What you carry at this position in your DNA and what research says about it.
Pain and Addiction Risk: 9/10 evidence, 45 publications.
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Sample genotype (not yours): C/C
Typical Pain Sensitivity and Baseline Addiction Risk
Baseline endocannabinoid breakdown results in typical pain sensitivity and standard risk levels for substance use. Standard responses to pain medications and antipsychotics are expected.
What this genotype means: Typical pain sensitivity; Standard risk of substance dependence; Typical response to opioid medications.
Sample genotype (not yours): A/A
Higher Pain Tolerance but Elevated Addiction Risk
Significantly reduced enzyme activity leads to elevated natural endocannabinoid levels, resulting in higher pain tolerance. This same biological shift is associated with an increased risk of developing substance use disorders.
What this genotype means: Lower physical pain sensitivity; Increased risk of substance use disorders; Higher risk of weight gain from certain antipsychotics.
Sample genotype (not yours): C/A
Typical Pain Sensitivity with Mild Medication Sensitivity
Intermediate enzyme activity maintains typical pain tolerance and baseline addiction risk. A slightly higher sensitivity to certain medications, including potential weight gain from antipsychotics, may be present.
What this genotype means: Typical pain sensitivity; Standard risk of substance dependence; Slightly increased risk of opioid-induced nausea.
Gene function and biological role
Gene Function: The FAAH gene encodes fatty acid amide hydrolase, a key enzyme responsible for breaking down endocannabinoids in the brain and body [1]. Endocannabinoids, such as anandamide, are lipid-based neurotransmitters that naturally regulate mood, pain perception, and reward pathways [1] [2]. By degrading these molecules, the FAAH enzyme controls the duration and strength of endocannabinoid signaling [1]. When FAAH activity is altered, it directly impacts how the brain processes stress, fear, and physical pain [2] [3]. Consequently, this gene plays a central role in emotional resilience and susceptibility to substance use disorders [2] [4].
Variant Impact: The rs324420 variant is a missense mutation in the FAAH gene that swaps the amino acid proline for threonine at position 129 [1]. This specific molecular change destabilizes the FAAH enzyme, making it highly susceptible to rapid cellular degradation [1]. As a result, individuals carrying the variant allele have significantly reduced FAAH enzyme activity and elevated levels of natural endocannabinoids like anandamide [1] [2]. This increase in endocannabinoid tone alters signaling within the brain's reward and pain-processing networks [2] [3]. Ultimately, this single nucleotide change influences pain sensitivity, emotional processing, and responses to various medications [3] [5].
Key Insight: The same genetic variant that makes you less sensitive to physical pain can also make you more vulnerable to substance addiction.
Location: FAAH. Chromosome 1 · 1p33 · 46.4 Mb
Estimated prevalence by population
Global 55.3%; European 62.9%; African 41.1%; East Asian 67.9%; South Asian 64.6%; Americas 48.5%; Ashkenazi 72.8%; Finnish 52.1%; Middle Eastern 72.1%; Amish 73.1%.
Estimated CC genotype frequency.
Global 37.5%; European 32.8%; African 46.0%; East Asian 29.0%; South Asian 31.5%; Americas 42.3%; Ashkenazi 25.0%; Finnish 40.2%; Middle Eastern 25.6%; Amish 24.8%.
Estimated CA genotype frequency.
Global 7.3%; European 4.3%; African 12.9%; East Asian 3.1%; South Asian 3.8%; Americas 9.2%; Ashkenazi 2.2%; Finnish 7.7%; Middle Eastern 2.3%; Amish 2.1%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Organ Systems
Chronic Pain
Pain Sensitivity. Evidence: 3/10. Source: PMID 26808012. Typical.
Neurology & Mental Health
Addiction & Reward
Addiction Risk. Evidence: 4/10. Source: PMID 12060782. Typical.
Nutrition & Metabolism
Blood Chemistry & Metabolites
Endocannabinoid Levels. Evidence: 9/10. Source: PMID 35050183. Typical.
Pharmacogenomics
Antidepressant & Psychiatric Drug Response
Antipsychotic Weight Gain. Evidence: 5/10. Source: PMID 20631561. Typical.
Anesthesia Response
Post-Surgery Nausea. Evidence: 5/10. Source: PMID 25558980. Typical.
Showing effects for A/A genotype
Pain Sensitivity. Evidence: 3/10. Source: PMID 26808012. Lower Sensitivity.
Addiction Risk. Evidence: 4/10. Source: PMID 12060782. Increased Risk.
Endocannabinoid Levels. Evidence: 9/10. Source: PMID 35050183. Elevated.
Antipsychotic Weight Gain. Evidence: 5/10. Source: PMID 20631561. Increased Risk.
Post-Surgery Nausea. Evidence: 5/10. Source: PMID 25558980. Increased Risk.
Showing effects for C/A genotype
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Standard levels of the fatty acid amide hydrolase enzyme are produced, leading to typical breakdown rates of the endocannabinoid anandamide [1]. This baseline enzymatic activity maintains standard signaling within the brain's pain and reward pathways [1] [2]. Physical pain sensitivity and emotional responses to stress generally fall within the typical population range [2] [3]. There is no genetically elevated risk for substance use disorders or addiction associated with this genotype [1] [4]. Additionally, standard responses to opioid pain medications and antipsychotic drugs are typical, with a lower likelihood of experiencing side effects like severe post-surgery nausea or rapid weight gain compared to variant carriers [5] [6].
Typical pain sensitivity; Standard risk of substance dependence; Typical response to opioid medications.
Sample genotype: AA (Homozygous)
A profound reduction in fatty acid amide hydrolase enzyme stability leads to significantly elevated levels of the endocannabinoid anandamide [1]. This high endocannabinoid tone alters signaling in pain-processing pathways, resulting in lower sensitivity to physical pain and a reduced need for postoperative pain relief [2]. However, the same altered signaling in the brain's reward center is linked to a significantly higher risk of developing substance use disorders [1] [3]. Responses to specific medications are also altered, including a higher likelihood of experiencing shortness of breath or nausea from morphine [4]. Furthermore, there is an increased risk of experiencing substantial weight gain when taking certain antipsychotic medications [5]. This genotype represents a clear biological trade-off between natural pain protection and vulnerability to addiction [2] [3].
Lower physical pain sensitivity; Increased risk of substance use disorders; Higher risk of weight gain from certain antipsychotics.
Sample genotype: CA (Heterozygous)
Carrying one copy of the variant allele leads to a moderate reduction in fatty acid amide hydrolase enzyme stability [1]. This intermediate activity level generally maintains typical pain sensitivity and standard baseline risk for substance use disorders [1] [2]. However, the subtle shift in endocannabinoid signaling can influence how the body responds to specific external substances [2] [3]. There is an increased likelihood of experiencing side effects such as post-surgery nausea and vomiting when treated with central opioids like morphine [4]. Additionally, treatment with certain antipsychotic medications may carry a higher risk of drug-induced weight gain [5]. Despite these pharmacogenomic sensitivities, overall emotional processing and pain thresholds remain close to the population average [2] [3].
Typical pain sensitivity; Standard risk of substance dependence; Slightly increased risk of opioid-induced nausea.
Variants with shared genetic architecture
rs2234918 · OPRD1 Gene · Chr 1 · Opioid Dependence Risk
rs2283265 · DRD2 Gene · Chr 11 · Dopamine Receptor Splicing
rs4818 · COMT Gene · Chr 22 · Pain Sensitivity
FAAH genetic variation enhances fronto-amygdala function in mouse and human.
A missense mutation in human fatty acid amide hydrolase associated with problem drug use.
Content updated August 2026.
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