What you carry at this position in your DNA and what research says about it.
Obesity Risk: 8/10 evidence, 62 publications.
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Sample genotype (not yours): T/T
Typical Obesity and Diabetes Risk
Possessing two copies of the T allele is associated with a typical body mass index and a lower risk of obesity and type 2 diabetes. This genotype promotes healthy appetite control and normal satiety responses after eating.
What this genotype means: Typical satiety and appetite control; Lower baseline body mass index; Reduced risk of type 2 diabetes.
Sample genotype (not yours): A/A
Significantly Increased Obesity and Diabetes Risk
Inheriting two copies of the A allele is associated with a higher body mass index and a significantly increased risk of obesity and type 2 diabetes. This genotype is linked to reduced satiety and a stronger drive to consume calorie-dense foods.
What this genotype means: Higher average body mass index; Reduced satiety and stronger food cravings; Significantly increased risk of type 2 diabetes.
Sample genotype (not yours): T/A
Moderately Increased Obesity and Diabetes Risk
Possessing a single copy of the A allele is linked to a moderately higher body mass index and an increased risk of type 2 diabetes. It may slightly reduce feelings of fullness after meals, leading to a preference for calorie-dense foods.
What this genotype means: Moderately higher average body mass index; Slightly reduced satiety after meals; Increased risk of type 2 diabetes.
Gene function and biological role
Gene Function: FTO stands for fat mass and obesity-associated gene. It is highly expressed in the brain, particularly in the hypothalamus, which regulates appetite and energy balance [1]. The FTO protein acts as an enzyme that modifies RNA, influencing how genes involved in metabolism are read [2]. Research has shown that FTO plays a critical role in controlling food intake, satiety, and energy expenditure [3]. Variants within this gene are among the most heavily studied genetic factors linked to body mass index and metabolic health [2].
Variant Impact: The rs9939609 variant is a single nucleotide polymorphism located in the first intron of the FTO gene [2]. Although it is an intron variant and does not directly alter the FTO protein structure, it is in strong linkage disequilibrium with causal variants that act as enhancers [4]. These enhancers influence the expression of FTO and neighboring genes like IRX3, which are involved in turning energy-storing white fat into energy-burning beige fat [4]. The risk-associated A allele is linked to increased appetite, reduced satiety, and a higher preference for calorie-dense foods [5].
Key Insight: The FTO gene primarily influences body weight by altering brain chemistry related to appetite and satiety, rather than slowing down resting metabolism. Personalized genetic feedback has been shown to help carriers of the risk allele lose more weight by increasing their motivation to adhere to diet and exercise programs.
Location: FTO. Chromosome 16 · 16q12.2 · 53.8 Mb
Origin Story: The thrifty gene hypothesis suggests that variants promoting fat storage, such as the FTO risk allele, were historically advantageous during periods of famine. These variants helped ancestral populations survive starvation by maximizing energy conservation, though they predispose individuals to obesity in modern environments with abundant food.
Estimated prevalence by population
Global 35.5%; European 35.1%; African 27.2%; East Asian 71.4%; South Asian 46.9%; Americas 46.9%; Ashkenazi 24.4%; Finnish 36.1%; Middle Eastern 37.9%; Amish 28.8%.
Estimated TT genotype frequency.
Global 47.3%; European 48.3%; African 49.9%; East Asian 26.2%; South Asian 43.1%; Americas 43.1%; Ashkenazi 50.0%; Finnish 48.0%; Middle Eastern 47.3%; Amish 49.7%.
Estimated TA genotype frequency.
Global 17.2%; European 16.6%; African 22.9%; East Asian 2.4%; South Asian 9.9%; Americas 9.9%; Ashkenazi 25.6%; Finnish 15.9%; Middle Eastern 14.8%; Amish 21.5%.
Estimated AA genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Obesity & Body Composition
Obesity. Evidence: 8/10. Source: PMID 17434869. Lower Risk.
Appetite Regulation. Evidence: 3/10. Source: PMID 28712975. Typical Satiety.
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 6/10. Source: PMID 17554300. Lower Risk.
Metabolic Syndrome & Insulin Resistance
Metabolic Syndrome. Evidence: 6/10. Source: PMID 38201907. Lower Risk.
Heart Disease
Cardiovascular Risk. Evidence: 6/10. Source: PMID 26555680. Typical Risk.
Showing effects for A/A genotype
Obesity. Evidence: 8/10. Source: PMID 17434869. High Risk.
Appetite Regulation. Evidence: 3/10. Source: PMID 28712975. Lowest Satiety.
Type 2 Diabetes. Evidence: 6/10. Source: PMID 17554300. ~1.6x Risk.
Metabolic Syndrome. Evidence: 6/10. Source: PMID 38201907. High Risk.
Cardiovascular Risk. Evidence: 6/10. Source: PMID 26555680. High Risk.
Showing effects for T/A genotype
Obesity. Evidence: 8/10. Source: PMID 17434869. Increased Risk.
Appetite Regulation. Evidence: 3/10. Source: PMID 28712975. Reduced Satiety.
Type 2 Diabetes. Evidence: 6/10. Source: PMID 17554300. ~1.3x Risk.
Metabolic Syndrome. Evidence: 6/10. Source: PMID 38201907. Increased Risk.
Cardiovascular Risk. Evidence: 6/10. Source: PMID 26555680. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Possessing two copies of the T allele protects against obesity and type 2 diabetes compared to carrying the A allele [1]. Studies indicate that individuals with this genotype experience normal satiety, meaning they feel full more easily after meals and are less prone to overeating [2]. This genotype is also linked to a lower baseline body mass index (BMI) and smaller waist circumference [3]. Furthermore, research suggests that T/T carriers have a lower risk of developing metabolic syndrome and cardiovascular complications [4]. Your body is genetically predisposed to regulate appetite and energy balance efficiently, making weight management more straightforward under typical lifestyle conditions [5].
Typical satiety and appetite control; Lower baseline body mass index; Reduced risk of type 2 diabetes.
Sample genotype: AA (Homozygous)
Inheriting the A allele from both parents is strongly associated with an increased risk of obesity and a higher average body mass index (BMI) [1]. This genotype is also linked to a roughly 1.6-fold increase in the risk of developing type 2 diabetes [2]. The biological mechanism involves altered appetite regulation in the hypothalamus, which reduces the feeling of fullness after eating and increases cravings for high-fat, energy-dense foods [3]. Individuals with the A/A genotype weigh, on average, about 3 kilograms more than those with the T/T genotype [1]. Despite this genetic predisposition, clinical trials show that carriers of the A/A genotype can lose weight just as effectively as others through targeted diet and exercise programs [4]. In fact, some studies suggest that personalized genetic feedback can enhance motivation and lead to greater weight loss success [5].
Higher average body mass index; Reduced satiety and stronger food cravings; Significantly increased risk of type 2 diabetes.
Sample genotype: TA (Heterozygous)
Possessing a single copy of the A allele is associated with a moderate increase in body mass index (BMI) and a higher risk of obesity [1]. This genotype is also linked to a roughly 1.3-fold increase in the risk of developing type 2 diabetes [2]. Research suggests that the A allele influences appetite regulation in the brain, often leading to reduced satiety and a higher preference for high-fat or sugary foods [3]. Individuals with this genotype may find themselves more responsive to food cues and prone to overeating [4]. However, lifestyle interventions, such as a high-protein diet or regular physical activity, have been shown to effectively mitigate these genetic risks [5]. Knowing you carry this variant can help you adopt proactive dietary habits to maintain metabolic health [6].
Moderately higher average body mass index; Slightly reduced satiety after meals; Increased risk of type 2 diabetes.
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
The FTO Gene and Measured Food Intake in 5- to 10-Year-Old Children Without Obesity.
Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls.
Content updated August 2026.
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