What you carry at this position in your DNA and what research says about it.
Obesity and BMI Risk: 7/10 evidence, 17 publications.
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Sample genotype (not yours): A/A
Typical Body Weight and BMI
This genotype is associated with a typical body weight and a standard genetic risk for obesity. You carry two copies of the protective A allele, which is the most common genetic profile.
What this genotype means: Typical genetic risk for obesity; Lower average body mass index; Standard waist-to-hip ratio.
Sample genotype (not yours): A/G
Slightly Higher Risk of Weight Gain
Carrying one copy of the G allele is associated with a slightly higher average body mass index and an increased predisposition to weight gain. Regular physical activity and dietary choices can successfully manage this genetic tendency.
What this genotype means: Slightly higher average body mass index; Increased susceptibility to weight gain; Appetite patterns may favor calorie-dense foods.
Sample genotype (not yours): G/G
Higher Risk of Weight Gain and Obesity
Carrying two copies of the G allele is linked to a higher average body mass index and a stronger genetic predisposition to obesity. Proactive lifestyle strategies, such as regular exercise and mindful eating, are highly effective at counteracting this genetic risk.
What this genotype means: Higher average body mass index; Increased genetic risk for obesity; Stronger predisposition to carrying abdominal fat.
Gene function and biological role
Gene Function: The FTO gene encodes an alpha-ketoglutarate dependent dioxygenase that plays a critical role in regulating energy homeostasis, appetite, and body fat accumulation [1]. It is highly expressed in the hypothalamus, a brain region that controls feeding behavior and satiety. Research shows that variants in this gene can influence food intake, particularly a preference for energy-dense foods [2]. Lifestyle interventions such as exercise and diet can significantly modulate the genetic risk associated with FTO variants [3].
Variant Impact: The rs9930506 variant is an intronic single nucleotide polymorphism located within the first intron of the FTO gene. This specific genomic region acts as a transcriptional enhancer that interacts with downstream genes involved in mitochondrial function and thermogenesis. The presence of the risk allele is associated with altered epigenetic methylation patterns and increased expression of nearby genes, leading to a shift from energy-burning brown fat to energy-storing white fat [4]. Studies have consistently linked this variant to differences in body mass index and waist circumference across diverse populations [5].
Key Insight: Carriers of the G allele may experience a higher baseline appetite and a natural preference for calorie-dense foods, but intensive lifestyle changes can completely offset this genetic predisposition.
Location: FTO. Chromosome 16 · 16q12.2 · 53.8 Mb
Estimated prevalence by population
Global 42.6%; European 30.9%; African 63.3%; East Asian 63.3%; South Asian 33.2%; Americas 46.4%; Ashkenazi 21.3%; Finnish 34.2%; Middle Eastern 40.0%; Amish 28.8%.
Estimated AA genotype frequency.
Global 43.5%; European 49.4%; African 32.5%; East Asian 32.5%; South Asian 48.8%; Americas 43.4%; Ashkenazi 49.7%; Finnish 48.6%; Middle Eastern 46.5%; Amish 49.7%.
Estimated AG genotype frequency.
Global 13.9%; European 19.7%; African 4.2%; East Asian 4.2%; South Asian 18.0%; Americas 10.2%; Ashkenazi 29.0%; Finnish 17.3%; Middle Eastern 13.5%; Amish 21.5%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Obesity & Body Composition
Body Mass Index. Evidence: 6/10. Source: PMID 17658951. Typical BMI.
Obesity. Evidence: 7/10. Source: PMID 40465716. Typical Risk.
Body Weight. Evidence: 4/10. Source: PMID 17658951. Typical Weight.
Waist-to-Hip Ratio. Evidence: 4/10. Source: PMID 17658951. Typical Ratio.
Heart Disease
Heart Health. Evidence: 6/10. Source: PMID 35915156. Typical Risk.
Showing effects for A/G genotype
Body Mass Index. Evidence: 6/10. Source: PMID 17658951. Slightly Higher BMI.
Obesity. Evidence: 7/10. Source: PMID 40465716. Increased Risk.
Body Weight. Evidence: 4/10. Source: PMID 17658951. Slightly Higher.
Waist-to-Hip Ratio. Evidence: 4/10. Source: PMID 17658951. Slightly Higher.
Heart Health. Evidence: 6/10. Source: PMID 35915156. Slightly Higher Risk.
Showing effects for G/G genotype
Body Mass Index. Evidence: 6/10. Source: PMID 17658951. Higher BMI.
Obesity. Evidence: 7/10. Source: PMID 40465716. Higher Risk.
Body Weight. Evidence: 4/10. Source: PMID 17658951. Higher Weight.
Waist-to-Hip Ratio. Evidence: 4/10. Source: PMID 17658951. Higher Ratio.
Heart Health. Evidence: 6/10. Source: PMID 35915156. Higher Risk.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Having two copies of the A allele is linked to a typical body mass index (BMI) and lower overall body fat accumulation compared to carriers of the G allele [1]. Large-scale genome-wide association studies have consistently shown that individuals with this genotype tend to have a lower baseline risk for obesity-related complications [2]. Research indicates that this genetic profile is associated with lower levels of promoter methylation in metabolic genes like PPARGC1A, which may support healthier metabolic programming [3]. While genetics play a role, maintaining a balanced diet and regular physical activity remain the most effective ways to support long-term metabolic health. This genotype is highly common across most global populations, especially in East Asian ancestries where the protective allele is highly prevalent [4]. Individuals with this profile typically do not experience the genetically driven appetite increases seen in G allele carriers. Consequently, maintaining a stable weight may feel more intuitive or straightforward. Overall, this genetic profile represents the baseline standard for metabolic risk at this locus.
Typical genetic risk for obesity; Lower average body mass index; Standard waist-to-hip ratio.
Sample genotype: AG (Heterozygous)
Carrying a single copy of the G allele is associated with a modest increase in body mass index (BMI) and overall body weight [1]. Studies show that each copy of the G allele can incrementally raise body weight and waist circumference by influencing appetite regulation and fat storage mechanisms [2]. This genetic variant is located within the FTO gene, which is highly active in brain regions controlling hunger and satiety, potentially leading to a preference for calorie-dense foods [3]. However, clinical trials demonstrate that lifestyle modifications, including intensive exercise and dietary adjustments, are highly effective at mitigating this genetic risk [4]. Individuals with this genotype can achieve and maintain a healthy weight through consistent healthy habits, as genetics are only one piece of the puzzle. Regular physical activity has been shown to be particularly powerful in overriding the genetic predisposition to weight gain. Mindful eating practices can also help manage any subtle increases in appetite. Ultimately, this genetic profile serves as a gentle reminder to prioritize daily movement and balanced nutrition.
Slightly higher average body mass index; Increased susceptibility to weight gain; Appetite patterns may favor calorie-dense foods.
Sample genotype: GG (Homozygous)
Having two copies of the G allele is associated with the highest genetic risk for elevated body mass index (BMI) and obesity at this locus [1]. On average, individuals with the G/G genotype weigh more and have larger waist circumferences than those with the A/A genotype [2]. This genetic variant influences how the body regulates appetite and stores fat, often predisposing individuals to a higher baseline appetite and a preference for energy-dense foods [3]. Additionally, this genotype is associated with an increased risk of developing obesity-related metabolic conditions, including coronary artery disease [4]. Despite this genetic predisposition, intensive lifestyle interventions, such as structured exercise programs and dietary changes, have been shown to significantly reduce or even eliminate the weight-related effects of this variant [5]. Engaging in regular physical activity is particularly beneficial for individuals with this genetic profile. Establishing consistent, healthy habits can completely offset the genetic tendency toward weight gain. Understanding this risk allows for proactive, personalized wellness planning. With the right strategies, maintaining a healthy weight is entirely achievable.
Higher average body mass index; Increased genetic risk for obesity; Stronger predisposition to carrying abdominal fat.
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
Maternal pregestational BMI is associated with methylation of the PPARGC1A promoter in newborns.
Genetic analyses of diverse populations improves discovery for complex traits.
Content updated August 2026.
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