What you carry at this position in your DNA and what research says about it.
Obesity and Weight Gain: 9/10 evidence, 47 publications.
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Sample genotype (not yours): G/G
Typical Obesity Risk and Standard Metabolism
A typical body weight profile and standard metabolic rate are associated with this genotype. This profile does not carry the elevated genetic risk for obesity or higher body mass index linked to this variant.
What this genotype means: Typical baseline risk for obesity; Standard appetite regulation and leptin levels; Slightly higher risk of breast cancer.
Sample genotype (not yours): A/A
Moderately Increased Obesity Risk
A moderately higher body mass index and an increased likelihood of obesity are associated with this genotype. This variation can significantly affect appetite control and metabolic efficiency, requiring more conscious weight management.
What this genotype means: Moderately higher average body mass index; Increased risk of obesity and higher fat mass; Elevated blood sugar and triglyceride levels.
Sample genotype (not yours): G/A
Slightly Increased Obesity Risk
A slightly higher body mass index and a modest increase in obesity risk are associated with this genotype. This variation can influence appetite and metabolic rate, making weight management slightly more challenging.
What this genotype means: Slightly higher average body mass index; Modestly increased risk of obesity; Slightly elevated blood sugar and lipid levels.
Gene function and biological role
Gene Function: The FTO gene encodes an RNA demethylase that plays a critical role in energy homeostasis and appetite regulation [1]. It is highly expressed in the hypothalamus, a brain region involved in controlling hunger and satiety [2]. Variations in this gene are strongly linked to differences in body mass index and susceptibility to obesity [3]. Research suggests that FTO helps regulate food intake and dietary preferences, particularly for energy-dense foods [4].
Variant Impact: An intronic nucleotide change at rs1121980 acts as a major genetic marker for body weight regulation [3]. This change is thought to alter the expression of FTO or neighboring genes, thereby influencing metabolic rate and appetite [5]. Carrying the A allele is consistently associated with higher body mass index and elevated obesity risk across diverse populations [6]. Conversely, the G allele is linked to a lower risk of obesity but shows a slight association with other traits like altered puberty timing [7].
Key Insight: Physical activity can almost entirely offset the genetic predisposition to weight gain associated with this variant.
Location: FTO. Chromosome 16 · 16q12.2 · 53.8 Mb
Estimated prevalence by population
Global 32.6%; European 31.7%; African 27.7%; East Asian 64.5%; South Asian 34.5%; Americas 41.5%; Ashkenazi 20.0%; Finnish 32.3%; Middle Eastern 35.1%; Amish 26.6%.
Estimated GG genotype frequency.
Global 48.4%; European 49.2%; African 49.9%; East Asian 31.6%; South Asian 48.5%; Americas 45.8%; Ashkenazi 49.4%; Finnish 49.1%; Middle Eastern 48.3%; Amish 50.0%.
Estimated GA genotype frequency.
Global 19.0%; European 19.1%; African 22.4%; East Asian 3.9%; South Asian 17.0%; Americas 12.6%; Ashkenazi 30.6%; Finnish 18.7%; Middle Eastern 16.6%; Amish 23.5%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Obesity & Body Composition
Obesity. Evidence: 6/10. Source: PMID 18159244. Typical Risk.
Body Mass Index. Evidence: 9/10. Source: PMID 18454148. Typical BMI.
Appetite Regulation. Evidence: 6/10. Source: PMID 32917775. Typical Leptin.
Diabetes & Glycemic Traits
Blood Glucose. Evidence: 8/10. Source: PMID 34594039. Typical Levels.
Lipids & Cholesterol
Blood Lipid Levels. Evidence: 6/10. Source: PMID 24097068. Typical Lipids.
Cancer & Oncology
Breast Cancer
Breast Cancer. Evidence: 6/10. Source: PMID 38538606. Slightly Higher Risk.
Showing effects for A/A genotype
Obesity. Evidence: 6/10. Source: PMID 18159244. ~2.76x Higher Risk.
Body Mass Index. Evidence: 9/10. Source: PMID 18454148. Higher BMI.
Appetite Regulation. Evidence: 6/10. Source: PMID 32917775. Elevated Leptin.
Blood Glucose. Evidence: 8/10. Source: PMID 34594039. Elevated Levels.
Blood Lipid Levels. Evidence: 6/10. Source: PMID 24097068. Elevated Lipids.
Breast Cancer. Evidence: 6/10. Source: PMID 38538606. Lower Risk.
Showing effects for G/A genotype
Obesity. Evidence: 6/10. Source: PMID 18159244. ~1.67x Higher Risk.
Body Mass Index. Evidence: 9/10. Source: PMID 18454148. Slightly Higher BMI.
Appetite Regulation. Evidence: 6/10. Source: PMID 32917775. Slightly Elevated.
Blood Glucose. Evidence: 8/10. Source: PMID 34594039. Slightly Elevated.
Blood Lipid Levels. Evidence: 6/10. Source: PMID 24097068. Slightly Elevated.
Breast Cancer. Evidence: 6/10. Source: PMID 38538606. Typical Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
The G/G genotype represents the baseline genetic profile for this FTO variant [1]. This genotype is associated with a typical body mass index and a lower risk of early-onset obesity compared to carriers of the A allele [2]. Research indicates that individuals with this profile have standard levels of appetite-regulating hormones like leptin [3]. They also tend to show a higher response to weight-loss interventions, such as hypocaloric diets, compared to those carrying the risk allele [4]. However, this genotype is associated with a slightly higher risk of breast cancer in some studies [5]. Overall, this genetic profile supports standard metabolic health and typical weight management.
Typical baseline risk for obesity; Standard appetite regulation and leptin levels; Slightly higher risk of breast cancer.
Sample genotype: AA (Homozygous)
The A/A genotype is associated with a 2.76-fold increase in the risk of obesity compared to the typical genotype [1]. This genotype is strongly linked to higher body mass index, elevated waist-to-hip ratio, and increased fat mass [2]. The biological mechanism involves altered expression of the FTO gene, which can lead to higher levels of appetite-stimulating hormones and reduced satiety [3]. Individuals with this profile often show higher circulating leptin and triglyceride levels [4]. Dietary factors, particularly a high intake of saturated fats, can further amplify the weight-promoting effects of this genotype [5]. Conversely, engaging in regular physical activity is highly effective at reducing the genetic influence on body weight [6]. Managing diet and exercise is particularly important for individuals with this genetic profile to support long-term metabolic health.
Moderately higher average body mass index; Increased risk of obesity and higher fat mass; Elevated blood sugar and triglyceride levels.
Sample genotype: GA (Heterozygous)
The G/A genotype is associated with a 1.67-fold increase in the risk of obesity compared to the typical genotype [1]. This genetic variation is linked to higher average body mass index and increased waist-to-hip ratio [2]. Research suggests that the A allele may influence appetite regulation, leading to higher levels of the hormone leptin and a potential preference for energy-dense foods [3]. The metabolic impact of this variant is often more pronounced in individuals with a high intake of saturated fatty acids [4]. However, regular physical activity has been shown to significantly attenuate this genetic predisposition to weight gain [5]. Individuals with this genotype may also experience slightly higher blood sugar and triglyceride levels [6].
Slightly higher average body mass index; Modestly increased risk of obesity; Slightly elevated blood sugar and lipid levels.
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
Regulation of Fto/Ftm gene expression in mice and humans.
Genetic analyses of diverse populations improves discovery for complex traits.
Genetic Studies of Leptin Concentrations Implicate Leptin in the Regulation of Early Adiposity.
New role of fat-free mass in cancer risk linked with genetic predisposition.
New genetic loci link adipose and insulin biology to body fat distribution.
Discovery and refinement of loci associated with lipid levels.
Content updated August 2026.
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