What you carry at this position in your DNA and what research says about it.
Obesity and Weight Gain: 9/10 evidence, 51 publications.
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Sample genotype (not yours): T/T
Typical Weight and BMI Risk
A baseline genetic predisposition supports a typical body weight and standard metabolic rate. Maintaining a balanced lifestyle is generally highly effective for weight management.
What this genotype means: Typical baseline risk for obesity and elevated BMI; Standard metabolic response to dietary protein and fat; Typical waist circumference and blood pressure ranges.
Sample genotype (not yours): A/A
Higher Weight and BMI Risk
Two copies of the risk allele are linked to a significantly higher body weight and stronger appetite signals. Prioritizing a high-protein diet can be an effective strategy to manage this genetic risk.
What this genotype means: Significantly increased risk of higher BMI and severe obesity; Elevated risk of type 2 diabetes and high blood pressure; Strongest weight loss and fat reduction response to high-protein diets.
Sample genotype (not yours): T/A
Moderately Higher Weight and BMI Risk
A single copy of the risk allele is linked to a moderately higher body weight and increased appetite. Adopting a high-protein diet may help counteract this genetic predisposition.
What this genotype means: Moderately increased risk of higher BMI and obesity; Slightly elevated waist circumference and body fat percentage; Enhanced weight loss response to high-protein diets.
Gene function and biological role
Gene Function: The FTO gene encodes an enzyme that plays a critical role in regulating energy homeostasis, appetite, and body weight [1]. It is highly expressed in the brain's hypothalamus, which acts as the control center for hunger and satiety signals [2]. Research suggests that FTO influences how the body senses nutrients and decides whether to burn energy or store it as fat [3]. Variations within this gene are the most widely replicated genetic factors influencing common obesity across diverse populations [4]. Understanding FTO function helps clarify why some individuals experience stronger food cravings or find weight management more challenging [5].
Variant Impact: The rs1558902 variant is a single nucleotide change located within the first intron of the FTO gene [2]. Although it does not directly alter the protein structure, this non-coding variant acts as a regulatory element that influences the expression of FTO and neighboring genes [3]. The risk-associated A allele is strongly linked to higher body mass index, increased waist circumference, and elevated body fat percentage [4]. Interestingly, this variant is in tight linkage disequilibrium with other famous obesity-associated markers, making it a primary indicator of genetic weight predisposition [6]. Clinical trials have shown that the metabolic effects of this variant are highly sensitive to dietary protein intake, offering a personalized path for weight management [7].
Key Insight: While the A allele predisposes to weight gain, carriers of this variant actually lose significantly more weight and body fat on a high-protein diet compared to a low-protein diet.
Location: FTO. Chromosome 16 · 16q12.2 · 53.8 Mb
Origin Story: According to the thrifty genotype hypothesis, variants that promote efficient fat storage may have been evolutionary advantageous during historical periods of famine, though they contribute to obesity in modern environments of food abundance.
Estimated prevalence by population
Global 49.9%; European 34.0%; African 80.7%; East Asian 71.6%; South Asian 44.7%; Americas 50.6%; Ashkenazi 23.9%; Finnish 33.2%; Middle Eastern 38.3%; Amish 26.1%.
Estimated TT genotype frequency.
Global 38.6%; European 48.6%; African 18.3%; East Asian 26.0%; South Asian 44.3%; Americas 41.1%; Ashkenazi 50.0%; Finnish 48.8%; Middle Eastern 47.2%; Amish 50.0%.
Estimated TA genotype frequency.
Global 11.5%; European 17.4%; African 1.0%; East Asian 2.4%; South Asian 11.0%; Americas 8.3%; Ashkenazi 26.1%; Finnish 17.9%; Middle Eastern 14.5%; Amish 23.9%.
Estimated AA genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Obesity & Body Composition
Obesity. Evidence: 9/10. Source: PMID 20421936. Typical Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 20935630. Typical BMI.
Waist Circumference. Evidence: 9/10. Source: PMID 19557197. Typical.
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 8/10. Source: PMID 38374256. Typical Risk.
Hypertension
Hypertension. Evidence: 8/10. Source: PMID 39024449. Typical Risk.
Neurology & Mental Health
Sleep & Circadian Rhythm
Sleep Apnea. Evidence: 8/10. Source: PMID 39024449. Typical Risk.
Showing effects for A/A genotype
Obesity. Evidence: 9/10. Source: PMID 20421936. ~1.37x Higher Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 20935630. Significantly Higher.
Waist Circumference. Evidence: 9/10. Source: PMID 19557197. Significantly Increased.
Type 2 Diabetes. Evidence: 8/10. Source: PMID 38374256. Increased Risk.
Hypertension. Evidence: 8/10. Source: PMID 39024449. Increased Risk.
Sleep Apnea. Evidence: 8/10. Source: PMID 39024449. Increased Risk.
Showing effects for T/A genotype
Obesity. Evidence: 9/10. Source: PMID 20421936. Increased Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 20935630. Moderately Higher.
Waist Circumference. Evidence: 9/10. Source: PMID 19557197. Moderately Increased.
Type 2 Diabetes. Evidence: 8/10. Source: PMID 38374256. Slightly Increased.
Hypertension. Evidence: 8/10. Source: PMID 39024449. Slightly Increased.
Sleep Apnea. Evidence: 8/10. Source: PMID 39024449. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Carrying two copies of the common T allele is associated with a typical body mass index and a standard risk of obesity [1]. Research indicates that this genotype does not carry the elevated appetite signals or altered fat storage patterns seen in carriers of the risk variant [2]. Metabolic markers, including waist circumference and blood pressure, typically fall within standard baseline ranges [3]. Because there is no genetically driven increase in appetite, standard dietary guidelines and moderate physical activity are highly effective for maintaining long-term health [4]. Additionally, this genotype shows a standard response to various macronutrient ratios, meaning extreme dietary restrictions are rarely necessary for weight control [5].
Typical baseline risk for obesity and elevated BMI; Standard metabolic response to dietary protein and fat; Typical waist circumference and blood pressure ranges.
Sample genotype: AA (Homozygous)
Carrying two copies of the A risk allele is strongly associated with an elevated body mass index and a higher risk of severe obesity [1]. This genetic variant alters the expression of the FTO gene, which plays a central role in regulating appetite and energy balance in the hypothalamus [2]. Consequently, individuals with this genotype often experience stronger food cravings and a higher baseline body fat percentage [3]. Metabolic assessments also link this genotype to increased waist circumference and a higher risk of type 2 diabetes [4]. Despite these genetic challenges, clinical evidence reveals a powerful tool for weight management [5]. In long-term dietary studies, individuals with two risk alleles experienced the most pronounced weight loss and visceral fat reduction when adhering to a high-protein diet [5]. This highlights that genetic risk can be effectively managed through targeted nutritional strategies.
Significantly increased risk of higher BMI and severe obesity; Elevated risk of type 2 diabetes and high blood pressure; Strongest weight loss and fat reduction response to high-protein diets.
Sample genotype: TA (Heterozygous)
Carrying one copy of the A risk allele is associated with a moderately higher body mass index and an increased likelihood of obesity [1]. This genetic change in the first intron of the FTO gene is thought to influence appetite regulation in the brain, leading to increased food intake [2]. Studies show that individuals with this genotype tend to have a slightly larger waist circumference and elevated leptin levels [3]. However, clinical trials demonstrate that this genetic predisposition is highly modifiable by lifestyle choices [4]. Specifically, during dietary interventions, carriers of this allele achieved significantly greater weight loss and fat reduction when following a high-protein diet compared to a low-protein diet [5]. This suggests that dietary composition plays a crucial role in managing the genetic risk.
Moderately increased risk of higher BMI and obesity; Slightly elevated waist circumference and body fat percentage; Enhanced weight loss response to high-protein diets.
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
Genetic studies of body mass index yield new insights for obesity biology.
Variations in the FTO gene are associated with severe obesity in the Japanese.
New genetic loci link adipose and insulin biology to body fat distribution.
Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index.
Whole-Genome Sequencing Coupled to Imputation Discovers Genetic Signals for Anthropometric Traits.
Dietary Fat Modifies the Effects of FTO Genotype on Changes in Insulin Sensitivity.
New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk.
Genomic and drug target evaluation of 90 cardiovascular proteins in 30,931 individuals.
Content updated August 2026.
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