic therapies.
Sample genotype (not yours): C/G
Slightly Elevated Mood and Stress Sensitivity
Carrying one copy of the C allele is linked to a slightly increased risk of depression and anxiety. It may also influence how the brain responds to stress and certain medications.
What this genotype means: Slightly increased risk of depression and anxiety; Mildly reduced serotonin release; Potential differences in response to certain psychiatric medications.
Sample genotype (not yours): G/G
Typical Mood and Stress Resilience
This genotype is associated with a typical risk of depression and anxiety. It represents the baseline genetic profile that allows normal regulation of serotonin levels in the brain.
What this genotype means: Typical risk of depression and anxiety; Normal serotonin receptor regulation; Favorable response to several common antidepressants.
Gene function and biological role
Gene Function: The HTR1A gene encodes the 5-hydroxytryptamine receptor 1A, a key subtype of serotonin receptor widely distributed in the brain [1]. It acts both as a presynaptic autoreceptor in the raphe nuclei, where it inhibits serotonin release, and as a postsynaptic heteroreceptor in regions like the hippocampus and prefrontal cortex [2]. Through these dual roles, the receptor plays a critical part in regulating mood, anxiety, and stress responses [1] [2]. Dysregulation of HTR1A expression or signaling has been heavily implicated in major depressive disorder and anxiety disorders [3]. It is also a primary target for many antidepressant and antipsychotic medications [4].
Variant Impact: The rs6295 variant, also known as C(-1019)G, is a functional single nucleotide polymorphism located in the promoter region of the HTR1A gene [2]. This genetic change alters a binding site for transcription factors, such as Deaf1, which normally repress receptor expression [5]. Because HTR1A sits on the minus strand, the risk allele reported in the literature as the promoter "G" corresponds to the C allele on this variant's forward strand: that C allele prevents these repressor proteins from binding, leading to an upregulation of 5-HT1A autoreceptors in the brain [5] [6]. This increase in autoreceptors reduces the overall release of serotonin into the synaptic cleft [6]. Consequently, this variant has been widely studied for its impact on susceptibility to mood disorders and individual differences in psychiatric drug response [2] [7].
Key Insight: This variant directly controls how much serotonin is released in the brain by altering the binding of a genetic repressor protein. On this variant's forward strand, the C allele prevents this repressor from working, leading to fewer active serotonin signals and higher stress sensitivity.
Location: HTR1A. Chromosome 5 · 5q12.3 · 64.0 Mb
Estimated prevalence by population
Global 26.3%; European 25.0%; African 31.3%; East Asian 5.9%; South Asian 17.2%; Americas 26.2%; Ashkenazi 22.0%; Finnish 33.0%; Middle Eastern 12.5%; Amish 9.1%.
Estimated CC genotype frequency.
Global 49.2%; European 50.0%; African 49.3%; East Asian 36.8%; South Asian 48.5%; Americas 50.0%; Ashkenazi 49.8%; Finnish 48.9%; Middle Eastern 45.7%; Amish 42.1%.
Estimated CG genotype frequency.
Global 24.6%; European 25.0%; African 19.4%; East Asian 57.3%; South Asian 34.2%; Americas 23.9%; Ashkenazi 28.2%; Finnish 18.1%; Middle Eastern 41.8%; Amish 48.8%.
Estimated GG genotype frequency.
Showing effects for C/C genotype
Neurology & Mental Health
Mood Disorders
Depression. Evidence: 5/10. Source: PMID 22752684. Higher Risk.
Anxiety & Stress Disorders
Anxiety and Stress. Evidence: 3/10. Source: PMID 32957930. Higher Risk.
Behavioral & Personality Traits
Impulsivity. Evidence: 3/10. Source: PMID 19725031. Higher Impulsivity.
Pharmacogenomics
Antidepressant & Psychiatric Drug Response
Antidepressant Response. Evidence: 5/10. Source: PMID 18484082. Poorer Response.
Showing effects for C/G genotype
Depression. Evidence: 5/10. Source: PMID 22752684. Slightly Higher Risk.
Anxiety and Stress. Evidence: 3/10. Source: PMID 32957930. Slightly Higher Risk.
Impulsivity. Evidence: 3/10. Source: PMID 19725031. Typical Impulsivity.
Antidepressant Response. Evidence: 5/10. Source: PMID 18484082. Variable Response.
Showing effects for G/G genotype
Depression. Evidence: 5/10. Source: PMID 22752684. Typical Risk.
Anxiety and Stress. Evidence: 3/10. Source: PMID 32957930. Typical Resilience.
Antidepressant Response. Evidence: 5/10. Source: PMID 18484082. Favorable Response.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Carrying two copies of the C allele prevents transcription repressors like Deaf1 from binding to the promoter region of the gene [1]. This lack of repression leads to a significant upregulation of 5-HT1A autoreceptors in the brain [2]. The excess of these autoreceptors dampens the activity of serotonin-producing neurons, leading to reduced serotonin levels in key brain regions [2] [3]. Clinical research has linked this genotype to an elevated risk of major depressive disorder and anxiety [4]. It is also associated with differences in how individuals respond to various psychiatric medications, including a poorer response to some antipsychotics like lurasidone [5].
Increased risk of depression and anxiety; Significantly reduced serotonin release; Poorer response to certain antidepressant and antipsychotic therapies.
Sample genotype: CG (Heterozygous)
Possessing one copy of the C allele partially disrupts the binding of transcription repressors in the promoter region of the receptor gene [1]. This disruption leads to a mild increase in the expression of presynaptic autoreceptors, which can slightly reduce serotonin release [2]. As a result, individuals with this heterozygous profile often exhibit a moderately increased sensitivity to stress and anxiety [3]. Some studies also suggest a higher susceptibility to mood disorders compared to those with the G/G genotype [4]. Furthermore, this genetic variation can influence the efficacy and side-effect profile of certain psychiatric medications [5].
Slightly increased risk of depression and anxiety; Mildly reduced serotonin release; Potential differences in response to certain psychiatric medications.
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele represents the typical genetic baseline for serotonin receptor regulation [1]. The G allele allows transcription factors like Deaf1 to bind properly to the promoter region, keeping receptor expression at balanced levels [2]. This normal regulation supports stable serotonin release throughout the brain's emotional processing centers [2] [3]. Clinical studies have associated this genotype with a lower susceptibility to depressive symptoms compared to C allele carriers [4]. Additionally, some research indicates that this profile may correlate with a more favorable response to standard antidepressant therapies [5].
Typical risk of depression and anxiety; Normal serotonin receptor regulation; Favorable response to several common antidepressants.
Variants with shared genetic architecture
rs25531 · SLC6A4 Gene · Chr 17 · Stress and Mood Regulation
rs4570625 · TPH2 Gene · Chr 12 · Anxiety and Mood Regulation
rs1360780 · FKBP5 Gene · Chr 6 · Depression Risk
Genetics of serotonin receptors and depression: state of the art.
Transcriptional regulation of the 5-HT1A receptor: implications for mental illness.
Transcriptional dysregulation of 5-HT1A autoreceptors in mental illness.
Pharmacogenetics of antidepressant response.
Effect of 5-HT1A gene polymorphisms on antidepressant response in major depressive disorder.
Content updated August 2026.
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