What you carry at this position in your DNA and what research says about it.
Inflammatory Response: 5/10 evidence, 55 publications.
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Sample genotype (not yours): G/G
Typical Inflammatory Response
A baseline level of interleukin-1 beta production helps maintain a balanced immune response. This genotype is associated with a typical risk of chronic inflammatory conditions.
What this genotype means: Typical risk of periodontal disease; Standard baseline inflammatory response; Typical response to anti-inflammatory biologics.
Sample genotype (not yours): A/A
Elevated Inflammatory Risk
Two copies of the A allele are linked to the highest levels of cytokine release. This significantly increases susceptibility to inflammatory conditions but may reduce weight gain from certain medications.
What this genotype means: Highest genetic risk for periodontal inflammation; Elevated susceptibility to joint and tissue inflammation; Reduced risk of weight gain on certain antipsychotics.
Sample genotype (not yours): G/A
Increased Inflammatory Risk
Carrying one copy of the A allele is linked to higher cytokine production. This can elevate the risk of chronic inflammation in the gums and joints.
What this genotype means: Moderately higher risk of gum inflammation; Increased susceptibility to joint discomfort; Variable response to opioid pain medications.
Gene function and biological role
Gene Function: The IL1B gene encodes interleukin-1 beta, a highly potent pro-inflammatory cytokine that acts as a primary chemical messenger in the innate immune system [1]. Upon cellular stimulation, this cytokine is produced and cleaved into its active form to initiate and amplify inflammatory cascades [1]. It plays a critical role in directing the body's response to infections, tissue injuries, and environmental stressors [2]. However, persistent or excessive production of interleukin-1 beta is a well-documented driver of chronic inflammatory diseases, joint destruction, and tissue damage [2] [3].
Variant Impact: The rs1143634 variant, historically referred to as +3953 C>T or +3954 C>T, is a synonymous genetic change located in exon 5 of the IL1B gene [1]. Although it does not alter the final amino acid sequence of the interleukin-1 beta protein, this specific nucleotide substitution has been shown to influence the rate of cytokine translation and secretion [1] [4]. Specifically, the minor A allele is associated with elevated levels of active interleukin-1 beta release from immune cells upon stimulation [4]. This heightened cytokine release can lead to an overactive inflammatory response, increasing susceptibility to various chronic inflammatory and autoimmune conditions [4] [2].
Key Insight: Although this genetic variant is synonymous and does not change the protein structure, it significantly alters how much active inflammatory cytokine the body releases during an immune response.
Location: IL1B. Chromosome 2 · 2q14.1 · 112.8 Mb
Estimated prevalence by population
Global 65.5%; European 58.6%; African 75.3%; East Asian 95.6%; South Asian 72.2%; Americas 68.6%; Ashkenazi 52.8%; Finnish 56.5%; Middle Eastern 42.7%; Amish 46.4%.
Estimated GG genotype frequency.
Global 30.4%; European 35.9%; African 22.9%; East Asian 4.3%; South Asian 25.6%; Americas 28.5%; Ashkenazi 39.7%; Finnish 37.3%; Middle Eastern 45.3%; Amish 43.5%.
Estimated GA genotype frequency.
Global 4.1%; European 5.5%; African 1.7%; East Asian < 0.1%; South Asian 2.3%; Americas 3.0%; Ashkenazi 7.5%; Finnish 6.2%; Middle Eastern 12.0%; Amish 10.2%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Organ Systems
Dental & Oral Health
Periodontitis. Evidence: 5/10. Source: PMID 31324923. Typical Risk.
Immunity & Inflammation
Chronic Inflammatory Diseases
Inflammatory Bowel Disease. Evidence: 5/10. Source: PMID 22960943. Typical Risk.
Autoimmune Diseases
Rheumatoid Arthritis. Evidence: 3/10. Source: PMID 31992083. Typical Severity.
Pharmacogenomics
Antidepressant & Psychiatric Drug Response
Antipsychotic Weight Gain. Evidence: 5/10. Source: PMID 25560300. Typical Weight Gain.
Showing effects for A/A genotype
Periodontitis. Evidence: 5/10. Source: PMID 31324923. ~4.9x Increased Risk.
Inflammatory Bowel Disease. Evidence: 5/10. Source: PMID 22960943. Increased Risk.
Rheumatoid Arthritis. Evidence: 3/10. Source: PMID 31992083. Increased Severity.
Antipsychotic Weight Gain. Evidence: 5/10. Source: PMID 25560300. Decreased Gain.
Showing effects for G/A genotype
Periodontitis. Evidence: 5/10. Source: PMID 31324923. ~2.8x Increased Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Inheriting two copies of the common G allele is associated with standard, baseline levels of interleukin-1 beta cytokine production [1]. Because the immune system does not overproduce this inflammatory signal under normal conditions, there is no elevated genetic risk for inflammatory tissue damage [1] [2]. Studies show a typical baseline susceptibility to periodontal disease and joint inflammation compared to carriers of the minor allele [2] [3]. Additionally, clinical data suggests a standard response to anti-inflammatory therapies such as infliximab [4]. Maintaining routine dental hygiene and a balanced lifestyle helps support long-term joint and tissue health.
Typical risk of periodontal disease; Standard baseline inflammatory response; Typical response to anti-inflammatory biologics.
Sample genotype: AA (Homozygous)
Carrying two copies of the minor A allele leads to the most pronounced increase in interleukin-1 beta cytokine production [1]. This genetic profile is strongly linked to heightened inflammatory responses throughout the body, particularly in the gums and joints [2] [3]. Research indicates a significantly higher risk of severe periodontitis and more rapid joint destruction in autoimmune conditions [2] [3]. On the positive side, clinical studies suggest that this genotype may protect against excessive weight gain if prescribed certain antipsychotic medications [4]. Proactive management of systemic inflammation through lifestyle, diet, and regular professional dental cleanings is highly beneficial.
Highest genetic risk for periodontal inflammation; Elevated susceptibility to joint and tissue inflammation; Reduced risk of weight gain on certain antipsychotics.
Sample genotype: GA (Heterozygous)
Presence of a single A allele alters the regulation of the IL1B gene, leading to moderately elevated levels of active interleukin-1 beta [1]. This increase in cytokine release can cause the immune system to overreact to minor irritants or infections [1] [2]. Clinical research associates this genotype with an increased susceptibility to chronic periodontitis and accelerated joint wear in rheumatoid arthritis [2] [3]. Some studies also suggest a variable response to certain pain medications, such as morphine, requiring careful clinical monitoring [4]. Prioritizing consistent dental care and anti-inflammatory dietary habits can help manage this genetic tendency.
Moderately higher risk of gum inflammation; Increased susceptibility to joint discomfort; Variable response to opioid pain medications.
Variants with shared genetic architecture
rs1143627 · IL1B Gene · Chr 2 · Inflammatory Response and Cancer Risk
rs16944 · IL1B Gene · Chr 2 · Osteoarthritis Risk
rs1143633 · IL1B Gene · Chr 2 · Allergy and Joint Health
Interleukin-1A and interleukin-1B gene polymorphisms in gastroesophageal reflux disease.
Interleukin-1 Genotype in Periodontitis.
Content updated August 2026.
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