What you carry at this position in your DNA and what research says about it.
Weight and Diabetes Risk: 10/10 evidence, 70 publications.
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Sample genotype (not yours): C/C
Typical Weight and Diabetes Risk
This genotype is associated with a baseline predisposition to typical body mass index and metabolic health. It does not carry the risk-increasing alleles that elevate appetite or weight gain.
What this genotype means: Typical metabolic rate; Standard baseline risk for type 2 diabetes.
Sample genotype (not yours): A/A
Increased Weight and Diabetes Risk
Carrying two copies of the A allele is associated with a higher average body mass index and an increased risk of type 2 diabetes.
What this genotype means: Higher average body mass index; Increased susceptibility to weight gain; Elevated risk of type 2 diabetes.
Sample genotype (not yours): C/A
Slightly Increased Weight and Diabetes Risk
Carrying one copy of the A allele is linked to a modest increase in average body mass index and a slightly higher risk of type 2 diabetes.
What this genotype means: Slightly elevated appetite drive; Modestly increased susceptibility to weight gain.
Gene function and biological role
Gene Function: The FTO gene encodes an enzyme that acts as an essential regulator of energy homeostasis and body fat accumulation. It is highly expressed in the brain regions that control appetite, where it influences food intake and satiety signaling. Genetic variations in this gene are among the most robustly replicated signals linked to common obesity and body mass index in diverse populations [1]. Research indicates that FTO plays a role in nucleic acid demethylation, thereby modulating the expression of downstream genes involved in mitochondrial function and thermogenesis [2].
Variant Impact: This variant is an intronic change located within a critical regulatory block of the FTO gene. It does not alter the protein sequence directly but acts as an expression modulator, influencing how actively the gene is transcribed. The risk-associated A allele is consistently linked to increased food intake and a preference for calorie-dense foods [3]. This genetic shift alters the regulatory landscape of the region, affecting metabolic pathways and adiposity traits across various age groups [4].
Key Insight: This variant influences body weight primarily by altering appetite and food intake patterns rather than slowing down how the body burns energy.
Location: FTO. Chromosome 16 · 16q12.2 · 53.8 Mb
Estimated prevalence by population
Global 36.9%; European 35.1%; African 31.7%; East Asian 71.9%; South Asian 47.0%; Americas 47.6%; Ashkenazi 24.5%; Finnish 36.1%; Middle Eastern 37.9%; Amish 28.8%.
Estimated CC genotype frequency.
Global 47.1%; European 48.3%; African 49.2%; East Asian 25.8%; South Asian 43.1%; Americas 42.8%; Ashkenazi 50.0%; Finnish 48.0%; Middle Eastern 47.3%; Amish 49.7%.
Estimated CA genotype frequency.
Global 16.1%; European 16.6%; African 19.1%; East Asian 2.3%; South Asian 9.9%; Americas 9.6%; Ashkenazi 25.5%; Finnish 15.9%; Middle Eastern 14.8%; Amish 21.5%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Obesity & Body Composition
Body Mass Index. Evidence: 10/10. Source: PMID 19079260. Typical BMI.
Obesity. Evidence: 6/10. Source: PMID 21706003. Typical Risk.
Body Weight. Evidence: 6/10. Source: PMID 19079260. Typical Weight.
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463248. Typical Risk.
Showing effects for A/A genotype
Body Mass Index. Evidence: 10/10. Source: PMID 19079260. Higher BMI.
Obesity. Evidence: 6/10. Source: PMID 21706003. ~1.5x Increased Risk.
Body Weight. Evidence: 6/10. Source: PMID 19079260. Higher.
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463248. ~1.4x Increased Risk.
Showing effects for C/A genotype
Body Mass Index. Evidence: 10/10. Source: PMID 19079260. Slightly Higher BMI.
Obesity. Evidence: 6/10. Source: PMID 21706003. Increased Risk.
Body Weight. Evidence: 6/10. Source: PMID 19079260. Slightly Higher.
Type 2 Diabetes. Evidence: 10/10. Source: PMID 17463248. ~1.2x Increased Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Carrying two copies of the C allele represents the typical genetic baseline for this metabolic locus. Large-scale genome-wide association studies show that this genotype is associated with a lower average body mass index and body weight compared to carriers of the A allele [1]. Individuals with this profile do not experience the genetically driven increases in food intake or fat accumulation linked to the variant form [2]. Consequently, the risk of developing type 2 diabetes remains at the standard population baseline [3]. This genotype is highly common globally, helping maintain typical metabolic signaling and energy balance under standard dietary conditions.
Typical metabolic rate; Standard baseline risk for type 2 diabetes.
Sample genotype: AA (Homozygous)
This genotype represents the highest risk category at this specific genetic marker. Carrying two copies of the A allele is associated with an approximate 1.4-fold increase in the risk of developing type 2 diabetes [1]. Clinical studies show a strong correlation with higher body mass index, increased body fat, and elevated overall body weight [2]. This genetic influence is primarily driven by altered appetite signaling, which can lead to increased food intake and a preference for high-calorie foods [3]. Despite this genetic predisposition, clinical trials suggest that the impact of this variant can be significantly mitigated through regular exercise and structured dietary interventions.
Higher average body mass index; Increased susceptibility to weight gain; Elevated risk of type 2 diabetes.
Sample genotype: CA (Heterozygous)
This heterozygous genotype is associated with intermediate metabolic effects between the typical and high-risk profiles. Having one copy of the A allele is linked to a roughly 1.2-fold increase in the risk of developing type 2 diabetes [1]. Research indicates that this variant influences appetite regulation, potentially leading to slightly higher overall calorie intake [2]. Studies across diverse ancestral groups confirm a modest but consistent upward shift in average body mass index and body fat percentage [3]. While this genetic predisposition plays a role, its impact is highly modifiable by regular physical activity and dietary habits.
Slightly elevated appetite drive; Modestly increased susceptibility to weight gain.
Variants with shared genetic architecture
rs11075995 · FTO Gene · Chr 16 · Breast Cancer Risk
rs11642015 · FTO Gene · Chr 16 · Weight and Diabetes Risk
rs1421085 · FTO Gene · Chr 16 · Obesity and Weight Gain
Genome-wide association analysis of body mass in chronic obstructive pulmonary disease.
Content updated August 2026.
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