What you carry at this position in your DNA and what research says about it.
Vitamin B12 and Gut Health: 9/10 evidence, 19 publications.
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Sample genotype (not yours): G/G
Active Secretor with Lower Vitamin B12
Active FUT2 enzymes support a diverse gut microbiome but are linked to lower circulating vitamin B12 levels. This pattern also leaves mucosal surfaces susceptible to common viral infections like norovirus.
What this genotype means: Active secretor status; Lower baseline vitamin B12; Typical susceptibility to stomach flu.
Sample genotype (not yours): A/A
Non-Secretor with Higher B12 and Norovirus Resistance
Inactive FUT2 enzymes prevent the secretion of mucosal sugars, conferring complete resistance to norovirus but raising the risk of inflammatory bowel issues.
What this genotype means: Non-secretor status; Higher baseline vitamin B12; Strong resistance to norovirus.
Sample genotype (not yours): G/A
Typical Secretor with Balanced Gut Health
One copy of each allele provides a balanced genetic profile, maintaining active secretor status and typical baseline vitamin B12 levels.
What this genotype means: Active secretor status; Typical vitamin B12 levels; Typical susceptibility to stomach flu.
Gene function and biological role
Gene Function: The FUT2 gene encodes the fucosyltransferase 2 enzyme, which plays a pivotal role in creating blood group antigens on mucosal surfaces and in bodily fluids [1]. This enzyme acts as a gatekeeper for the digestive tract by attaching fucose sugars to the lining of the gut [2]. These sugars serve as a crucial food source for beneficial gut bacteria, particularly Bifidobacteria [3]. Individuals with a fully functional FUT2 gene are classified as secretors, meaning they secrete these antigens into their saliva and mucus [1]. Conversely, those with inactive FUT2 are non-secretors, which significantly alters their gut microbiome composition and nutrient absorption [2].
Variant Impact: The rs602662 variant is a missense mutation in the FUT2 gene that results in a glycine-to-serine amino acid substitution at position 258 of the enzyme [4]. This specific change alters the enzyme's stability and activity, directly influencing whether a person exhibits a secretor or non-secretor phenotype [5]. The G allele represents the highly active reference enzyme, while the A allele is associated with significantly reduced enzyme function [5]. This single molecular swap has widespread systemic effects, ranging from the diversity of the gut microbiome to the absorption efficiency of essential vitamins in the small intestine [6].
Key Insight: Being a non-secretor protects you from the stomach flu but increases your susceptibility to inflammatory bowel diseases.
Location: FUT2. Chromosome 19 · 19q13.33 · 48.7 Mb
Origin Story: The non-secretor phenotype is believed to have been maintained in human populations through pathogen-driven balancing selection, as lacking mucosal antigens prevents certain highly contagious viruses from binding to gastrointestinal cells.
Estimated prevalence by population
Global 30.2%; European 24.6%; African 24.8%; East Asian 99.2%; South Asian 49.9%; Americas 37.7%; Ashkenazi 27.8%; Finnish 34.8%; Middle Eastern 16.9%; Amish 41.3%.
Estimated GG genotype frequency.
Global 47.6%; European 50.0%; African 50.0%; East Asian 0.8%; South Asian 41.5%; Americas 47.4%; Ashkenazi 49.8%; Finnish 48.4%; Middle Eastern 48.4%; Amish 45.9%.
Estimated GA genotype frequency.
Global 22.2%; European 25.4%; African 25.2%; East Asian < 0.1%; South Asian 8.6%; Americas 14.9%; Ashkenazi 22.3%; Finnish 16.8%; Middle Eastern 34.7%; Amish 12.8%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Nutrition & Metabolism
Vitamin & Mineral Metabolism
Vitamin B12 Levels. Evidence: 9/10. Source: PMID 18776911. Lower B12 Levels.
Immunity & Inflammation
Chronic Inflammatory Diseases
Crohn's Disease. Evidence: 6/10. Source: PMID 20570966. Lower Risk.
Infection Susceptibility & Resistance
Norovirus Resistance. Evidence: 3/10. Source: PMID 30376117. Typical Risk.
Organ Systems
Digestive & Gut Disorders
Gut Microbiome. Evidence: 4/10. Source: PMID 33462482. Healthy Secretor.
Cardiovascular & Metabolic
Lipids & Cholesterol
Cholesterol Levels. Evidence: 7/10. Source: PMID 35213538. Lower Cholesterol.
Showing effects for A/A genotype
Vitamin B12 Levels. Evidence: 9/10. Source: PMID 18776911. Higher B12 Levels.
Crohn's Disease. Evidence: 6/10. Source: PMID 20570966. Higher Risk.
Norovirus Resistance. Evidence: 3/10. Source: PMID 30376117. Highly Resistant.
Gut Microbiome. Evidence: 4/10. Source: PMID 33462482. Non-Secretor Profile.
Cholesterol Levels. Evidence: 7/10. Source: PMID 35213538. Higher Cholesterol.
Showing effects for G/A genotype
Vitamin B12 Levels. Evidence: 9/10. Source: PMID 18776911. Typical B12 Levels.
Crohn's Disease. Evidence: 6/10. Source: PMID 20570966. Typical Risk.
Cholesterol Levels. Evidence: 7/10. Source: PMID 35213538. Typical.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Full enzyme activity ensures that fucose sugars are abundantly secreted onto mucosal linings, providing a vital prebiotic source that nourishes beneficial gut microbes [1]. This active secretor status is highly protective against inflammatory bowel conditions like Crohn's disease [2]. However, the presence of these mucosal sugars also provides docking sites for pathogens, making individuals with this genotype more susceptible to norovirus and rotavirus infections [3]. Additionally, active secretors consistently show lower baseline levels of circulating vitamin B12, possibly due to differences in gut absorption pathways [4]. Maintaining a diet rich in B12 can help offset this natural metabolic tendency.
Active secretor status; Lower baseline vitamin B12; Typical susceptibility to stomach flu; Lower risk of Crohn's disease.
Sample genotype: AA (Homozygous)
Two copies of the inactive A allele result in a non-secretor phenotype, meaning mucosal surfaces lack the fucose sugars that many pathogens use to bind and infect cells [1]. This lack of binding sites provides robust, natural resistance to common stomach flu strains like norovirus [1]. On the other hand, the absence of these prebiotic sugars can compromise gut microbiome diversity, leading to lower levels of friendly Bifidobacteria [2]. This altered gut environment is associated with an increased risk of inflammatory bowel diseases, including Crohn's disease and ulcerative colitis [3]. Interestingly, non-secretors consistently exhibit significantly higher circulating levels of vitamin B12, likely due to altered absorption dynamics in the gut [4].
Non-secretor status; Higher baseline vitamin B12; Strong resistance to norovirus; Increased risk of Crohn's disease.
Sample genotype: GA (Heterozygous)
A single copy of the functional G allele is generally sufficient to maintain active secretor status, meaning fucose sugars are still secreted into the digestive tract [1]. This supports a healthy, diverse gut microbiome with adequate levels of beneficial Bifidobacteria [2]. Baseline vitamin B12 levels tend to fall into the typical range, avoiding the lower extremes seen in G/G homozygotes [3]. While this genotype remains susceptible to common gastrointestinal viruses like norovirus, it also maintains a typical, non-elevated risk for autoimmune and inflammatory bowel diseases [4]. Overall, this represents a balanced, highly common genetic profile.
Active secretor status; Typical vitamin B12 levels; Typical susceptibility to stomach flu; Typical risk of Crohn's disease.
Variants with shared genetic architecture
rs516246 · FUT2 Gene · Chr 19 · Gut Health and Immunity
rs1047781 · FUT2 Gene · Chr 19 · Norovirus and Gut Health
rs492602 · FUT2 Gene · Chr 19 · Cholesterol and Gut Health
Widespread balancing selection and pathogen-driven selection at blood group antigen genes.
Fucosyltransferase 2 (FUT2) non-secretor status is associated with Crohn's disease.
Common variants of FUT2 are associated with plasma vitamin B12 levels.
FUT2 Genetic Variants and Reported Respiratory and Gastrointestinal Illnesses During Infancy.
Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway.
Content updated August 2026.
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